Disclaimer: I wrote a post based on notes I compiled in a text editor, formatted it, and accidentally hit the back button and lost all of my changes, so this thread may seem a bit all over the place and disorganized. I apologize for this in advance.
And I will first state: I do not encourage mass market junk cigarettes, I can't even smoke those. I smoke pure tobacco in a pipe, sometimes I roll it into a cigarette (no filter) if I'm driving long distances or out and about. Actually, this COVID hysteria situation caused the local tobacco store to close down and I had to go to the pipe shop that sells moist, flavored tobacco. Shops will usually sell cheap, large bags of rolling tobacco (pure, dry, additive-free tobacco) relabelled as "pipe tobacco" to avoid taxes. This addition of more flavored, regular pipe tobacco might be giving me more issues, or maybe not. An increased mucous layer could help to pathogens away from the epithelial cells, thereby protecting it. That is why towards the end of a cold (another coronavirus) the mucus layer is coughed up. This is just my theorizing and I could be mistaken, so I will get on to the point:
Are tobacco smokers [all else equal] better off when it comes to COVID-19?
If you contract COVID-19 as a smoker and are taken to the hospital and deprived your ability to smoke, could that actually exacerbate the respiratory issues?
Should already-smokers cut down or try to quit entirely during this outbreak, or even increase their smoking rates (along with additional vitamins)?
There is also more touching of the face when it comes to smokers. Many confounding variables exist here that can muddy the results of this sort of research.
I say "all else equal" because people who smoke tobacco are often worse off in many health categories, so it is not scientifically sound to statistically compare COVID reactions in smokers versus non-smokers and make conclusions regarding a causal role of smoking. The main issue I see here we have with the data is that these are correlations in non-randomized samples, not taking into account that tobacco smokers are on average poorer, eat less healthy foods, exercise less, do more drugs, are more sleep deprived, etc. One can claim it's BECAUSE they smoke, but you can use that same "logic" to "prove" that people who take allergy medications have more runny noses, but actually these drugs are protective. All-in-all, tobacco smokers are a group who are generally less health conscious.
Ray peat: "Stress seems to be perceived as a need for sugar. In the absence of sucrose, satisfying this need with starch and fat is more likely to lead to obesity."
This should also apply to smokers, who go take a smoke break when they feel stressed. This is a self-medication mechanism. To date, there are no randomized controlled trials on humans showing that smokers have higher cancer rates or die sooner. Many centenarians smoked, the oldest man (Shigechiyo Izumi or Christian Mortensen), oldest woman (Madamme Jeanne Calment, smoked since teens), and marathon runner (Buster Martin, smoked since 7) were smokers.
The animal studies (the only randomized trials we have on this) show that smoking animals live longer, about 20%, compared to non-smoking animals. Randomized intervention trials also failed to show benefits for cessation.
Now, some info on COVID and smoking I have located:
- A 19 Feb 2020 study on COVID in 140 Chinese patients found a: "lower incidence of COVID‐19 in current smokers" Clinical characteristics of 140 patients infected with SARS-CoV-2 in Wuhan, China. - PubMed - NCBI
- An 4 Apr 2020 study on COVID, "Smoking, vaping and hospitalization for COVID-19" found:
"A systematic research of the literature (PubMed) was performed on April 1. Out of 432 studies, we identified 13 studies examining the clinical characteristics of a total of 5960 hospitalized COVID-19 patients that presented data on the smoking status...
This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19. Instead, these consistent observations, which are further emphasized by the low prevalence of current smoking among COVID-19 patients in the US (1.3%), raises the hypothesis that nicotine may have beneficial effects on COVID-19
... no recommendation can be currently made concerning the effects of smoking on the risk of hospitalization for COVID-19. In fact, the consistently low prevalence of current smoking among Chinese patients with COVID-19 was further supported by the recent data recently released from the US CDC.28 From a total of 7162 patients in the US, only 1.3% were current smokers. low smoking prevalence was also observed among hospitalized non-ICU (2.1%) and ICU cases (1.1%), while the population smoking prevalence in the US is 13.8%. These observations raise a possible hypothesis that nicotine might reduce the risk for severe COVID-19. Hospitalization for COVID-19 will inevitably result in abrupt withdrawal of nicotine and its beneficial effect linked to this hypothesis in smokers or users of other nicotine products. This could, at least partly, explain the association between smoking and COVID-19 severity among hospitalized patients.27 Nicotine has been found to prevent acute lung injury in an animal ARDS model and has immunomodulatory effects.29,30 There is also evidence for an interaction between nicotine and the renin-angiotensin-aldosterone axis, although such interactions remain unclear.2-5 In any case, the observations of a consistently low prevalence of smoking among COVID-19 cases in China and the US, together with the potential mechanisms through which nicotine interacts with the inflammatory process and the renin-angiotensin-aldosterone axis involved in the development of COVID-19, warrant an urgent investigation of the clinical effects of pharmaceutical nicotine on COVID-19 susceptibility, progression and severity. The potential need to provide pharmaceutical nicotine products to smokers who experience an abrupt withdrawal of nicotine when hospitalized for COVID-19 or aim to follow medical advice to quit smoking to relieve underlying conditions that may increase vulnerability to serious or fatal symptoms should also be examined." Smoking, vaping and hospitalization for COVID-19 - Article (Preprint v13) | Qeios
There is not too much info since this is such a new virus and there can really only be anti-smoking research published in the west today. But there are various studies showing that smokers exposed to dangerous inhalants were the least likely to have lung problems:
Protective and therapeutic effects of smoking on lung function in people exposed to environmental carcinogens -- predictably, ex-smokers were worst off:
"Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers" Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workers
- Smoking has a protective effect on immunological abnormalities in asbestos workers. See: Redirecting and: Redirecting
Also for asbestos workers, relative risk of lung cancer for asbestos workers was: "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant." Combined effect of asbestos and smoking on mortality from lung cancer and mesothelioma in factory workers. - PubMed - NCBI
In dogs exposed to carcinogen radon: While the radon alone had no problems in inducing lung cancers in dogs (or any other animals), the combined effect of tobacco smoke and radon resulted in significant protection against lung cancers in smoking dogs -- while the nonsmoking dogs exposed to radon had 37% incidence of lung tumors, the smoking dogs exposed to radon had only 5% lung tumor incidence: https://doi.org/10.1093/oxfordjournals.rpd.a083030
And:
"Results of this experiment indicate that cigarette-smoke exposure, under the conditions of the experiment, had a mitigating effect of radon-daughter induced respiratory tract cancer in dogs..." https://doi.org/10.1097/00004032-198201000-00004
More:
"The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers" The interaction of asbestos and smoking in lung cancer: a modified measure of effect. - PubMed - NCBI
and:
"Over the 22 years of follow-up, exposed workers have had a very high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has been much higher in nonsmokers and ex-smokers than in current smokers." The cigarette factor in lung cancer due to chloromethyl ethers. - PubMed - NCBI
and:
"Presence of chronic respiratory symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment was positively associated with smoking cessation." Smoking cessation among coal miners as predicted by baseline respiratory function and symptoms: a 5-year prospective study. - PubMed - NCBI
Nicotine stimulates and upregulates growth and branching of blood vessels (via upregulation of vascular growth factor), especially of capillaries, which improves the nutrient delivery and cleanup (antioxidant & detox enzyme supplies) to all tissues, including brain and skin (provided person's intake of nutrients and supplements is adequate -- it is probably the case that smokers need to increase intake of specific vitamins, like vitamin C, to compensate for their habit).
Tobacco smoke (not nicotine) also increases internal detox and antioxidant enzymes, glutathione, catalase and SOD to nearly double the levels. Specifically, some still unknown components of tobacco smoke upregulate substantially the key internal antioxidants and detox enzymes (glutathione [or more recent ref cf. Fig 4, p. L1076], upregulation of 16 internal antioxidants, plus catalase and SOD, all nearly doubled). These (families of) enzymes are responsible for neutralizing and excreting many environmental or industrial toxins and carcinogens we are exposed to (wiki: glutathione, SOD, catalase). I am not quite sure about the link of these enzymes with COVID-19.
Also, carbon monoxide in very low concentration (as delivered in tobacco smoke) may act as a signaling mechanism to increase blood circulation, oxygenation and reduce inflammation, helping prevent burnout and excitotoxic effects from stimulants or excessive work..
I recognize that CO is a poisonous gas that has been used in gas chambers, but we're talking about very low doses (see also on protective role of CO in pre-eclampsia and "Therapeutic CO" whitepaper, miracle medicine, mithochondrial ROS inhibition, protects against endotoxic shock, multiple sclerosis, IBD, hypertension, neurotransmitter, beneficial digestive effects...).
More info on potential benefits of very low dose CO:
- https://www.atsjournals.org/doi/full/10.1164/rccm.201309-1615ED
- Carbon monoxide is a poison. Can it also be a medicine?
- Carbon Monoxide Has Unexpected Benefits, But Dont Try It At Home
- Therapeutic Applications of Carbon Monoxide
Many more exist if you just google for it,
There are a lot of articles coming out now, jumping in on the anti-tobacco bandwagon, saying to quit smoking ASAP because of this COVID-19 outbreak. But as shown above, former smokers often were worse off than never smokers when it came to inhaling environmental contaminants.
There's also a study from india:
"Are lung cancers triggered by stopping smoking? The clinically high correlation between smoking and carcinoma of the lungs has been the focal point in societal campaigns against the habit and the tobacco lobby. In an overview of personal history in a number of lung cancer patients locally, we am struck by the more than casual relationship between the appearance of lung cancer – and an abrupt and recent cessation of the smoking habit in many, if not most cases. The association is more than just casual – development of cancer within a few months of eschewing cigarette smoking. Over a period of 4 years, a total of 312 cases were treated for carcinoma of pulmonary origin [...] Each one of had been addicted to the habit for no less than twenty-five years, smoking in excess of twenty sticks a day. The striking direct statistical correlation between cessation of smoking to the development of lung malignancies, more than 60% plus, is too glaring to be dismissed as coincidental." Are lung cancers triggered by stopping smoking? - PubMed - NCBI
In congruence with the above finding, randomized animal studies require the experimenters to quit smoking to actually observe lung cancer:
"The 4-month recovery period is absolutely necessary for observation of increased lung tumor multiplicity, but the reason for this is not clear."
Carcinogenicity studies of inhaled cigarette smoke in laboratory animals: old and new
So a "Recovery period" where they don't smoke is necessary to observe increased lung cancer, but smoking itself is the cause? Doesn't compute.
There is also this that I found:
"…While nicotine has anti-inflammatory properties in this disease, the therapeutic value of nicotine does not exceed that of more conventional treatments such as aminosalicylates.48
Therefore, while cells are present that are primed for activation, the immune and inflammatory response may be dampened, as has been observed in many smokers.62 Expanding upon this possibility, Floto and Smith64 suggested that the inflammatory response to the stimulatory components of tobacco may be counteracted by the anti-inflammatory effects of nicotine, which offers a rational explanation for why few smokers generate pulmonary Langerhans’ cell histiocytosis. It has also been pointed out that there is a significantly lower incidence of sarcoidosis in smokers65 and decreased incidence of immunoglobulin G (IgG) precipitins that develop during allergic alveolitis as occurs both in humans and guinea pigs.66,67…A notable outcome of this effect may be that the anti-inflammatory properties of nicotine actually enhance the survival of influenza virus in mice and induce significantly higher titers of virus following infection.63" Neuronal nicotinic acetylcholine receptor expression and function on nonneuronal cells. - PubMed - NCBI
COVID-19 is not an influenza though, even the common cold is a coronavirus.
According to a study on respiratory conditions of Whites, Amerindians, and White-Amerind mixed inidividuals it was found that the mixed group race had a higher rate of asthma, hay fever, sinusitis and COPD. With the exception of COPD, the difference between Amerindian-White mixes was larger than the difference between current and never smokers. Smoking status was highest in Amerindian-White mixes, and lowest in Whites. A comparison of respiratory conditions between multiple race adults and their single race counterparts: an analysis based on American Indian/Alaska... - PubMed - NCBI
But another confounding variable exists here, in that the highest frequency of eczema, and the highest frequency of EAH (eczema with asthma and/or hay fever) exists in "mixed raced" individuals (but sometimes Blacks, who are themselves a mixed group in the USA at 15-20% White admixture), even when controlled for smoking: Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. - PubMed - NCBI
Interesting, but inconclusive.
I will also point out that a curious genetic link: indeed, there are exactly known alleles within a nicotinic acetylcholine receptor gene cluster which simultaneously make people more likely to get lung cancer, as well as, independently make them more likely to smoke: https://www.nature.com/articles/nature06846
This is perhaps why the only two people I ever knew who had lung cancer: a young woman who contracted it in adolescence, and my 50+ year old aunt, neither were ever smokers.
This is a lot of information (there is much more I did not post) but I think a proper thread needs to exist on this subject - Tobacco smoking and COVID-19 - for those of us who do smoke and are now found in this pandemic situation. I would just like to hear some thoughts on the topic of people who are smoking and what they should do differently (if anything; in regards to smoking) during this COVID outbreak.
And I will first state: I do not encourage mass market junk cigarettes, I can't even smoke those. I smoke pure tobacco in a pipe, sometimes I roll it into a cigarette (no filter) if I'm driving long distances or out and about. Actually, this COVID hysteria situation caused the local tobacco store to close down and I had to go to the pipe shop that sells moist, flavored tobacco. Shops will usually sell cheap, large bags of rolling tobacco (pure, dry, additive-free tobacco) relabelled as "pipe tobacco" to avoid taxes. This addition of more flavored, regular pipe tobacco might be giving me more issues, or maybe not. An increased mucous layer could help to pathogens away from the epithelial cells, thereby protecting it. That is why towards the end of a cold (another coronavirus) the mucus layer is coughed up. This is just my theorizing and I could be mistaken, so I will get on to the point:
Are tobacco smokers [all else equal] better off when it comes to COVID-19?
If you contract COVID-19 as a smoker and are taken to the hospital and deprived your ability to smoke, could that actually exacerbate the respiratory issues?
Should already-smokers cut down or try to quit entirely during this outbreak, or even increase their smoking rates (along with additional vitamins)?
There is also more touching of the face when it comes to smokers. Many confounding variables exist here that can muddy the results of this sort of research.
I say "all else equal" because people who smoke tobacco are often worse off in many health categories, so it is not scientifically sound to statistically compare COVID reactions in smokers versus non-smokers and make conclusions regarding a causal role of smoking. The main issue I see here we have with the data is that these are correlations in non-randomized samples, not taking into account that tobacco smokers are on average poorer, eat less healthy foods, exercise less, do more drugs, are more sleep deprived, etc. One can claim it's BECAUSE they smoke, but you can use that same "logic" to "prove" that people who take allergy medications have more runny noses, but actually these drugs are protective. All-in-all, tobacco smokers are a group who are generally less health conscious.
Ray peat: "Stress seems to be perceived as a need for sugar. In the absence of sucrose, satisfying this need with starch and fat is more likely to lead to obesity."
This should also apply to smokers, who go take a smoke break when they feel stressed. This is a self-medication mechanism. To date, there are no randomized controlled trials on humans showing that smokers have higher cancer rates or die sooner. Many centenarians smoked, the oldest man (Shigechiyo Izumi or Christian Mortensen), oldest woman (Madamme Jeanne Calment, smoked since teens), and marathon runner (Buster Martin, smoked since 7) were smokers.
The animal studies (the only randomized trials we have on this) show that smoking animals live longer, about 20%, compared to non-smoking animals. Randomized intervention trials also failed to show benefits for cessation.
Now, some info on COVID and smoking I have located:
- A 19 Feb 2020 study on COVID in 140 Chinese patients found a: "lower incidence of COVID‐19 in current smokers" Clinical characteristics of 140 patients infected with SARS-CoV-2 in Wuhan, China. - PubMed - NCBI
- An 4 Apr 2020 study on COVID, "Smoking, vaping and hospitalization for COVID-19" found:
"A systematic research of the literature (PubMed) was performed on April 1. Out of 432 studies, we identified 13 studies examining the clinical characteristics of a total of 5960 hospitalized COVID-19 patients that presented data on the smoking status...
This preliminary analysis does not support the argument that current smoking is a risk factor for hospitalization for COVID-19. Instead, these consistent observations, which are further emphasized by the low prevalence of current smoking among COVID-19 patients in the US (1.3%), raises the hypothesis that nicotine may have beneficial effects on COVID-19
... no recommendation can be currently made concerning the effects of smoking on the risk of hospitalization for COVID-19. In fact, the consistently low prevalence of current smoking among Chinese patients with COVID-19 was further supported by the recent data recently released from the US CDC.28 From a total of 7162 patients in the US, only 1.3% were current smokers. low smoking prevalence was also observed among hospitalized non-ICU (2.1%) and ICU cases (1.1%), while the population smoking prevalence in the US is 13.8%. These observations raise a possible hypothesis that nicotine might reduce the risk for severe COVID-19. Hospitalization for COVID-19 will inevitably result in abrupt withdrawal of nicotine and its beneficial effect linked to this hypothesis in smokers or users of other nicotine products. This could, at least partly, explain the association between smoking and COVID-19 severity among hospitalized patients.27 Nicotine has been found to prevent acute lung injury in an animal ARDS model and has immunomodulatory effects.29,30 There is also evidence for an interaction between nicotine and the renin-angiotensin-aldosterone axis, although such interactions remain unclear.2-5 In any case, the observations of a consistently low prevalence of smoking among COVID-19 cases in China and the US, together with the potential mechanisms through which nicotine interacts with the inflammatory process and the renin-angiotensin-aldosterone axis involved in the development of COVID-19, warrant an urgent investigation of the clinical effects of pharmaceutical nicotine on COVID-19 susceptibility, progression and severity. The potential need to provide pharmaceutical nicotine products to smokers who experience an abrupt withdrawal of nicotine when hospitalized for COVID-19 or aim to follow medical advice to quit smoking to relieve underlying conditions that may increase vulnerability to serious or fatal symptoms should also be examined." Smoking, vaping and hospitalization for COVID-19 - Article (Preprint v13) | Qeios
There is not too much info since this is such a new virus and there can really only be anti-smoking research published in the west today. But there are various studies showing that smokers exposed to dangerous inhalants were the least likely to have lung problems:
Protective and therapeutic effects of smoking on lung function in people exposed to environmental carcinogens -- predictably, ex-smokers were worst off:
"Smokers in the potroom group had a lower prevalence of respiratory symptoms than never smokers or ex-smokers, which was significant for wheezing (2.6% v 17.4% and 28.6% respectively, both p < 0.01), whereas respiratory symptoms in controls tended to be highest in smokers (NS). No effects of potroom work on the prevalence of respiratory symptoms could be detected. In potroom workers, impairment of lung function due to occupational exposure was found only in non-smokers" Lack of combined effects of exposure and smoking on respiratory health in aluminium potroom workers
- Smoking has a protective effect on immunological abnormalities in asbestos workers. See: Redirecting and: Redirecting
Also for asbestos workers, relative risk of lung cancer for asbestos workers was: "highest for those who had never smoked, lowest for current smokers, and intermediate for ex-smokers. The trend was statistically significant." Combined effect of asbestos and smoking on mortality from lung cancer and mesothelioma in factory workers. - PubMed - NCBI
In dogs exposed to carcinogen radon: While the radon alone had no problems in inducing lung cancers in dogs (or any other animals), the combined effect of tobacco smoke and radon resulted in significant protection against lung cancers in smoking dogs -- while the nonsmoking dogs exposed to radon had 37% incidence of lung tumors, the smoking dogs exposed to radon had only 5% lung tumor incidence: https://doi.org/10.1093/oxfordjournals.rpd.a083030
And:
"Results of this experiment indicate that cigarette-smoke exposure, under the conditions of the experiment, had a mitigating effect of radon-daughter induced respiratory tract cancer in dogs..." https://doi.org/10.1097/00004032-198201000-00004
More:
"The excess relative risk of lung cancer from asbestos exposure is about three times higher in non-smokers than in smokers" The interaction of asbestos and smoking in lung cancer: a modified measure of effect. - PubMed - NCBI
and:
"Over the 22 years of follow-up, exposed workers have had a very high risk of respiratory cancer, mostly of the lung. The risk has been dose related and has been much higher in nonsmokers and ex-smokers than in current smokers." The cigarette factor in lung cancer due to chloromethyl ethers. - PubMed - NCBI
and:
"Presence of chronic respiratory symptoms at baseline was inversely related to cessation of smoking. Respiratory impairment was positively associated with smoking cessation." Smoking cessation among coal miners as predicted by baseline respiratory function and symptoms: a 5-year prospective study. - PubMed - NCBI
Nicotine stimulates and upregulates growth and branching of blood vessels (via upregulation of vascular growth factor), especially of capillaries, which improves the nutrient delivery and cleanup (antioxidant & detox enzyme supplies) to all tissues, including brain and skin (provided person's intake of nutrients and supplements is adequate -- it is probably the case that smokers need to increase intake of specific vitamins, like vitamin C, to compensate for their habit).
Tobacco smoke (not nicotine) also increases internal detox and antioxidant enzymes, glutathione, catalase and SOD to nearly double the levels. Specifically, some still unknown components of tobacco smoke upregulate substantially the key internal antioxidants and detox enzymes (glutathione [or more recent ref cf. Fig 4, p. L1076], upregulation of 16 internal antioxidants, plus catalase and SOD, all nearly doubled). These (families of) enzymes are responsible for neutralizing and excreting many environmental or industrial toxins and carcinogens we are exposed to (wiki: glutathione, SOD, catalase). I am not quite sure about the link of these enzymes with COVID-19.
Also, carbon monoxide in very low concentration (as delivered in tobacco smoke) may act as a signaling mechanism to increase blood circulation, oxygenation and reduce inflammation, helping prevent burnout and excitotoxic effects from stimulants or excessive work..
I recognize that CO is a poisonous gas that has been used in gas chambers, but we're talking about very low doses (see also on protective role of CO in pre-eclampsia and "Therapeutic CO" whitepaper, miracle medicine, mithochondrial ROS inhibition, protects against endotoxic shock, multiple sclerosis, IBD, hypertension, neurotransmitter, beneficial digestive effects...).
More info on potential benefits of very low dose CO:
- https://www.atsjournals.org/doi/full/10.1164/rccm.201309-1615ED
- Carbon monoxide is a poison. Can it also be a medicine?
- Carbon Monoxide Has Unexpected Benefits, But Dont Try It At Home
- Therapeutic Applications of Carbon Monoxide
Many more exist if you just google for it,
There are a lot of articles coming out now, jumping in on the anti-tobacco bandwagon, saying to quit smoking ASAP because of this COVID-19 outbreak. But as shown above, former smokers often were worse off than never smokers when it came to inhaling environmental contaminants.
There's also a study from india:
"Are lung cancers triggered by stopping smoking? The clinically high correlation between smoking and carcinoma of the lungs has been the focal point in societal campaigns against the habit and the tobacco lobby. In an overview of personal history in a number of lung cancer patients locally, we am struck by the more than casual relationship between the appearance of lung cancer – and an abrupt and recent cessation of the smoking habit in many, if not most cases. The association is more than just casual – development of cancer within a few months of eschewing cigarette smoking. Over a period of 4 years, a total of 312 cases were treated for carcinoma of pulmonary origin [...] Each one of had been addicted to the habit for no less than twenty-five years, smoking in excess of twenty sticks a day. The striking direct statistical correlation between cessation of smoking to the development of lung malignancies, more than 60% plus, is too glaring to be dismissed as coincidental." Are lung cancers triggered by stopping smoking? - PubMed - NCBI
In congruence with the above finding, randomized animal studies require the experimenters to quit smoking to actually observe lung cancer:
"The 4-month recovery period is absolutely necessary for observation of increased lung tumor multiplicity, but the reason for this is not clear."
Carcinogenicity studies of inhaled cigarette smoke in laboratory animals: old and new
So a "Recovery period" where they don't smoke is necessary to observe increased lung cancer, but smoking itself is the cause? Doesn't compute.
There is also this that I found:
"…While nicotine has anti-inflammatory properties in this disease, the therapeutic value of nicotine does not exceed that of more conventional treatments such as aminosalicylates.48
Therefore, while cells are present that are primed for activation, the immune and inflammatory response may be dampened, as has been observed in many smokers.62 Expanding upon this possibility, Floto and Smith64 suggested that the inflammatory response to the stimulatory components of tobacco may be counteracted by the anti-inflammatory effects of nicotine, which offers a rational explanation for why few smokers generate pulmonary Langerhans’ cell histiocytosis. It has also been pointed out that there is a significantly lower incidence of sarcoidosis in smokers65 and decreased incidence of immunoglobulin G (IgG) precipitins that develop during allergic alveolitis as occurs both in humans and guinea pigs.66,67…A notable outcome of this effect may be that the anti-inflammatory properties of nicotine actually enhance the survival of influenza virus in mice and induce significantly higher titers of virus following infection.63" Neuronal nicotinic acetylcholine receptor expression and function on nonneuronal cells. - PubMed - NCBI
COVID-19 is not an influenza though, even the common cold is a coronavirus.
According to a study on respiratory conditions of Whites, Amerindians, and White-Amerind mixed inidividuals it was found that the mixed group race had a higher rate of asthma, hay fever, sinusitis and COPD. With the exception of COPD, the difference between Amerindian-White mixes was larger than the difference between current and never smokers. Smoking status was highest in Amerindian-White mixes, and lowest in Whites. A comparison of respiratory conditions between multiple race adults and their single race counterparts: an analysis based on American Indian/Alaska... - PubMed - NCBI
But another confounding variable exists here, in that the highest frequency of eczema, and the highest frequency of EAH (eczema with asthma and/or hay fever) exists in "mixed raced" individuals (but sometimes Blacks, who are themselves a mixed group in the USA at 15-20% White admixture), even when controlled for smoking: Adult eczema prevalence and associations with asthma and other health and demographic factors: a US population-based study. - PubMed - NCBI
Interesting, but inconclusive.
I will also point out that a curious genetic link: indeed, there are exactly known alleles within a nicotinic acetylcholine receptor gene cluster which simultaneously make people more likely to get lung cancer, as well as, independently make them more likely to smoke: https://www.nature.com/articles/nature06846
This is perhaps why the only two people I ever knew who had lung cancer: a young woman who contracted it in adolescence, and my 50+ year old aunt, neither were ever smokers.
This is a lot of information (there is much more I did not post) but I think a proper thread needs to exist on this subject - Tobacco smoking and COVID-19 - for those of us who do smoke and are now found in this pandemic situation. I would just like to hear some thoughts on the topic of people who are smoking and what they should do differently (if anything; in regards to smoking) during this COVID outbreak.
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