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While the COVID-19 pandemic surges, other pandemics continue, albeit in the shadow of COVID-19. The global tobacco pandemic has been in progress for a century, dating to the 1913 release of Camel, the first mass-marketed cigarette brand. In the United States, the Surgeon General attributes 480,000 premature deaths annually to tobacco, a number greatly exceeding the current death toll from COVID-19 of over 150,000 deaths. But, this is a comparison that should not be made. The COVID-19 deaths are identifiable and each has a death certificate listing COVID-19 as the underlying cause, while the death certificates of those killed prematurely by smoking list coronary heart disease, COPD, lung cancer, and the many other diseases causally linked to smoking. And, there is the tobacco industry but no COVID-19 industry.
With 34 million current smokers and far more former smokers, we ask if smokers and former smokers are at higher risk for infection with SARS-CoV-2 infection, more severe COVID-19, and more deaths from COVID-19. Affirmative answers to these questions would point to opportunities for intervention with a susceptible population.
Plausibly, smoking might lead to "yes" answers to these questions. The lungs of those who smoke are inflamed and the lining of the lung, the epithelium, is more permeable. These changes could prime the lung for ready entry of the SARS-CoV-2 into its cells and, furthermore, the immune system of the lung is compromised by smoking. In fact, the 2014 50th anniversary report of the Surgeon General concluded that "the evidence is sufficient to infer that cigarette smoking compromises the immune system and that altered immunity is associated with increased risk for pulmonary infections." Does this conclusion apply to SARS-CoV-2?
For SARS-CoV-2, the story has particular complexities. With its spike protein, the virus binds to the angiotensin-converting enzyme-2 (ACE-2) receptor, which is abundant in the lung. Smoking upregulates the ACE-2 receptor, i.e., increases the number of receptors, which might increase the risk for infection or more severe disease. There are potential countering effects of nicotine mediated by the nicotinic acetylcholine receptor. To simplify and summarize, the underlying biology is complicated.
The relevant epidemiological studies, carried out within the constraints posed by a deadly pandemic, provide a mixed picture. The most informative is the OpenSAFELY Study in the United Kingdom, a follow-up study of 17 million people carried out through record linkage within the National Health Service. After adjusting for underlying diseases, being a current smoker was not associated with increased risk for in-hospital death, while being a former smoker was. Diabetes, heart disease, and lung disease other than asthma were associated with increased risk for dying. Inequities were captured as well; Blacks and South Asians were at 50% greater risk for dying compared with whites.
There are multiple systematic reviews of varying quality on smoking and COVID-19. Fortunately, various groups have taken on the tedious task of maintaining updated systematic reviews. I have found the "Living Rapid Evidence Review" maintained by a group in the United Kingdom to be up-to-date and informative. The evidence available is limited and weak with suggestive evidence of lower test positivity and also poorer outcomes in current versus never smokers.
One pathway for increased risk from smoking is supported: the presence of underlying chronic disease in those who smoke. The prevalence of these diseases is far too high and has been increasing. In Colorado, the prevalence of COPD is about 4%, diabetes 7%, and 5% with cardiovascular disease. Inevitably, there are striking disparities in the occurrence of these drivers of morbidity and mortality from COVID-19.
There will be more research. Studies involving nicotine patches are underway in France involving healthcare workers and patients. But, COVID-19 has not changed the narrative on smoking: don't smoke, and wear your mask.
Until next week,
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