Smoking, SARS-CoV-2 and COVID-19: a review of reviews considering implications for public health policy and practice

IntroductionThere has been significant speculation regarding the association between Severe Acute RespiratorySyndrome Coronavirus 2 (SARS-CoV-2) pathogen, coronavirus disease (COVID-19) and smoking.We provide an overview of the available literature regarding the association between smoking, risk ofSARS-CoV-2 infection, and risk of severe COVID-19 and poor clinical outcomes, with the aim ofinforming public health policy and practice in England.MethodsPublications were identified utilising a systematic search approach on PUBMED and Google Scholar.Publications presenting a systematic review or meta-analysis considering the association betweensmoking and SARS-COV-2 infection or COVID-19 outcomes were included.ResultsEight studies were identified. One considered the relationship between smoking and the probability ofSARS-CoV-2 infection, three considered the association between COVID-19 hospitalisation andsmoking history and six reviewed the association between smoking history and development ofsevere COVID-19. One study specifically investigated the risk of mortality. The studies consideringrisk of severe disease indicate that there is a significant association between COVID-19 and currentor ever smoking.ConclusionsThis is a rapidly evolving topic. Current analysis remains limited due to the quality of primary data,although early results indicate an association between smoking and COVID-19 severity. We highlyrecommend public health messaging to continue focusing on smoking cessation efforts

Targeting cyclooxygenase-2 in depression is not a viable therapeutic approach and may even aggravate the pathophysiology underpinning depression

Depression is a complex progressive disorder accompanied by activation of inflammatory and Th-1 driven pathways, oxidative and nitrosative stress (O&amp;NS), lowered antioxidant levels, mitochondrial dysfunctions, neuroprogression and increased bacterial translocation. In depression, activation of immuno-inflammatory pathways is associated with an increased risk for cardio-vascular disorder (CVD). Because of the inflammatory component, the use of cyclooxygenase 2 (COX-2) inhibitors, such as celecoxib, has been advocated to treat depression. Electronic databases, i.e. PUBMED, Scopus and Google Scholar were used as sources for this selective review on the effects of COX-2 inhibitors aggravating the abovementioned pathways. COX-2 inhibitors may induce neuroinflammation, exacerbate Th1 driven responses, increase lipid peroxidation, decrease the levels of key antioxidants, damage mitochondria and aggravate neuroprogression. COX-2 inhibitors may aggravate bacterial translocation and CVD through Th1-driven mechanisms. COX-2 inhibitors may aggravate the pathophysiology of depression. Since Th1 and O&amp;NS pathways are risk factors for CVD, the use of COX-2 inhibitors may further aggravate the increased risk for CVD in depression. Selectively targeting COX-2 may not be a viable therapeutic approach to treat depression. Multi-targeting of the different pathways that play a role in depression is more likely to yield good treatment results. <br /