新型冠狀病毒肺炎（簡稱新冠肺炎）是本世紀最重要的傳染病。許多研究已經證實吸菸抑制肺部免疫力，增加呼吸道傳染性疾病風險。早期新冠肺炎的研究對吸菸的資料較少，中國學者發表的研究及美國哈佛大學團隊發表的研究，皆顯示吸菸的新冠肺炎病人約有兩倍的風險發展為重症。最早的統合分析研究顯示吸菸與新冠肺炎重症無統計學顯著相關，亦有少數學者報告新冠肺炎病人吸菸率低於人口平均值，導致「尼古丁保護論」的產生。然而後續學者的論文指出最初的統合分析有數據引用及統計方法的錯誤，經更正後吸菸與新冠肺炎重症應有統計學顯著相關。人口學研究方面，使用統合回歸及時空模型等方法，顯示吸菸率較高的地區新冠肺炎發生率較高。美國克里夫蘭醫學中心分析吸菸量與新冠肺炎預後的關係，發現吸菸量越高，新冠肺炎住院、入住加護病房及死亡率皆越高，顯示有劑量效應，進一步推論有因果關係。英國約42萬人的Biobank發表結合流行病學及基因研究的資料，亦顯示吸菸與新冠肺炎重症有因果關係。在致病機轉方面，吸菸增加ACE2(angiotensin converting enzyme-2)受體的表現，導致感染率較高。吸菸也增加手口接觸的機會，提高接觸傳染的風險。在大型的統合分析方面，有數萬人的研究證實除了年齡、高血壓、糖尿病、心血管疾病、慢性阻塞性肺病、慢性腎病以外，吸菸增加住院病人死亡的風險。本文結論吸菸增加新冠肺炎感染、重症及死亡的風險，吸菸者應盡速戒菸。

COVID-19 is one of the most prevalent infectious diseases in this century. While many studies have proved that smoking suppresses pulmonary immunity and increases the risk of lung infections, there are fewer reports on the association between smoking and the severity of COVID-19 infection. Studies of both Chinese researchers and a Harvard University research team revealed that the risk of developing severe outcomes doubled in smoking COVID-19 patients. The first meta-analysis showed that there was no statistically significant effect of smoking on developing severe COVID-19 outcomes, and the report of several researchers that the smoking rate of COVID-19 patients was lower than that of the general population even led to the emergency of the “nicotine protection” theory. However, subsequent studies found the data collection and analysis methods of the first meta-analysis invalid. The corrected analysis indicated a statistically significant correlation between smoking and the severity of COVID-19 outcomes. Population studies using meta-regression and spatiotemporal models also identified a higher COVID-19 prevalence in areas with higher smoking rates. According to the COVID-19 registry developed by the US-based Cleveland Clinic, greater smoking exposure was associated with higher rates of COVID-19 hospitalization, ICU admission, and mortality. The results unveiled a dose-response relationship indicating the causal effect of smoking and COVID-19 outcomes. The UK Biobank recruited around 420,000 participants, and a combination of epidemiology and genetic studies concluded the causal effect of smoking on the risk of severe COVID-19 outcomes. As reported by studies on transmission mechanisms, smoking increased the expression of ACE2 (angiotensin converting enzyme-2) receptors, thereby increasing the risk of infection. Hand and mouth contact during smoking was also a risk to increase viral transmission. In a large-scale meta-analysis that studied tens of thousands of patients, in addition to hypertension, diabetes, cardiovascular diseases, COPD, and chronic renal diseases, smoking was one of the in-hospital mortality risks. This review article concludes that smoking increases the risks of infection, severe outcomes, and mortality of COVID-19. Smokers are urged to stop smoking as soon as possible.