The association between current smoking and coronavirus disease 2019 (COVID-19) progression remains uncertain. We aim to provide up-to-date evidence of the role of cigarette smoking in COVID-19 hospitalisation, severity and mortality. On 23 February 2022 we conducted an umbrella review and a traditional systematic reviewviaPubMed/Medline and Web of Science. We used random-effects meta-analyses to derive pooled odds ratios of COVID-19 outcomes for smokers in cohorts of severe acute respiratory syndrome coronavirus 2 infected individuals or COVID-19 patients. We followed the Meta-analysis of Observational Studies in Epidemiology reporting guidelines. PROSPERO: CRD42020207003. 320 publications were included. The pooled odds ratio for currentversusnever or nonsmokers was 1.08 (95% CI 0.98–1.19; 37 studies) for hospitalisation, 1.34 (95% CI 1.22–1.48; 124 studies) for severity and 1.32 (95% CI 1.20–1.45; 119 studies) for mortality. Estimates for formerversusnever-smokers were 1.16 (95% CI 1.03–1.31; 22 studies), 1.41 (95% CI: 1.25–1.59; 44 studies) and 1.46 (95% CI 1.31–1.62; 44 studies), respectively. Estimates for ever-versusnever-smokers were 1.16 (95% CI 1.05–1.27; 33 studies), 1.44 (95% CI 1.31–1.58; 110 studies) and 1.39 (95% CI 1.29–1.50; 109 studies), respectively. We found a 30–50% excess risk of COVID-19 progression for current and former smokers compared with never-smokers. Preventing serious COVID-19 outcomes, including death, seems the newest compelling argument against smoking.

Objective Cervical cancer (CC) is the fourth most frequent cancer worldwide. Cigarette smoking has been shown to influence CC risk in conjunction with human papillomavirus (HPV) infection. The aim of this study is to provide the most accurate and updated estimate of this association and its dose-response relationship. Methods Using an innovative approach for the identification of original publications, we conducted a systematic review and meta-analysis of studies published up to January 2021. Random effects models were used to provide pooled relative risks (RRs) of CC for smoking status. Dose-response relationships were evaluated using one-stage random effects models with linear or restricted cubic splines models. Results We included 109 studies providing a pooled RR of invasive CC and preinvasive lesions, respectively, of 1.70 [95% confidence interval (CI), 1.53–1.88] and 2.11 (95% CI, 1.85–2.39) for current versus never smokers, and, respectively, 1.13 (95% CI, 1.02–1.24) and 1.29 (95% CI, 1.15–1.46) for former versus never smokers. Considering HPV does not alter the positive association or its magnitude. Risks of CC sharply increased with few cigarettes (for 10 cigarettes/day, RR = 1.72; 95% CI, 1.34–2.20 for invasive CC and RR = 2.13; 95% CI, 1.86–2.44 for precancerous lesions). The risk of CC increased with pack-years and smoking duration and decreased linearly with time since quitting, reaching that of never smokers about 15 years after quitting. Conclusion This comprehensive review and meta-analysis confirmed the association of smoking with CC, independently from HPV infection. Such association rose sharply with smoking intensity and decreased after smoking cessation.

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