Abstract
Implications: This commentary addresses the state of the evidence on tobacco products, nicotine, and COVID-19. The evidence of the effects of smoking on respiratory infections and the immune ...system in general are examined and the current understanding of tobacco products and risk for SARS-CoV-2 infection and the course of COVID-19 is addressed.
Abstract
This commentary celebrates the 40th year of Carcinogenesis, spanning 1980–2020 with a focus on lung cancer. For lung cancer, these 40 years come toward the end of a century of scientific ...inquiry that began with descriptions of this highly fatal malignancy and that closes with emphasis on molecular processes and genomics. This commentary gives a historical perspective of lung cancer research as well as a look into the questions that remain to be addressed. Over the 20th century and into the first two decades of the 21st, a series of issues have more or less sequentially been the focus of epidemiological investigation of lung cancer, as questions have been answered and methodologies have evolved. These questions began with whether an epidemic was occurring and continue now with exploration of causal mechanisms and molecular risk predictors. With tobacco smoking firmly established decades ago as a cause of lung cancer, the evidence has long been sufficient to motivate tobacco prevention and control. There is unfinished business as tobacco smoking remains widespread and the industry continues to market new, addicting, products.
We conducted a systematic review and 3-part meta-analysis to characterize the relationship between smoking and perinatal death, defined as the combination of stillbirth and neonatal death. The PubMed ...database was searched (1956-August 31, 2011) with keywords, and manual reference searches of included articles and Surgeon Generals' reports were conducted. The full texts of 1,713 articles were reviewed, and 142 articles that examined the associations between active or passive smoking and perinatal death were included in the meta-analyses. Data were abstracted by 2 reviewers. Any active maternal smoking was associated with increased risks of stillbirth (summary relative risk (sRR) = 1.46, 95% confidence interval (CI): 1.38, 1.54 (n = 57 studies)), neonatal death (sRR = 1.22, 95% CI: 1.14, 1.30 (n = 28)), and perinatal death (sRR = 1.33, 95% CI: 1.25, 1.41 (n = 46)). The risks of stillbirth, neonatal death, and perinatal death increased with the amount smoked by the mother. Biases in study publication, design, and analysis were present but did not significantly affect the results. These findings strengthen the evidence that women should not smoke while pregnant, and all women of reproductive age should be warned that smoking increases the risks of stillbirth, neonatal death, and perinatal death.
Use of electronic cigarettes (e-cigarettes), vape pens, e-hookah, e-cigars, e-pipes, or other electronic nicotine delivery systems (ENDS) has increased rapidly since their introduction in the US in ...2007, growing to a $2 billion market. Numerous flavored products that have seeming appeal to adolescents and young adults are on the market, such as Cherry Crush, Chocolate Treat, Snappin' Apple, and Vanilla Dreams flavors; their availability may generate an entirely new population of nicotine-addicted users among never-users of combustible tobacco products. Here, Barrington-Trimis et al examine the unrecognized respiratory health hazard of flavorings in e-cigarettes.
Summary Background Overweight and obesity are increasing worldwide. To help assess their relevance to mortality in different populations we conducted individual-participant data meta-analyses of ...prospective studies of body-mass index (BMI), limiting confounding and reverse causality by restricting analyses to never-smokers and excluding pre-existing disease and the first 5 years of follow-up. Methods Of 10 625 411 participants in Asia, Australia and New Zealand, Europe, and North America from 239 prospective studies (median follow-up 13·7 years, IQR 11·4–14·7), 3 951 455 people in 189 studies were never-smokers without chronic diseases at recruitment who survived 5 years, of whom 385 879 died. The primary analyses are of these deaths, and study, age, and sex adjusted hazard ratios (HRs), relative to BMI 22·5–<25·0 kg/m2. Findings All-cause mortality was minimal at 20·0–25·0 kg/m2 (HR 1·00, 95% CI 0·98–1·02 for BMI 20·0–<22·5 kg/m2 ; 1·00, 0·99–1·01 for BMI 22·5–<25·0 kg/m2 ), and increased significantly both just below this range (1·13, 1·09–1·17 for BMI 18·5–<20·0 kg/m2 ; 1·51, 1·43–1·59 for BMI 15·0–<18·5) and throughout the overweight range (1·07, 1·07–1·08 for BMI 25·0–<27·5 kg/m2 ; 1·20, 1·18–1·22 for BMI 27·5–<30·0 kg/m2 ). The HR for obesity grade 1 (BMI 30·0–<35·0 kg/m2 ) was 1·45, 95% CI 1·41–1·48; the HR for obesity grade 2 (35·0–<40·0 kg/m2 ) was 1·94, 1·87–2·01; and the HR for obesity grade 3 (40·0–<60·0 kg/m2 ) was 2·76, 2·60–2·92. For BMI over 25·0 kg/m2 , mortality increased approximately log-linearly with BMI; the HR per 5 kg/m2 units higher BMI was 1·39 (1·34–1·43) in Europe, 1·29 (1·26–1·32) in North America, 1·39 (1·34–1·44) in east Asia, and 1·31 (1·27–1·35) in Australia and New Zealand. This HR per 5 kg/m2 units higher BMI (for BMI over 25 kg/m2 ) was greater in younger than older people (1·52, 95% CI 1·47–1·56, for BMI measured at 35–49 years vs 1·21, 1·17–1·25, for BMI measured at 70–89 years; pheterogeneity <0·0001), greater in men than women (1·51, 1·46–1·56, vs 1·30, 1·26–1·33; pheterogeneity <0·0001), but similar in studies with self-reported and measured BMI. Interpretation The associations of both overweight and obesity with higher all-cause mortality were broadly consistent in four continents. This finding supports strategies to combat the entire spectrum of excess adiposity in many populations. Funding UK Medical Research Council, British Heart Foundation, National Institute for Health Research, US National Institutes of Health.
There has been little research examining whether e-cigarette use increases the risk of cigarette initiation among adolescents in the transition to adulthood when the sale of cigarettes becomes legal.
...The Children's Health Study is a prospectively followed cohort in Southern California. Data on e-cigarette use were collected in 11th and 12th grade (mean age = 17.4); follow-up data on tobacco product use were collected an average of 16 months later from never-smoking e-cigarette users at initial evaluation (n = 146) and from a sample of never-smoking, never e-cigarette users (n = 152) frequency matched to e-cigarette users on gender, ethnicity, and grade.
Cigarette initiation during follow-up was reported by 40.4% of e-cigarette users (n = 59) and 10.5% of never users (n = 16). E-cigarette users had 6.17 times (95% confidence interval: 3.30-11.6) the odds of initiating cigarettes as never e-cigarette users. Results were robust to adjustment for potential confounders and in analyses restricted to never users of any combustible tobacco product. Associations were stronger in adolescents with no intention of smoking at initial evaluation. E-cigarette users were also more likely to initiate use of any combustible product (odds ratio = 4.98; 95% confidence interval: 2.37-10.4), including hookah, cigars, or pipes.
E-cigarette use in never-smoking youth may increase risk of subsequent initiation of cigarettes and other combustible products during the transition to adulthood when the purchase of tobacco products becomes legal. Stronger associations in participants with no intention of smoking suggests that e-cigarette use was not simply a marker for individuals who would have gone on to smoke regardless of e-cigarette use.
Conclusions as to the causation of adverse effects by environmental and occupational agents may have powerful societal consequences, leading to measures to control exposure through removal of ...products from the marketplace, changes in design and manufacturing processes, regulation, and litigation. We are at a moment when massive and widely publicized litigation is underway in the United States related to carcinogenicity and causation of cancer by two agents, talcum powder and the herbicide glyphosate, sold as Roundup. Verdicts amounting to hundreds of millions of dollars (as much as $4 billion in the case of talc and ovarian cancer) have been reached: for ovarian cancer in talcum powder users and for nonHodgkin's lymphoma in persons exposed to glyphosate. Conclusions of the World Health Organization's International Agency for Research on Cancer (IARC) have figured in this litigation. Through its IARC Monographs, the agency offers evidence-based classifications of the strength of evidence for carcinogenicity of selected agents and exposures.In this issue of AJPH, Rosner et al. (p. 969) comment on how exposure to talc contaminated with asbestos might have occurred, thus leading to increased risk for ovarian cancer. The manufacturers' strategy was to label talcum powder as having "nondetected" amounts of asbestos, leaving the possibility that cancer-causing asbestos fibers were present. Today's litigation may be a legacy of this strategy.Here, I focus on the IARC classification of the herbicide glyphosate as "probably carcinogenic to humans" (Group 2A) and the aftermath of the classification.1 IARC Monographs have also covered both talc and asbestos and ovarian cancer. Monograph 93 classified talc applied to the perineum as "possibly carcinogenic to humans" (Group 2B) while Monograph 100C concluded that asbestos causes cancer of the ovary.There are critical lessons learned from the IARC glyphosate classification and its aftermath around transparency, journals, and unrevealed conflict ofinterest (COI), and on potential consequences for those serving on expert panels. First, I state my own potential biases and COIs; for more than three decades, I have participated in and chaired multiple IARC Working Groups, including chairing the group that recently revised the Preamble to the IARC Monographs. I support the program and have defended it and called out its accomplishments.2 My views are shared by many.
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