Tobacco smoking and cancer: a brief review of recent epidemiological evidence
Summary
This report summarises the epidemiological evidence on the association between tobacco smoking and cancer, which was reviewed by an international group of scientists convened by IARC. Studies published since the 1986 IARC Monograph on “Tobacco smoking” provide sufficient evidence to establish a causal association between cigarette smoking and cancer of the nasal cavities and paranasal sinuses, nasopharynx, stomach, liver, kidney (renal cell carcinoma) and uterine cervix, and for adenocarcinoma of the oesophagus and myeloid leukaemia. These sites add to the previously established list of cancers causally associated with cigarette smoking, namely cancer of the lung, oral cavity, pharynx, larynx, oesophagus, pancreas, urinary bladder and renal pelvis. Other forms of tobacco smoking, such as cigars, pipes and bidis, also increase risk for cancer, including cancer of the lung and parts of the upper aerodigestive tract. A meta-analysis of over 50 studies on involuntary smoking among never smokers showed a consistent and statistically significant association between exposure to environmental tobacco smoke and lung cancer risk. Smoking is currently responsible for a third of all cancer deaths in many Western countries. It has been estimated that every other smoker will be killed by tobacco.
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Cited by (563)
Recirculating bioavailable nicotine metabolite using ascorbic acid: A pragmatic approach for treating nicotine dependence
2024, Advances in Redox ResearchNicotine undergoes metabolism, converting into the oxidized metabolite cotinine, which can persist in the body for several weeks and potentially lead to fatal conditions, such as cancer. Conventional nicotine replacement therapy provides additional nicotine to the body, thereby increasing the chance of accumulating the toxic metabolite cotinine. Consequently, we proposed a hypothesis: converting cotinine back into nicotine using a suitable reducing agent, such as ascorbic acid, could be a practical approach. This conversion would allow cotinine to be reutilized for its central nervous system effects before its eventual elimination from the body. In the current study, we examined this hypothesis by using plasma samples from smokers. Volunteers (both non-smokers and smokers) were screened and recruited for this study. In the initial time- and dose-dependent studies, we incubated plasma samples from non-smokers with cotinine and ascorbic acid. Changes in cotinine and nicotine levels were quantified using HPLC-PDA. Based on the findings of these experiments, we selected a concentration of 1 µM ascorbic acid and incubated it with plasma samples from 25 smokers for 10 min. A time-dependent study revealed that nicotine was detected in non-smokers' plasma samples after a 10-minute incubation with 28.38 µM of both cotinine and ascorbic acid. In a subsequent dose-dependent study, the maximum concentration of nicotine was observed at 1 µM ascorbic acid. Among the 25 samples of smokers’ plasma, the mean nicotine concentration increased from 0.565 ± 0.196 to 1.937 ± 0.622 µM (P = 0.0081), while cotinine levels decreased from 1.278 ± 0.253 to 0.754 ± 0.137 µM (P = 0.0087). This study conclusively demonstrated that ascorbic acid, at a specified concentration, effectively converts cotinine back into nicotine in smokers' plasma. Importantly, this conversion did not occur in water or in the absence of ascorbic acid in the plasma, indicating enzyme involvement.
Cancer mortality in Germany-born Americans and Germans
2024, Cancer EpidemiologyComparing cancer mortality and associated risk factors among immigrant populations in a host country to those in their country of origin reveals disparities in cancer risk, access to care, diagnosis, and disease management. This study compares cancer mortality between the German resident population and Germany-born individuals who migrated to the US.
Cancer mortality data from 2008–2018 were derived for Germans from the World Health Organization database and for Germany-born Americans resident in four states (California, Florida, Massachusetts, and New York) from respective Departments of Vital Statistics. We calculated age-standardized mortality rates (ASMRs) using the European standard population and standardized mortality ratios (SMR) compared to the German resident population along with 95% confidence intervals (CIs).
Germany-born American males had lower ASMRs (253.8 per 100,000) than German resident population (325.6 per 100,000). The difference in females was modest, with ASMRs of 200.7 and 203.7 per 100,000, respectively. For all cancers, Germany-born American males had an SMR of 0.72 (95% CI: 0.70–0.74) and females 0.98 (95% CI: 0.95–1.00). Male SMRs among Germany-born Americans were significantly below one for oral cavity, stomach, colorectal, liver, lung, prostate, and kidney cancer. Among females, SMRs were below one for oral cavity, stomach, colorectal, gallbladder, breast, cervix uteri, and kidney cancer. For both sexes, SMRs were over one for bladder cancer (1.14 for males, 1.21 for females). Mortality was higher for lung cancer (SMR: 1.68), non-Hodgkin’s lymphoma (1.18) and uterine cancer (1.22) among Germany-born American females compared to the German resident population.
Germany-born American males but not females showed lower cancer mortality than German resident population. Disparities may stem from variations in risk factors (e.g., smoking and alcohol use) as well as differences in screening practices and participation, cancer treatment, besides some residual potential "healthy immigrant effect".
Risk of Parkinson's disease-related death in cancer survivors: A population-based study in Japan
2024, Parkinsonism and Related DisordersThe risk of Parkinson's disease (PD)-related death in patients with cancer largely unexplored.
We analyzed data from the Neoplasms ANd other causes of DEath (NANDE) study, which investigates the causes of death in patients with cancer in Japan. Standardized mortality ratios (SMRs) were calculated to compare the risk of PD-related deaths in patients with cancer to that of the general population. Poisson regression models were employed to estimate the relative risk of PD-related death in the subgroups.
The cohort included 548,485 patients with cancer, yielding 2,047,398 person-years at risk from 1995 to 2013. During the study period, 242,250 patients died and 145 deaths were attributable to PD. The SMR for PD-related death was 2.34 (95% confidence interval [CI]: 1.99–2.75). Patients who were diagnosed with cancer before 70 years of age had a high SMR (>5) for PD-related deaths. The SMR of patients with mouth-to-stomach cancers (lip, oral cavity, pharynx, esophagus, and stomach cancers) was 3.72 (95% CI: 2.84–4.86), while that of those with other cancers was 1.93 (95% CI: 1.57–2.37). The multivariate Poisson regression model revealed that patients with mouth-to-stomach cancers were more likely to die of PD than those without (relative risk 2.07, 95 % CI; 1.46–2.93).
Patients with cancer are at a high risk of PD-related death; particularly, mouth-to-stomach cancers and potentially obstructing medication for PD are attributable to a high mortality risk. Careful management, including adequate PD treatment, would benefit cancer survivors with PD and reduce the risk of PD-related death.
Dysregulation of immunity by cigarette smoking promotes inflammation and cancer: A review
2023, Environmental PollutionSmoking is a serious global health issue. Cigarette smoking contains over 7000 different chemicals. The main harmful components include nicotine, acrolein, aromatic hydrocarbons and heavy metals, which play the key role for cigarette-induced inflammation and carcinogenesis. Growing evidences show that cigarette smoking and its components exert a remarkable impact on regulation of immunity and dysregulated immunity promotes inflammation and cancer. Therefore, this comprehensive and up-to-date review covers four interrelated topics, including cigarette smoking, inflammation, cancer and immune system. The known harmful chemicals from cigarette smoking were summarized. Importantly, we discussed in depth the impact of cigarette smoking on the formation of inflammatory or tumor microenvironment, primarily by affecting immune effector cells, such as macrophages, neutrophils, and T lymphocytes. Furthermore, the main molecular mechanisms by which cigarette smoking induces inflammation and cancer, including changes in epigenetics, DNA damage and others were further summarized. This article will contribute to a better understanding of the impact of cigarette smoking on inducing inflammation and cancer.
Comparative analyses of transcriptome sequencing and carcinogenic exposure toxicity of nicotine and 6-methyl nicotine in human bronchial epithelial cells
2023, Toxicology in VitroElectronic cigarettes have become a purported safer alternative to the conventional cigarettes in recent years. Nicotine is the main component of electronic cigarettes, and other nicotinic compounds are synthesized as alternatives to nicotine. However, scientific data on the potential health effects of electronic cigarettes are scarce. Herein, we evaluated the cytotoxicity of nicotine and its analog 6-methyl nicotine (6-MN) on human bronchial epithelial cells (BEAS-2B cells) in vitro. Furthermore, we performed transcriptome sequencing to systematically assess the effects of nicotine and 6-MN on BEAS-2B cells. The cytotoxicity assay revealed that BEAS-2B cells were more sensitive to 6-MN than to nicotine. Transcriptome sequencing revealed 1208 differentially expressed cancer-related proteins (CRP) in the 6-MN groups relative to that with CRP in the control group. In addition, 6-MN had a greater negative effect on the CRP expression than nicotine. Bioinformatic analysis revealed that the differentially expressed genes and proteins in the 6-MN group were significantly enriched in the cancer-related pathways, unlike those in the nicotine group. Further validations of some lung cancer-related proteins, such as NF-κB p65, EGFR, and MET, were conducted by immunoblotting and real-time PCR, which revealed that 6-MN may have a greater negative effect on tumor development and metastasis than nicotine. Taken together, our findings suggest that new electronic cigarettes with 6-MN might offer some advantages over conventional electronic cigarettes containing nicotine.
Effect of environmental exposures on cancer risk: Emerging role of non-coding RNA shuttled by extracellular vesicles
2023, Environment InternationalEnvironmental and lifestyle exposures have a huge impact on cancer risk; nevertheless, the biological mechanisms underlying this association remain poorly understood. Extracellular vesicles (EVs) are membrane-enclosed particles actively released by all living cells, which play a key role in intercellular communication. EVs transport a variegate cargo of biomolecules, including non-coding RNA (ncRNA), which are well-known regulators of gene expression. Once delivered to recipient cells, EV-borne ncRNAs modulate a plethora of cancer-related biological processes, including cell proliferation, differentiation, and motility. In addition, the ncRNA content of EVs can be altered in response to outer stimuli. Such changes can occur either as an active attempt to adapt to the changing environment or as an uncontrolled consequence of cell homeostasis loss. In either case, such environmentally-driven alterations in EV ncRNA might affect the complex crosstalk between malignant cells and the tumor microenvironment, thus modulating the risk of cancer initiation and progression.
In this review, we summarize the current knowledge about EV ncRNAs at the interface between environmental and lifestyle determinants and cancer. In particular, we focus on the effect of smoking, air and water pollution, diet, exercise, and electromagnetic radiation. In addition, we have conducted a bioinformatic analysis to investigate the biological functions of the genes targeted by environmentally-regulated EV microRNAs.
Overall, we draw a comprehensive picture of the role of EV ncRNA at the interface between external factors and cancer, which could be of great interest to the development of novel strategies for cancer prevention, diagnosis, and therapy.