A review of human carcinogens—Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish

Secretan, Béatrice; Straif, Kurt; Baan, R.A.; Grosse, Yann; Ghissassi, Fatiha El; Bouvard, Véronique; Benbrahim‐Tallaa, Lamia; Guha, Neela; Freeman, Crystal; Galichet, Laurent; Cogliano, Vincent

doi:10.1016/s1470-2045(09)70326-2

Cited by 968 publications

(807 citation statements)

References 16 publications

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“…Increased risk for cancer in spouses is assumed to be caused by common lifestyle and shared environmental exposures, such as smoking, 15 alcohol consumption, 16 UV radiation 17,18 and physical inactivity. 19 Assuming similar exposure to these non-genetic risk factors among couples and nuclear families, the difference between familial risk estimates and calculated risks for spouses can reflect the cancer risk that is due to shared genes or gene-environment interactions.…”

Section: Discussionmentioning

confidence: 99%

The population impact of familial cancer, a major cause of cancer

Christoph

Fallah

et al. 2013

Int. J. Cancer

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The population attributable fraction (PAF) defines the proportion of a disease that would be prevented if the exposure to a particular risk factor was avoided. Familial risk is a known risk factor for many cancers, but an unbiased estimation of the PAF for familial risk requires a large study population to include rare cancers. PAFs and their corresponding standardized incidence ratios (SIRs) were calculated for familial relative risk among first-degree relatives (FDRs) and second-degree relatives (SDRs) diagnosed with the same (concordant) invasive or in situ cancers. Calculations were based on the Swedish Family-Cancer Database considering 8,148,737 individuals. To assess environmental effects, PAFs were also calculated for concordant cancers among spouses. Almost all cancers showed a significant familial risk. The highest PAFs were found for the common cancers of the prostate (13.94%), breast (7.46%) and colorectum (6.78%) among the FDRs. In the FDRs, the overall PAF for any concordant cancer was 4.20%, but in the SDRs, it was only 0.34%. The overall PAFs for in situ cancers were 0.86% and 0.56% for the FDRs and SDRs, respectively. The overall independent familial PAF was 5.96% for the invasive and in situ cancers in the FDRs and SDRs. The cancers between spouses yielded an overall PAF of 0.14%. For esophageal cancer, the risk among spouses was higher than the familial risk. Our study shows that the overall familial PAF of 5.96%, although underestimated for sex-specific cancers, ranks as the third most common population burden after tobacco smoking and unhealthy diet.Twin data suggest that cancer is an environmental disease with a significant genetic component. 1 The population attributable fraction (PAF) is an epidemiological measure that estimates the population impact of various risk factors to the etiology of a disease. The PAF depends on the magnitude of the effect and the size of the exposed population. 2 The PAF has been traditionally used to assess modifiable environmental risk factors, but it has also been increasingly used in disease genetics to gain an understanding of the population impact of identified gene variants. 3,4 A recent PAF estimate concerning lifestyle and environmental factors on all cancer types in the British population ranked tobacco first (19.4%), followed by unhealthy diet (9.2%), overweight and obesity (5.5%), alcohol use (4.0%) and occupation (3.5%). 5 Increased cancer incidence among family members is most likely due to having more shared genes than the population at large, but family members also share habits and lifestyle more than the general population. However, the main argument that the familial clustering of most cancers is largely a result of genetics is the generally low spousal correlation for cancer risk after long cohabitation. 6 Even if familial cancer has a main genetic component, the risk may be modifiable through genetic counseling and management. Family history is a risk factor for which advice and management may bring medical benefits. 7 Many cancer screening...

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Section: Discussionmentioning

confidence: 99%

The population impact of familial cancer, a major cause of cancer

Christoph

Fallah

et al. 2013

Int. J. Cancer

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“…Examples include the role of tobacco, alcohol, and human papilloma virus (HPV) infections in oral cavity cancers; 168,169 sun exposure in melanoma; 170 and hepatitis C virus (HCV) infections, autoimmune diseases, and sun exposure in certain NHLs. 171 However, the role of these risk factors in SN after allogeneic HCT is largely unknown.…”

Section: Non-transplant-related Risk Factorsmentioning

confidence: 99%

National Institutes of Health Hematopoietic Cell Transplantation Late Effects Initiative: The Subsequent Neoplasms Working Group Report

Morton

Saber

Baker

et al. 2017

Biology of Blood and Marrow Transplantation

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Subsequent neoplasms (SN) following hematopoietic cell transplantation (HCT) cause significant patient morbidity and mortality. Risks for specific SN types vary substantially, with particularly elevated risks for post-transplant lymphoproliferative disorders, myelodysplastic syndrome/acute myeloid leukemia, and squamous cell malignancies. This consensus document provides an overview of the current state of knowledge regarding SN after HCT and recommends priorities and approaches to overcome challenges and gaps in understanding. Numerous factors have been suggested to impact risk, including patient-related (e.g., age), primary disease-related (e.g., disease type, pre-HCT therapies), and HCT-related characteristics (e.g., type and intensity of conditioning regimen, stem cell source, development of graft-versus-host disease). However, gaps in understanding remain for each of these risk factors, particularly for patients receiving HCT in the current era due to substantial advances in clinical transplantation practices. Additionally, the influence of non-transplant-related risk factors (e.g., germline genetic susceptibility, oncogenic viruses, lifestyle factors) is poorly understood. Clarification of the magnitude of SN risks and identification of etiologic factors will require large-scale, long-term, systematic follow-up of HCT survivors with detailed clinical data. Most investigations of the mechanisms of SN pathogenesis after HCT have focused on immune drivers. Expansion of our understanding in this area will require interdisciplinary laboratory collaborations utilizing measures of immune function and availability of archival tissue from SN diagnoses. Consensus-based recommendations for optimal preventative, screening, and therapeutic approaches have been developed for certain SN after HCT, whereas for other SN, general population guidelines are recommended. Further evidence is needed to specifically tailor preventative, screening, and therapeutic guidelines for SN after HCT, particularly for unique patient populations. Accomplishment of this broad research agenda will require increased investment in systematic data collection with engagement from patients, clinicians, and interdisciplinary scientists in order to reduce the burden of SN in the rapidly growing population of HCT survivors.

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“…Recently, ACH production associated with the consumption of alcoholic beverages has been reclassified as highly carcinogenic (Group 1) by the International Agency for Research on Cancer of the World Health Organization [2]. In particular, increased ACH levels in saliva have been associated with increased risk for upper aerodigestive tract cancer [3–5], which was the seventh most common cancer in Japan in 2011 with one million newly diagnosed cases annually worldwide [6,7].…”

Section: Introductionmentioning

confidence: 99%

Characterization of oral microbiota and acetaldehyde production

Yokoyama

Takeuchi

Shibata

et al. 2018

Journal of Oral Microbiology

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Background: Neisseria has been reported to be a high producer of acetaldehyde (ACH), a carcinogen, from ethanol in vitro, but no information exists regarding whether the ACH production depends on oral microbiota profiles.Objective and Design: To explore the salivary microbiota profiles with respect to ACH production ability in the oral cavity using a cross-sectional design.Results: Using 16S rRNA gene amplicon sequencing, we classified 100 saliva samples into two types of communities (I and II). Salivary ACH production ability from ethanol was measured using gas chromatography and was found to vary over a 30-fold range. ACH production ability was significantly higher in the type I community, wherein the relative abundance of Neisseria species was significantly lower. Multivariate logistic regression analysis showed that the subjects with the type I community exhibited significantly higher probability of high ACH production ability than those with the type II community (P = 0.014). Moreover, the relative abundance of Neisseria species was inversely correlated with the ACH production ability (P = 0.002).Conclusion: The salivary microbiota profile with a lower relative abundance of Neisseria species was independently associated with high ACH production ability, despite Neisseria species are dominant producers of ACH in vitro.

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A review of human carcinogens—Part E: tobacco, areca nut, alcohol, coal smoke, and salted fish

Cited by 968 publications

References 16 publications

The population impact of familial cancer, a major cause of cancer

The population impact of familial cancer, a major cause of cancer

National Institutes of Health Hematopoietic Cell Transplantation Late Effects Initiative: The Subsequent Neoplasms Working Group Report

Characterization of oral microbiota and acetaldehyde production

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