Gastric cancer is one of the most common causes of cancer-related mortality worldwide. The objective of this article is to review the epidemiology and biology of gastric cancer risk. This literature review explores the biological, clinical, and environmental factors that influence the rates of this disease and discuss the different intervention methods that may not only increase the awareness of gastric cancer but also increase screening in efforts to reduce the risk of gastric cancer. Helicobacter pylori infection is the primary risk factor for gastric cancer. Additional risk factors include geographical location, age, sex, smoking, socioeconomic status, dietary intake, and genetics. Primary and secondary prevention strategies such as dietary modifications and screenings are important measures for reducing the risk of gastric cancer. Interventions, such as H. pylori eradication through chemoprevention trials, have shown some potential as a preventative strategy. Although knowledge about gastric cancer risk has greatly increased, future research is warranted on the differentiation of gastric cancer epidemiology by subsite and exploring the interactions between H. pylori infection, genetics, and environmental factors. Better understanding of these relationships can help researchers determine the most effective intervention strategies for reducing the risk of this disease.

Use of non-cigarette tobacco products such as cigars and pipe has been increasing, even though these products entail exposure to similar carcinogens to those in cigarettes. More research is needed to explore the risk of these products to guide cancer prevention efforts. To measure the association between cigars and/or pipe smoking, and cancer incidence in men, we performed meta-analyses of data from five prospective cohorts. Cox regression was used to evaluate the association between different aspects of cigars and pipe smoking and risk of each smoking-related cancer (head and neck, esophagus, lung, stomach, liver, pancreas, kidney, and bladder) for each study. Adjusted HRs were combined using random-effects models. Cigars and/or pipe smokers were at increased risk for head and neck [HR, 1.51; 95% confidence interval (CI), 1.22-1.87], lung (HR, 2.04; 95% CI, 1.68-2.47), and liver cancers (HR, 1.56; 95% CI, 1.08-2.26). Ever-smokers of cigars and/or pipe had an increased risk of developing a smoking-related cancer when compared with never smokers of any tobacco product (overall HR, 1.07; 95% CI, 1.03-1.12). The risk for smoking-related cancers was also increased in mixed smokers who smoked cigars or pipe as well as cigarettes, even when they were smoking predominantly pipe or cigars. This pooled analysis highlights the increased risk for smoking-related cancers, particularly for lung and head and neck cancers in exclusive and predominant smokers (former and current) of cigars and pipe. Tobacco prevention efforts should include these products in addition to cigarettes. .

Background: Exposure to high levels of arsenic in drinking water has been associated with an increased risk of lung and bladder cancer, but the presence of an increased risk at low levels is questionable. Methods: A systematic review and a dose–response meta-analysis were conducted on risk estimates of lung and bladder cancer for exposure to arsenic in drinking water up to 150 µg/L, using a 2-stage approach based on a random-effects model. Results: Five studies of lung cancer were identified; the meta-relative risk (RR) for an increase of 10 µg/L arsenic level was 1.03 (95% confidence interval [CI]: 0.99-1.06; P heterogeneity = .05). The meta-analysis of bladder cancer included 8 studies; the meta-RR for an increase of 10 µg/L arsenic level was 1.02 (95% CI: 0.97-1.07, P heterogeneity = .01). Sensitivity analyses, including a 1-stage meta-regression, confirmed the main findings. Conclusion: This systematic review and meta-analysis provided evidence of a lack of an increased risk of lung and bladder cancer for exposure to arsenic in drinking water up to 150 µg/L, the highest concentration studied.

Background: Exposure to high arsenic concentrations in drinking water has been associated with skin lesions. Our goal was to conduct a systematic review of studies on skin lesions and arsenic exposure, with emphasis on results at low level of exposure. Methods: We conducted a systematic review of studies reporting estimates of either prevalence or risk of skin lesions associated with exposure to more than 2 levels of arsenic in drinking water. We reviewed and abstracted the relevant results, with the aim of conducting a dose-response meta-analysis. Results: Nine studies of skin lesions were reviewed. Strong heterogeneity in the results did not meet the criteria for performing a meta-analysis. The relative risks for an increase of 10 μg/L arsenic in drinking water ranged from 1.002 to 1.140 (p-value of heterogeneity < 0.0001). Protection from bias and confounding was inadequate in most studies. Conclusion: Current studies are inadequate to conduct meta-analysis on dose-response relationship between exposure to arsenic in drinking water and skin lesions. Studies with complete exposure histories indicate skin lesions are associated with arsenic exposure in excess of 50 µg/L or higher.