scholarly journals The Associations of Fruit and Vegetable Intake with Lung Cancer Risk in Participants with Different Smoking Status: A Meta-Analysis of Prospective Cohort Studies

Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1791 ◽  
Author(s):  
Chong Wang ◽  
Ting Yang ◽  
Xiao-fei Guo ◽  
Duo Li

The results of epidemiological studies on the relationship between fruit and vegetable intake and lung cancer risk were inconsistent among participants with different smoking status. The purpose of this study was to investigate these relationships in participants with different smoking status with prospective cohort studies. A systematic literature retrieval was conducted using PubMed and Scopus databases up to June 2019. The summary relative risks (RRs) and the corresponding 95% confidence intervals (CIs) were calculated by random-effects model. The nonlinear dose-response analysis was carried out with restricted cubic spline regression model. Publication bias was estimated using Begg’s test. Nine independent prospective studies were included for data synthesis. Dietary consumption of fruit was negatively correlated with lung cancer risk among current smokers and former smokers, and the summery RRs were 0.86 (95% CI: 0.78, 0.94) and 0.91 (95% CI: 0.84, 0.99), respectively. Consumption of vegetable was significantly associated with reduced risk of lung cancer for current smokers (summary RR = 87%; 95% CI: 0.78, 0.94), but not for former smokers and never for smokers. Dose-response analysis suggested that risk of lung cancer was reduced by 5% (95% CI: 0.93, 0.97) in current smokers, and reduced by 4% (95% CI: 0.93, 0.98) in former smokers with an increase of 100 grams of fruit intake per day, respectively. Besides, dose-response analysis indicated a 3% reduction in lung cancer risk in current smokers for 100 gram per day increase of vegetable intake (95% CI: 0.96, 1.00). The findings of this study provide strong evidence that higher fruit consumption is negatively associated with the risk of lung cancer among current smokers and former smokers, while vegetable intake is significantly correlated with reducing the risk of lung cancer in current smokers. These findings might have considerable public health significance for the prevention of lung cancer through dietary interventions.

1992 ◽  
Vol 2 (3) ◽  
pp. 177-194 ◽  
Author(s):  
Leslie Stayner ◽  
Randall Smith ◽  
Michael Thun ◽  
Teresa Schnorr ◽  
Richard Lemen

2016 ◽  
Vol 32 (5) ◽  
pp. 1196-1205 ◽  
Author(s):  
Frances C. Sherratt ◽  
Michael W. Marcus ◽  
Jude Robinson ◽  
John K. Field

Purpose: The current project sought to examine whether delivery of lung cancer risk projections (calculated using the Liverpool Lung Project [LLP] risk model) predicted follow-up smoking status. Design: Two single-blinded randomized controlled trials. Setting: Stop Smoking Services in Liverpool (United Kingdom). Participants: Baseline current smokers (N = 297) and baseline recent former smokers (N = 216) were recruited. Intervention: Participants allocated to intervention groups were provided with personalized lung cancer risk projections, calculated using the LLP risk model. Measures: Baseline and follow-up questionnaires explored sociodemographics, smoking behavior, and lung cancer risk perceptions. Analysis: Bivariate analyses identified significant differences between randomization groups, and logistic regression models were developed to investigate the intervention effect on the outcome variables. Results: Lung cancer risk projections were not found to predict follow-up smoking status in the trial of baseline current smokers; however, they did predict follow-up smoking status in the trial of baseline recent former smokers (odds ratio: 1.91; 95% confidence interval: 1.03-3.55). Conclusion: The current study suggests that lung cancer risk projections may help maintain abstinence among individuals who have quit smoking, but the results did not provide evidence to suggest that lung cancer risk projections motivate current smokers to quit.


2010 ◽  
Vol 28 (16) ◽  
pp. 2719-2726 ◽  
Author(s):  
Anil K. Chaturvedi ◽  
Neil E. Caporaso ◽  
Hormuzd A. Katki ◽  
Hui-Lee Wong ◽  
Nilanjan Chatterjee ◽  
...  

Purpose Chronic inflammation could play a role in lung carcinogenesis, underscoring the potential for lung cancer prevention and screening. We investigated the association of circulating high-sensitivity C-reactive protein (CRP, an inflammation biomarker) and CRP single nucleotide polymorphisms (SNPs) with prospective lung cancer risk. Patients and Methods We conducted a nested case-control study of 592 lung cancer patients and 670 controls with available prediagnostic serum and 378 patients and 447 controls with DNA within the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (N = 77,464). Controls were matched to patients on age, sex, entry year, follow-up time, and smoking. We measured CRP levels in baseline serum samples and genotyped five common CRP SNPs. Results Elevated CRP levels were associated with increased lung cancer risk (odds ratio [OR], 1.98; 95% CI, 1.35 to 2.89; P-trend < .001 for fourth quartile [Q4, ≥ 5.6 mg/L] v Q1 [< 1.0 mg/L]). The CRP association did not differ significantly by histology, follow-up time, or smoking status, but was most apparent for squamous cell carcinomas (OR, 2.92; 95% CI, 1.30 to 6.54), 2 to 5 years before lung cancer diagnosis (OR, 2.33; 95% CI, 1.24 to 4.39), and among former smokers (OR, 2.48; 95% CI, 1.53 to 4.03) and current smokers (OR, 1.90; 95% CI, 1.06 to 3.41). Although CRP SNPs and haplotypes were associated with CRP levels, they were not associated with lung cancer risk. Ten-year standardized absolute risks of lung cancer were higher with elevated CRP levels among former smokers (Q4: 2.55%; 95% CI, 1.98% to 3.27% v Q1: 1.39%; 95% CI, 1.07% to 1.81%) and current smokers (Q4: 7.37%; 95% CI, 5.81% to 9.33% v Q1: 4.03%; 95% CI, 3.01% to 5.40%). Conclusion Elevated CRP levels are associated with subsequently increased lung cancer risk, suggesting an etiologic role for chronic pulmonary inflammation in lung carcinogenesis.


2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
You Chen ◽  
Bao-ling Zhu ◽  
Cong-cong Wu ◽  
Rui-fang Lin ◽  
Xi Zhang

Background. The associations between periodontal disease, tooth loss, and lung cancer risk remain debatable. Therefore, the purpose of the present study is to evaluate whether periodontal disease and tooth loss are associated with lung cancer risk. Methods. A literature search was performed for relevant studies using PubMed and Embase databases. Risk ratio (RR) with 95% confidence interval (CI) was applied as effect size to summarize the associations between periodontal disease, tooth loss, and lung cancer risk. A further dose-response analysis was also performed. Results. A total of twelve studies comprising 263,238 participants were included. The results indicated that periodontal disease was positively associated with lung cancer risk (RR=1.37, 95%CI=1.16‐1.63). There was a positive association between tooth loss and lung cancer risk (RR=1.69, 95%CI=1.46‐1.96). Moreover, there was a significantly linear dose-response relationship between tooth loss and lung cancer risk, and every 5 increment in tooth loss was associated with 10% increased lung cancer risk. Similar results were obtained in subgroup analysis. Conclusions. Periodontal disease and tooth loss are increased risk factors for lung cancer. Prevention and treatment of periodontal disease may be effective potential prevention strategies for lung cancer.


BMJ Open ◽  
2018 ◽  
Vol 8 (9) ◽  
pp. e021059 ◽  
Author(s):  
Maureen Sanderson ◽  
Melinda C Aldrich ◽  
Robert S Levine ◽  
Barbara Kilbourne ◽  
Qiuyin Cai ◽  
...  

ObjectivesTo examine the association between neighbourhood deprivation and lung cancer risk.DesignNested case–control study.SettingSouthern Community Cohort Study of persons residing in 12 states in the southeastern USA.Participants1334 cases of lung cancer and 5315 controls.Primary outcome measureRisk of lung cancer.ResultsAfter adjustment for smoking status and other confounders, and additional adjustment for individual-level measures of socioeconomic status (SES), there was no monotonic increase in risk with worsening deprivation score overall or within sex and race groups. There was an increase among current and shorter term former smokers (p=0.04) but not among never and longer term former smokers. There was evidence of statistically significant interaction by sex among whites, but not blacks, in which the effect of worsening deprivation on lung cancer existed in males but not in females.ConclusionsArea-level measures of SES were associated with lung cancer risk in current and shorter term former smokers only in this population.


2016 ◽  
Vol 31 (1) ◽  
Author(s):  
Wei Jie Seow ◽  
Qing Lan

AbstractWhile there is strong evidence for the association between household air pollution and lung cancer among non-smoking women, the association between domestic incense use and lung cancer risk has been inconsistent. We conducted a systematic review of PubMed articles authored between 1969 and August 25, 2015 before performing a manual review of each study, and found a total of seven published studies on this topic. Most of the studies are case-control in design and did not further stratify by sex and smoking status. Of the seven studies, three reported positive associations, three reported null associations and one study found a negative association between incense use and lung cancer. Only one study reported estimates for non-smoking women. Future studies should be larger in sample size, stratify by both sex and smoking status in their analyses, and collect more detailed information on incense use in order to facilitate the understanding of the association between domestic incense use and lung cancer risk among non-smoking women in Asia.


2012 ◽  
Vol 30 (15_suppl) ◽  
pp. e21155-e21155
Author(s):  
Nagi B. Kumar ◽  
Gwendolyn P. Quinn ◽  
Theresa Crocker ◽  
Mark Alexandrow ◽  
Jhanelle Elaine Gray ◽  
...  

e21155 Background: Over 50% of new lung cancers occur in former smokers, who often are seeking strategies to reduce their lung cancer risk. However, recruitment and retention of participants in chemoprevention trials continues to be costly and presents unique challenges. Evaluation of feasibility and knowledge of challenges are critical to inform design and ensure accrual in chemoprevention trials.The study assessed interest and willingness of former heavy smokers to participate in a chemoprevention clinical trial using a botanical agent to prevent lung cancer. Methods: An introductory letter and survey instrument that included the goal of the survey, epidemiological and smoking history, acceptability of trial procedures, perception of lung cancer risk and interest in participating in this trial were mailed to 500 consecutive, former heavy smokers with no cancer from a database of 826 subjects at the Moffitt Cancer Center. Results: 202 (40.4%) men and women returned completed surveys. 98% of respondents were over age 60 and 56% had an undergraduate education or higher. The average years smoked was 40.7 (SD 11.9) pack years. 76% believed there was a 50% chance or greater of developing lung cancer. In response to interest and motivation to participate, 92-96% reported interest in receiving free lung exams, health status monitoring and knowing their lung cancer risk. 88% were interested in being a part of a trial to evaluate a botanical agent for lung cancer prevention. Over 92% of subjects reported a willingness to comply with study requirements, multiple blood draws and trips to the Center, spiral CTs and chest x-rays. Subjects were relatively less enthusiastic (73-79%) about undergoing bronchoscopy, taking multiple study agents and possible assignment to a placebo arm. Conclusions: Our study strongly suggests feasibility, highlights potential challenges and the significant interest and willingness of former smokers to participate in chemoprevention trials.


Epidemiology ◽  
1997 ◽  
Vol 8 (3) ◽  
pp. 304 ◽  
Author(s):  
Fredrik Nyberg ◽  
Inger Isaksson ◽  
Jennifer R. Harris ◽  
Göran Pershagen

Dose-Response ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 155932581983690 ◽  
Author(s):  
Louis Anthony (Tony) Cox

Chronic inflammation mediates an extraordinarily wide range of diseases. Recent progress in understanding intracellular inflammasome assembly, priming, activation, cytokine signaling, and interactions with mitochondrial reactive oxygen species, lysosome disruption, cell death, and prion-like polymerization and spread of inflammasomes among cells, has potentially profound implications for dose–response modeling. This article discusses mechanisms of exposure concentration and duration thresholds for NOD-like receptor protein 3 (NLRP3)-mediated inflammatory responses and develops a simple biomathematical model of the onset of exposure-related tissue-level chronic inflammation and resulting disease risks, focusing on respirable crystalline silica (RCS) and lung cancer risk as an example. An inflammation-mediated 2-stage clonal expansion model of RCS-induced lung cancer is proposed that explains why relatively low estimated concentrations of RCS (eg, <1 mg/m3) do not increase lung cancer risk and why even high occupational concentrations increase risk only modestly (typically relative risk <2). The model of chronic inflammation implies a dose–response threshold for excess cancer risk, in contrast to traditional linear-no-threshold assumptions. If this implication is correct, then concentrations of crystalline silica (or amphibole asbestos fibers, or other environmental challenges that act via the NLRP3 inflammasome) below the threshold do not cause chronic inflammation and resulting elevated risks of inflammation-mediated diseases.


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