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Background: A ban on the sale of menthol cigarettes in the United States is currently under consideration. A justification is that menthol cigarettes are harder to quit, particularly for African American smokers who use menthols much more frequently than White smokers, but epidemiologic data are limited.Methods: In a cohort of 16 425 mostly low-income African American and White current cigarette smokers enrolled during 2002-2009, we computed smoking quit and reuptake rates at 3 follow-ups conducted means of 4.6, 7.7, and 11 years after entry. Generalized estimation equations were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) for quitting and resuming smoking for menthol vs nonmenthol smokers adjusted for race, age, education, income, and smoking pack-years.Results: Crude annual quit rates among current smokers were 4.3% for menthol and 4.5% for nonmenthol smokers, with adjusted odds ratios of quitting for menthol vs nonmenthol smokers of 1.01 (95% CI = 0.91 to 1.11) overall, 0.99 (95% CI = 0.87 to 1.12) among African American smokers, and 1.02 (95% CI = 0.88 to 1.20) among White smokers. Crude annual smoking reuptake rates were somewhat higher among menthol smokers (8.4%) than nonmenthol smokers (7.1%), with an adjusted odds ratio of 1.19 (95% CI = 0.97 to 1.47), but net quit rates remained similar (OR = 1.01, 95% CI = 0.90 to 1.13 overall; OR = 1.00, 95% CI = 0.86 to 1.15 among African American participants; and OR = 1.04, 95% CI = 0.87 to 1.24 among White participants).Conclusions: This large-scale prospective survey revealed similar quit rates among menthol and nonmenthol smokers. Results contribute to policy discussions, especially if, as a meta-analysis suggests, lung cancer risk is higher for nonmenthol smokers and a ban leads menthol smokers to switch to nonmenthol cigarettes. [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection has been suggested to be associated with lung cancer risk. However, information is lacking on whether the association differs by H. pylori antigen. We conducted a nested case-control study within the Southern Community Cohort Study, including 295 incident lung cancer cases and 295 controls. Helicobacter pylori multiplex serology assay was performed to detect antibodies to 15 H. pylori proteins. Conditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals (95% CIs) after adjustment for covariates. Overall H. pylori + was associated with a non-statistically significant increased risk of lung cancer (OR: 1.29; 95% CI: 0.85–1.95). Significant associations, however, were observed for H. pylori + VacA+ (OR: 1.64; 95% CI: 1.02–2.62) and H. pylori + Catalase+ (OR: 1.75; 95% CI: 1.11–2.77). The positive association of H. pylori + Catalase+ with lung cancer risk was predominantly seen among African Americans (OR: 2.09; 95% CI: 1.11–3.95) but not European Americans (OR: 1.20; 95% CI: 0.56–2.54). Among participants who smoked ≥ 30 pack-years, overall H. pylori + (OR: 1.85; 95% CI: 1.02–3.35), H. pylori + CagA+ (OR: 2.77; 95% CI: 1.35–5.70), H. pylori + VacA+ (OR: 2.53; 95% CI: 1.25–5.13) and H. pylori + HP1564+ (OR: 2.01; 95% CI: 1.07–3.77) were associated with increased risk of lung cancer. Our study provides novel evidence that associations of H. pylori infection with lung cancer risk differ by H. pylori biomarker, may be more evident among African Americans and may be modified by smoking habits. Furthermore, studies are warranted to confirm our findings. [ABSTRACT FROM AUTHOR]

Background: The history of gestational diabetes mellitus (GDM) has been associated with breast cancer risk in some studies, particularly in young women, but results of cohort studies are conflicting.Methods: We pooled data from 257 290 young (age <55 years) women from five cohorts. We used multivariable Cox proportional-hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between GDM history and risk of breast cancer, overall and by oestrogen receptor (ER) status, before age 55 years, adjusted for established breast cancer risk factors.Results: Five percent of women reported a history of GDM and 6842 women reported an incident breast-cancer diagnosis (median follow-up = 16 years; maximum = 24 years). Compared with parous women without GDM, women with a history of GDM were not at increased risk of young-onset breast cancer overall (HR = 0.90; 95% CI: 0.78, 1.03) or by ER status (HR = 0.96; 95% CI: 0.79, 1.16 for ER-positive; HR = 1.07; 95% CI: 0.78, 1.47 for ER-negative). Compared with nulliparous women, parous women with a history of GDM had a lower risk of breast cancer overall (HR = 0.79; 95% CI: 0.68, 0.91) and of ER-positive (HR = 0.82; 95% CI: 0.66, 1.02) but not ER-negative (HR = 1.09; 95% CI: 0.76, 1.54) invasive breast cancer. These results were consistent with the HRs comparing parous women without GDM to nulliparous women.Conclusions: Results of this analysis do not support the hypothesis that GDM is a risk factor for breast cancer in young women. Our findings suggest that the well-established protective effect of parity on risk of ER-positive breast cancer persists even for pregnancies complicated by GDM. [ABSTRACT FROM AUTHOR]

Background Breast cancer–related lymphedema (BCRL) is a well-known side effect of cancer and its treatment with wide-ranging prevalence estimates. Objective This study describes associations between breast cancer–related lymphedema (BCRL) signs, symptoms, and diagnosis for women who were African American, white, or had a low income and survived breast cancer. Design This is a cross-sectional, observational study that used a computer-assisted telephone interview. Methods Women who had survived breast cancer were queried on the presence of 5 lymphedema signs and symptoms (edema in the breast, axilla, arm, and/or hand; tissue fibrosis; pitting; hemosiderin staining; heaviness) and whether they had a diagnosis of BCRL. Relationships between signs/symptoms and diagnosis for each group were evaluated with kappa and chi-square statistics. Results The study sample included 528 women who had survived breast cancer (266 white and 262 African American), with 514 reporting complete data on household income; 45% of the latter reported an annual household income of ≤$20,000. Women who were African American or had a low income were nearly twice as likely as women who were white to have any of 8 signs/symptoms of BCRL. Regardless of race and income, >50% of women with all BCRL signs and symptoms reported that they were not diagnosed with BCRL. Limitations The main limitations of our study are the lack of medical chart data and longitudinal design. Conclusions Women who were African American or had a low income and had survived breast cancer had a greater burden of BCRL signs and symptoms than women who were white. The lack of a strong association between BCRL signs, symptoms, and diagnosis suggests that BCRL may be underdiagnosed. These findings suggest that more rigorous screening and detection of BCRL—especially for women who are African American or have a low income—may be warranted. Cancer rehabilitation programs may be able to fill this gap. [ABSTRACT FROM AUTHOR]

Motivation The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern Identifier (SIPI) approach to evaluate 45 SNP interaction patterns/patterns. SIPI is statistically powerful but suffers from a large computation burden. For large-scale studies, it is necessary to use a powerful and computation-efficient method. The objective of this study is to develop an evidence-based mini-version of SIPI as the screening tool or solitary use and to evaluate the impact of inheritance mode and model structure on detecting SNP–SNP interactions. Results We tested two candidate approaches: the 'Five-Full' and 'AA9int' method. The Five-Full approach is composed of the five full interaction models considering three inheritance modes (additive, dominant and recessive). The AA9int approach is composed of nine interaction models by considering non-hierarchical model structure and the additive mode. Our simulation results show that AA9int has similar statistical power compared to SIPI and is superior to the Five-Full approach, and the impact of the non-hierarchical model structure is greater than that of the inheritance mode in detecting SNP–SNP interactions. In summary, it is recommended that AA9int is a powerful tool to be used either alone or as the screening stage of a two-stage approach (AA9int+SIPI) for detecting SNP–SNP interactions in large-scale studies. Availability and implementation The 'AA9int' and 'parAA9int' functions (standard and parallel computing version) are added in the SIPI R package, which is freely available at https://linhuiyi.github.io/LinHY%5fSoftware/. Supplementary information Supplementary data are available at Bioinformatics online. [ABSTRACT FROM AUTHOR]

Background: Self-reported smoking is the principal measure used to assess lung cancer risk in epidemiological studies. We evaluated if circulating cotinine-a nicotine metabolite and biomarker of recent tobacco exposure-provides additional information on lung cancer risk.Methods: The study was conducted in the Lung Cancer Cohort Consortium (LC3) involving 20 prospective cohort studies. Pre-diagnostic serum cotinine concentrations were measured in one laboratory on 5364 lung cancer cases and 5364 individually matched controls. We used conditional logistic regression to evaluate the association between circulating cotinine and lung cancer, and assessed if cotinine provided additional risk-discriminative information compared with self-reported smoking (smoking status, smoking intensity, smoking duration), using receiver-operating characteristic (ROC) curve analysis.Results: We observed a strong positive association between cotinine and lung cancer risk for current smokers [odds ratio (OR ) per 500 nmol/L increase in cotinine (OR500): 1.39, 95% confidence interval (CI): 1.32-1.47]. Cotinine concentrations consistent with active smoking (≥115 nmol/L) were common in former smokers (cases: 14.6%; controls: 9.2%) and rare in never smokers (cases: 2.7%; controls: 0.8%). Former and never smokers with cotinine concentrations indicative of active smoking (≥115 nmol/L) also showed increased lung cancer risk. For current smokers, the risk-discriminative performance of cotinine combined with self-reported smoking (AUCintegrated: 0.69, 95% CI: 0.68-0.71) yielded a small improvement over self-reported smoking alone (AUCsmoke: 0.66, 95% CI: 0.64-0.68) (P = 1.5x10-9).Conclusions: Circulating cotinine concentrations are consistently associated with lung cancer risk for current smokers and provide additional risk-discriminative information compared with self-report smoking alone. [ABSTRACT FROM AUTHOR]

Multiple myeloma (MM) incidence and mortality are higher among African Americans (AAs) than among other population groups. The prevalence of obesity is also elevated among AAs, but few studies have examined risk of this cancer in relation to body size among AAs. We combined data from seven prospective cohorts tracking mortality among 239 597 AA adults and used Cox proportional hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for death because of MM according to body mass index (BMI) at cohort entry, adjusted for age (as time-scale) and sex. Relative to those with normal BMIs (18.5-25 kg/m(2)), mortality increased monotonically as BMI increased, with hazard ratios reaching 1.43 (95% CI = 1.03 to 1.97) for BMIs of 35 kg/m(2) or greater. The findings suggest that obesity is a risk factor for MM and a contributor to the elevated rates and rising incidence trends of MM among AAs in the United States. [ABSTRACT FROM AUTHOR]

Although much research has been conducted on the role adult body mass index (BMI) plays in mortality, there have been fewer studies that evaluated the associations of BMI in young adulthood and adult weight trajectory with mortality, and it remains uncertain whether associations differ by race or sex. We prospectively examined the relationships of BMI in young adulthood (21 years of age) and adult obesity trajectory with later-life mortality rates among 75,881 men and women in the Southern Community Cohort Study. Study participants were enrolled between 2002 and 2009 at ages 40-79 years and were followed through December, 2011. Multivariable Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals. There were 7,301 deaths in the 474,970 person-years of follow-up. Participants who reported being overweight or obese as young adults had mortality rates that were 19% (95% confidence interval: 12, 27) and 64% (95% confidence interval: 52, 78) higher, respectively, than those of their normal weight counterparts. The results did not significantly differ by race or sex. Participants who reported being obese in young adulthood only or in both young and middle adulthood experienced mortality rates that were 40%-90% higher than those of participants who were non-obese at either time. These results suggest that obesity in young adulthood is associated with higher mortality risk regardless of race, sex, and obesity status in later life. [ABSTRACT FROM AUTHOR]

The article focuses on quantitative estimates of cancer risks made by researchers Richard Doll and Richard Peto. Topics discussed include their review of factors known at the time to affect cancer risk; cigarette smoking as the major single preventable cause of cancer in the U.S.; and estimate that cigarette smoking accounted for about 30 percent of all cancer deaths in 1978 in the country.

We investigated genetic variation in CYP2A6 in relation to lung cancer risk among African American smokers, a high-risk population. Previously, we found that CYP2A6, a nicotine/nitrosamine metabolism gene, was associated with lung cancer risk in European Americans, but smoking habits, lung cancer risk and CYP2A6 gene variants differ significantly between European and African ancestry populations. Herein, African American ever-smokers, drawn from two independent lung cancer case–control studies, were genotyped for reduced activity CYP2A6 alleles and grouped by predicted metabolic activity. Lung cancer risk in the Southern Community Cohort Study (n = 494) was lower among CYP2A6 reduced versus normal metabolizers, as estimated by multivariate conditional logistic regression [odds ratio (OR) = 0.44; 95% confidence interval (CI) = 0.26–0.73] and by unconditional logistic regression (OR = 0.62; 95% CI = 0.41–0.94). The association was replicated in an independent study from MD Anderson Cancer Center (n = 407) (OR = 0.64; 95% CI = 0.42–0.98), and pooling the studies yielded an OR of 0.64 (95% CI = 0.48–0.86). Exploratory analyses revealed a significant interaction between CYP2A6 genotype and sex on the risk for lung cancer (Southern Community Cohort Study: P = 0.04; MD Anderson: P = 0.03; Pooled studies: P = 0.002) with a CYP2A6 effect in men only. These findings support a contribution of genetic variation in CYP2A6 to lung cancer risk among African American smokers, particularly men, whereby CYP2A6 genotypes associated with reduced metabolic activity confer a lower risk of developing lung cancer. [ABSTRACT FROM AUTHOR]

There is limited evidence demonstrating the benefits of physical activity with regard to mortality risk or the harms associated with sedentary behavior in black adults, so we examined the relationships between these health behaviors and cause-specific mortality in a prospective study that had a large proportion of black adults. Participants (40–79 years of age) enrolled in the Southern Community Cohort Study between 2002 and 2009 (n = 63,308) were prospectively followed over 6.4 years, and 3,613 and 1,394 deaths occurred in blacks and whites, respectively. Black adults who reported the highest overall physical activity level (≥32.3 metabolic equivalent-hours/day vs. <9.7 metabolic equivalent-hours/day) had lower risks of death from all causes (hazard ratio (HR) = 0.76. 95% confidence interval (CI): 0.69, 0.85), cardiovascular disease (HR = 0.81, 95% CI: 0.67, 0.98), and cancer (HR = 0.76, 95% CI: 0.62, 0.94). In whites, a higher physical activity level was associated with a lower risk of death from all causes (HR = 0.76, 95% CI: 0.64, 0.90) and cardiovascular disease (HR = 0.69, 95% CI: 0.49, 0.99) but not cancer (HR = 0.95, 95% CI: 0.67, 1.34). Spending more time being sedentary (>12 hours/day vs. <5.76 hours/day) was associated with a 20%–25% increased risk of all-cause mortality in blacks and whites. Blacks who reported the most time spent being sedentary (≥10.5 hours/day) and lowest level of physical activity (<12.6 metabolic equivalent-hours/day) had a greater risk of death (HR = 1.47, 95% CI: 1.25, 1.71). Our study provides evidence that suggests that health promotion efforts to increase physical activity level and decrease sedentary time could help reduce mortality risk in black adults. [ABSTRACT FROM PUBLISHER]

Among 2258 Helicobacter pylori-seropositive subjects randomly assigned to receive one-time H. pylori treatment with amoxicillin-omeprazole or its placebo, we evaluated the 15-year effect of treatment on gastric cancer incidence and mortality in subgroups defined by age, baseline gastric histopathology, and post-treatment infection status. We used conditional logistic and Cox regressions for covariable adjustments in incidence and mortality analyses, respectively. Treatment was associated with a statistically significant decrease in gastric cancer incidence (odds ratio = 0.36; 95% confidence interval [Cl] = 0.17 to 0.79) and mortality (hazard ratio = 0.26; 95% Cl = 0.09 to 0.79) at ages 55 years and older and a statistically significant decrease in incidence among those with intestinal metaplasia or dysplasia at baseline (odds ratio = 0.56; 95% Cl = 0.34 to 0.91). Treatment benefits for incidence and mortality among those with and without post-treatment infection were similar. Thus H. pylori treatment can benefit older members and those with advanced baseline histopathology, and benefits are present even with post-treatment infection, suggesting treatment can benefit an entire population, not just the young or those with mild histopathology. [ABSTRACT FROM AUTHOR]

The beneficial biologic effects attributed to vitamin D suggest a potential to influence overall mortality. Evidence addressing this hypothesis is limited, especially for African Americans who have a high prevalence of vitamin D insufficiency. The authors conducted a nested case-control study within the prospective Southern Community Cohort Study to relate baseline serum levels of 25-hydroxyvitamin D (25(OH)D) with subsequent mortality. Cases were 1,852 participants who enrolled from 2002 to 2009 and died >12 months postenrollment. Controls (n = 1,852) were matched on race, sex, age, enrollment site, and blood collection date. The odds ratios for quartile 1 (<10.18 ng/mL) versus quartile 4 (>21.64 ng/mL) levels of 25(OH)D were 1.60 (95% confidence interval (CI): 1.20, 2.14) for African Americans and 2.11 (95% CI: 1.39, 3.21) for non-African Americans. The effects were strongest for circulatory disease death, where quartile 1 versus quartile 4 odds ratios were 2.53 (95% CI: 1.44, 4.46) and 3.25 (95% CI: 1.33, 7.93) for African Americans and non-African Americans, respectively. The estimated odds of total mortality were minimized in the 25(OH)D range of 35–40 ng/mL. These findings provide support for the hypothesis that vitamin D status may have an important influence on mortality for both African Americans and non-African Americans. [ABSTRACT FROM PUBLISHER]

Type 2 diabetes (T2D) is up to twice as prevalent among African Americans as Caucasians. Recent genome-wide association studies (GWAS) have identified multiple common genetic risk variants for T2D; however, none of these studies were conducted exclusively among subjects of African ancestry. Investigating these known loci in other populations would be an expedient way to evaluate the generalizability of the current findings. The authors evaluated 29 known T2D loci in a large southeastern US cohort study including 4,288 African Americans (1,554 cases and 2,734 controls) enrolled during 2002–2009. Seven of the 29 single nucleotide polymorphisms (SNPs) examined were found to be associated with T2D risk at P ≤ 0.05, including rs6769511 (IGF2BP2), 2 SNPs in the WFS1 gene (rs4689388 and rs1801214), rs7903146 (TCF7L2), and 3 SNPs in the KCNQ1 gene (rs231362, rs2237892, and rs2237897). Notably, the association for rs7903146 reached the GWAS significance level (P = 3.6 × 10−8), with an odds ratio per T allele of 1.32 (95% confidence interval: 1.20, 1.46). Regional analyses using GWAS data from Vanderbilt University's BioVU DNA biobank showed significant associations (P < 0.05) with 9 loci, though no association was observed for the index SNPs reported in European- or Asian-ancestry populations. These results extend some of the recent GWAS findings to African Americans and may guide future efforts to identify causal variants for T2D. [ABSTRACT FROM PUBLISHER]

Prospective epidemiologic studies generally rely on 1 baseline biologic sample from participants for measurement of prediagnostic biomarkers, assuming that 1 measurement adequately represents the participant's “typical” level. The body of work assessing the reproducibility of circulating serum 25-hydroxyvitamin D (25(OH)D) levels over time focuses almost exclusively on populations of European descent, and data for vitamin D-binding protein (VDBP) are virtually nonexistent. Thus, the authors measured levels of serum 25(OH)D and VDBP twice in samples collected between 2005 and 2008 from 225 participants (155 black, 70 white) in the Southern Community Cohort Study. Reproducibility for 25(OH)D was uniformly high, with adjusted intraclass correlation coefficients (ICCs) of 0.84 (95% confidence interval (CI): 0.79, 0.88) for blacks and 0.92 (95% CI: 0.87, 0.95) for whites, and there was substantial agreement for assignment of 25(OH)D quartile (κ = 0.83, 95% CI: 0.78, 0.87) and vitamin D adequacy status (κ = 0.76, 95% CI: 0.69, 0.83). VDBP levels were highly stable over time, with adjusted ICCs of 0.97 (95% CI: 0.96, 0.98) for blacks and 0.96 (95% CI: 0.93, 0.97) for whites. These findings suggest that single, baseline 25(OH)D and VDBP serum measurements provide reasonably representative measures of these compounds for both white and black adults, demonstrating their utility as epidemiologic biomarkers in prospective studies. [ABSTRACT FROM PUBLISHER]

In recent pooled analyses among whites and Asians, mortality was shown to rise markedly with increasing body mass index (BMI; weight (kg)/height (m)2), but much less is known about this association among blacks. This study prospectively examined all-cause mortality in relation to BMI among 22,014 black males, 9,343 white males, 30,810 black females, and 14,447 white females, aged 40–79 years, from the Southern Community Cohort Study, an epidemiologic cohort of largely low-income participants in 12 southeastern US states. Participants enrolled in the cohort from 2002 to 2009 and were followed up to 8.9 years. Hazard ratios and 95% confidence intervals for mortality were obtained from sex- and race-stratified Cox proportional hazards models in association with BMI at cohort entry, adjusting for age, education, income, cigarette smoking, and alcohol consumption. Elevated BMI was associated with increased mortality among whites (hazard ratios for BMI >40 vs. 20–24.9 = 1.37 (95% confidence interval (CI): 1.02, 1.84) and 1.47 (95% CI: 1.15, 1.89) for white males and white females, respectively) but not significantly among blacks (hazard ratios = 1.13 (95% CI: 0.89, 1.43) and 0.87 (95% CI: 0.72, 1.04) for black males and black females, respectively). In this large cohort, obesity in mid-to-late adulthood among blacks was not associated with the same excess mortality risk seen among whites. [ABSTRACT FROM PUBLISHER]

In the Shandong Intervention Trial, 2 weeks of antibiotic treatment for Helicobacter pylori reduced the prevalence of precancerous gastric lesions, whereas 7.3 years of oral supplementation with garlic extract and oil (garlic treatment) or vitamin C, vitamin E, and selenium (vitamin treatment) did not. Here we report 14.7-year follow-up for gastric cancer incidence and cause-specific mortality among 3365 randomly assigned subjects in this masked factorial placebo-controlled trial. Conditional logistic regression was used to estimate the odds of gastric cancer incidence, and the Cox proportional hazards model was used to estimate the relative hazard of cause-specific mortality. All statistical tests were two-sided. Gastric cancer was diagnosed in 3.0% of subjects who received H pylori treatment and in 4.6% of those who received placebo (odds ratio = 0.61, 95% confidence interval = 0.38 to 0.96, P = .032). Gastric cancer deaths occurred among 1.5% of subjects assigned H pylori treatment and among 2.1% of those assigned placebo (hazard ratio [HR] of death = 0.67, 95% CI = 0.36 to 1.28). Garlic and vitamin treatments were associated with non-statistically significant reductions in gastric cancer incidence and mortality. Vitamin treatment was associated with statistically significantly fewer deaths from gastric or esophageal cancer, a secondary endpoint (HR = 0.51, 95% CI = 0.30 to 0.87; P = .014). [ABSTRACT FROM PUBLISHER]

Background: Research suggests individuals with diabetes are twice as likely as those without diabetes to be clinically depressed. Still unknown is the relationship between diabetes and depression in socioeconomically disadvantaged populations. Purpose: We examined the relationship between diabetes and depressive symptoms in a large, racially diverse, low-income cohort in the southeastern USA. Methods: A total of 69,068 adults were recruited from community health centers in 12 southeastern states. A fully adjusted polytomous logistic regression model tested the relationship between demographics, lifestyle behaviors, antidepressant use, body mass index, diabetes diagnosis, diabetes duration, diabetes medication compliance, and depressive symptoms using the Centers for Epidemiological Studies Depression scale. Results: Diabetes was present in 21.7% of sample. While a diabetes diagnosis was associated with having severe depressive symptoms (AOR, 1.24; 95% CI, 1.14-1.34), demographics, lifestyle behaviors, body mass index and antidepressant use were more strongly associated with severe depressive symptoms than a diabetes diagnosis. Conclusions: Having diabetes was associated with the presence and severity of depressive symptoms in a large, low-income sample of racially diverse adults. However, the relationship between diabetes and depressive symptoms was weaker than in other studies with higher socioeconomic groups. [ABSTRACT FROM AUTHOR]

Background Menthol cigarettes, preferred by African American smokers, have been conjectured to be harder to quit and to contribute to the excess lung cancer burden among black men in the Unites States. However, data showing an association between smoking menthol cigarettes and increased lung cancer risk compared with smoking nonmenthol cigarettes are limited. The Food and Drug Administration is currently considering whether to ban the sale of menthol cigarettes in the United States. Methods We conducted a prospective study among 85 806 racially diverse adults enrolled in the Southern Community Cohort Study during March 2002 to September 2009 according to cigarette smoking status, with smokers classified by preference for menthol vs nonmenthol cigarettes. Among 12 373 smokers who responded to a follow-up questionnaire, we compared rates of quitting between menthol and nonmenthol smokers. In a nested case–control analysis of 440 incident lung cancer case patients and 2213 matched control subjects, using logistic regression modeling we computed odds ratios (ORs) and accompanying 95% confidence intervals (CIs) of lung cancer incidence, and applied Cox proportional hazards modeling to estimate hazard ratios (HRs) of lung cancer mortality, according to menthol preference. Results Among both blacks and whites, menthol smokers reported smoking fewer cigarettes per day; an average of 1.6 (95% CI = 1.3 to 2.0) fewer for blacks and 1.8 (95% CI = 1.3 to 2.3) fewer for whites, compared with nonmenthol smokers. During an average of 4.3 years of follow-up, 21% of participants smoking at baseline had quit, with menthol and nonmenthol smokers having equal odds of quitting (OR = 1.02, 95% CI = 0.89 to 1.16). A lower lung cancer incidence was noted in menthol vs nonmenthol smokers (for smokers of <10, 10–19, and ≥20 cigarettes per day, compared with never smokers, OR = 5.0 vs 10.3, 8.7 vs 12.9, and 12.2 vs 21.1, respectively). These trends were mirrored for lung cancer mortality. In multivariable analyses adjusted for pack-years of smoking, menthol cigarettes were associated with a lower lung cancer incidence (OR = 0.65, 95% CI = 0.47 to 0.90) and mortality (hazard ratio of mortality = 0.69, 95% CI = 0.49 to 0.95) than nonmenthol cigarettes. Conclusions The findings suggest that menthol cigarettes are no more, and perhaps less, harmful than nonmenthol cigarettes. [ABSTRACT FROM PUBLISHER]

Few food frequency questionnaires (FFQs) have been developed specifically for use among African Americans, and reports of FFQ performance among African Americans or low-income groups assessed using biochemical indicators are scarce. The authors conducted a validation study within the Southern Community Cohort Study to evaluate FFQ-estimated intakes of α-carotene, β-carotene, β-cryptoxanthin, lutein/zeaxanthin, lycopene, folate, and α-tocopherol in relation to blood levels of these nutrients. Included were 255 nonsmoking participants (125 African Americans, 130 non-Hispanic whites) who provided a blood sample at the time of study enrollment and FFQ administration in 2002–2004. Levels of biochemical indicators of each micronutrient (α-tocopherol among women only) significantly increased with increasing FFQ-estimated intake (adjusted correlation coefficients: α-carotene, 0.35; β-carotene, 0.28; β-cryptoxanthin, 0.35; lutein/zeaxanthin, 0.28; lycopene, 0.15; folate, 0.26; α-tocopherol, 0.26 among women; all P's < 0.05). Subjects in the top decile of FFQ intake had blood levels that were 27% (lycopene) to 178% (β-cryptoxanthin) higher than those of subjects in the lowest decile. Satisfactory FFQ performance was noted even for participants with less than a high school education. Some variation was noted in the FFQ's ability to predict blood levels for subgroups defined by race, sex, and other characteristics, but overall the Southern Community Cohort Study FFQ appears to generate useful dietary exposure rankings in the cohort. [ABSTRACT FROM PUBLISHER]

A letter to the editor is presented in response to the article on the commentary in cancer epidemiology's false-positive results by Boffetta and colleagues.

False-positive results are inherent in the scientific process of testing hypotheses concerning the determinants of cancer and other human illnesses. Although much of what is known about the etiology of human cancers has arisen from well-conducted epidemiological studies, epidemiology has been increasingly criticized for producing findings that are often sensationalized in the media and fail to be upheld in subsequent studies. Herein we describe examples from cancer epidemiology of likely false-positive findings and discuss conditions under which such results may occur. We suggest general guidelines or principles, including the endorsement of editorial policies requiring the prominent listing of study caveats, which may help reduce the reporting of misleading results. Increased epistemological humility regarding findings in epidemiology would go a long way to diminishing the detrimental effects of false-positive results on the allocation of limited research resources, on the advancement of knowledge of the causes and prevention of cancer, and on the scientific reputation of epidemiology and would help to prevent oversimplified interpretations of results by the media and the public. [ABSTRACT FROM AUTHOR]

Background: Randomized trials have yielded mixed results on the effects of treatment for Helicobacter pylori and little information on the effects of vitamins or garlic supplements on precancerous gastric lesions. We conducted a randomized trial to test the effects of one-time H. pylori treatment and long-term vitamin or garlic supplements in reducing the prevalence of advanced precancerous gastric lesions. Methods: Most of the adults aged 35-64 years in 13 randomly selected villages in Linqu County, Shandong Province, China, were identified and given baseline endoscopies in 1994. In 1995, 3365 eligible subjects were randomly assigned in a factorial design to three interventions or placebos: amoxicillin and omeprazole for 2 weeks in 1995 (H. pylori treatment); vitamin C, vitamin E, and selenium for 7.3 years (vitamin supplement); and aged garlic extract and steam-distilled garlic oil for 7.3 years (garlic supplement). Subjects underwent endoscopies with biopsies in 1999 and 2003, and the prevalence of precancerous gastric lesions was determined by histopathologic examination of seven standard biopsy sites. The 3365 eligible randomized subjects represented 93.5% of those with baseline endoscopy and included all baseline histologic categories except gastric cancer. Only 0.18% had normal gastric mucosa. Logistic regression was used to estimate the intervention effects on the odds of advanced precancerous gastric lesions, and t-tests were used to assess effects on histologic severity. All statistical tests were two-sided. Results: H. pylori treatment resulted in statistically significant decreases in the combined prevalence of severe chronic atrophic gastritis, intestinal metaplasia, dysplasia, or gastric cancer in 1999 (odds ratio [OR] = 0.77; 95% confidence interval [CI] = 0.62 to 0.95) and in 2003 (OR = 0.60; 95% CI = 0.47 to 0.75), and had favorable effects on the average histopathologic severity and on progression and regression of precancerous gastric lesions in 2003. H. pylori treatment did not reduce the combined prevalence of dysplasia or gastric cancer. However, fewer subjects receiving H. pylori treatment (19/1130; 1.7%) than receiving placebo (27/1128; 2.4%) developed gastric cancer (adjusted P= .14). No statistically significant favorable effects were seen for garlic or vitamin supplements. Conclusion: H. pylori treatment reduces the prevalence of precancerous gastric lesions and may reduce gastric cancer incidence, but further data are needed to prove the latter point. Long-term vitamin or garlic supplementation had no beneficial effects on the prevalence of precancerous gastric lesions or on gastric cancer incidence. [ABSTRACT FROM AUTHOR]

Carbonated soft drinks (CSDs) have been associated with gastroesophageal reflux, an established risk factor for esophageal adenocarcinoma. As both CSD consumption and esophageal adenocarcinoma incidence have sharply increased in recent decades, we examined CSD as a risk factor for esophageal and gastric cancers in a U.S. multicenter, population-based case-control study. Associations between CSD intake and risk were estimated by adjusted odds ratios (ORs), comparing the highest versus lowest quartiles of intake. All statistical tests were two-sided. Contrary, to the proposed hypothesis, CSD consumption was inversely associated with esophageal adenocarcinoma risk (highest versus lowest quartiles, OR = 0.47, 95% confidence interval = 0.29 to 0.76; Ptrend = .005), due primarily to intake of diet CSD. High CSD consumption did not increase risk of any esophageal or gastric cancer subtype in men or women or when analyses were restricted to nonproxy interviews. These findings indicate that CSD consumption (especially diet CSD) is inversely associated with risk of esophageal adenocarcinoma, and thus it is not likely to have contributed to the rising incidence rates. [ABSTRACT FROM AUTHOR]

Background: An inverse association between Helicobacter pylori infection and esophageal adenocarcinoma has been reported that may be attributed to reduced acidity from inducing atrophic gastritis and from producing ammonia. We examined associations between H. pylori infection, gastric atrophy, and the risk of esophageal adenocarcinoma, esophageal squamous-cell carcinoma, and gastric cardia adenocarcinoma in a large population-based case-control study in Sweden.Methods: Self-reported data were obtained during interviews, and serum was collected from 97 patients with incident esophageal adenocarcinoma, 85 patients with incident esophageal squamous-cell carcinoma, 133 patients with incident gastric cardia adenocarcinoma, and 499 randomly selected control subjects. Serum antibodies against whole H. pylori cell-surface antigens (HP-CSAs) and cytotoxin-associated gene A (CagA) antigens were assessed by an IgG enzyme-linked immunosorbent assay and immunoblotting, respectively. Gastric atrophy was assessed by serum levels of pepsinogen I. Multivariable logistic regression with adjustment for potential confounding factors was used to evaluate associations.Results: H. pylori infection, assayed by HP-CSA or CagA antibodies, was statistically significantly associated with a reduced risk for esophageal adenocarcinoma (for HP-CSA antibodies, odds ratio [OR] = 0.3, 95% confidence interval [CI] = 0.2 to 0.6; for CagA antibodies, OR = 0.5, 95% CI = 0.3 to 0.8; for both, OR = 0.2, 95% CI = 0.1 to 0.5). Gastric atrophy was not associated with the risk for esophageal adenocarcinoma (OR = 1.1, 95% CI = 0.5 to 2.5). Serum CagA antibodies and gastric atrophy were associated with an increased risk for esophageal squamous-cell carcinoma (OR = 2.1, 95% CI = 1.1 to 4.0, and OR = 4.3, 95% CI = 1.9 to 9.6, respectively). The risk of gastric cardia adenocarcinoma was not associated with H. pylori infection. However, gastric atrophy was associated with an increased risk for gastric cardia adenocarcinoma (OR = 4.5, 95% CI = 2.5 to 7.8).Conclusions: Infection with H. pylori may reduce the risk of esophageal adenocarcinoma, but it is unlikely to do so by atrophy-reduced acidity. Gastric atrophy and infection with CagA-positive strains of H. pylori may increase the risk for esophageal squamous-cell carcinoma. [ABSTRACT FROM AUTHOR]

Background: An inverse association between Helicobacter pylori infection and esophageal adenocarcinoma has been reported that may be attributed to reduced acidity from inducing atrophic gastritis and from producing ammonia. We examined associations between H. pylori infection, gastric atrophy, and the risk of esophageal adenocarcinoma, esophageal squamous-cell carcinoma, and gastric cardia adenocarcinoma in a large population-based case-control study in Sweden. Methods: Self-reported data were obtained during interviews, and serum was collected from 97 patients with incident esophageal adenocarcinoma, 85 patients with incident esophageal squamous-cell carcinoma, 133 patients with incident gastric cardia adenocarcinoma, and 499 randomly selected control subjects. Serum antibodies against whole H. pylori cell-surface antigens (HP-CSAs) and cytotoxin-associated gene A (CagA) antigens were assessed by an IgG enzyme-linked immunosorbent assay and immunoblotting, respectively. Gastric atrophy was assessed by serum levels of pepsinogen I. Multivariable logistic regression with adjustment for potential confounding factors was used to evaluate associations. Results: H. pylori infection, assayed by HP-CSA or CagA antibodies, was statistically significantly associated with a reduced risk for esophageal adenocarcinoma (for HP-CSA antibodies, odds ratio [OR] = 0.3, 95% confidence interval [CI] = 0.2 to 0.6; for CagA antibodies, OR = 0.5, 95% CI = 0.3 to 0.8; for both, OR = 0.2, 95% CI = 0.1 to 0.5). Gastric atrophy was not associated with the risk for esophageal adenocarcinoma (OR = 1.1, 95% CI = 0.5 to 2.5). Serum CagA antibodies and gastric atrophy were associated with an increased risk for esophageal squamous-cell carcinoma (OR = 2.1, 95% CI = 1.1 to 4.0, and OR = 4.3, 95% CI = 1.9 to 9.6, respectively). The risk of gastric cardia adenocarcinoma was not associated with H. pylori infection. However, gastric atrophy was associated with an increased risk for gastric cardia adenocarcinoma (OR = 4.5, 95% CI = 2.5 to 7.8). Conclusions: Infection with H. pylori may reduce the risk of esophageal adenocarcinoma, but it is unlikely to do so by atrophyreduced acidity. Gastric atrophy and infection with CagApositive strains of H. pylori may increase the risk for esophageal squamous-cell carcinoma. [ABSTRACT FROM AUTHOR]

Background: Several risk factors have been identified for esophageal adenocarcinoma, gastric cardia adenocarcinoma, esophageal squamous cell carcinoma, and noncardia gastric adenocarcinoma, but no study has comprehensively examined their contributions to the cancer burden in the general population. Herein, we estimate the population attributable risks (PARs) for various risk factors observed in a multicenter population-based case-control study. Methods: We calculated PARs by using 293 patients with esophageal adenocarcinoma, 261 with gastric cardia adenocarcinoma, 221 with esophageal squamous cell carcinoma, 368 with noncardia gastric adenocarcinoma, and 695 control subjects. We included smoking for all four tumor types and Helicobacter pylori infection for noncardia gastric adenocarcinoma as established causal risk factors as well as several other factors for which causality is under evaluation. Results: Ever smoking, body mass index above the lowest quartile, history of gastroesophageal reflux, and low fruit and vegetable consumption accounted for 39.7% (95% confidence interval [CI] = 25.6% to 55.8%), 41.1% (95% CI = 23.8% to 60.9%), 29.7% (95% CI = 19.5% to 42.3%), and 15.3% (95% CI = 5.8% to 34.6%) of esophageal adenocarcinomas, respectively, with a combined PAR of 78.7% (95% CI = 66.5% to 87.3%). Ever smoking and body mass index above the lowest quartile were responsible for 45.2% (95% CI = 31.3% to 59.9%) and 19.2% (95% CI = 4.9% to 52.0%) of gastric cardia adenocarcinomas, respectively, with a combined PAR of 56.2% (95% CI = 38.1% to 72.8%). Ever smoking, alcohol consumption, and low fruit and vegetable consumption accounted for 56.9% (95% CI = 36.6% to 75.1%), 72.4% (95% CI = 53.3% to 85.8%), and 28.7% (95% CI = 11.1% to 56.5%) of esophageal squamous cell carcinomas, respectively, with a combined PAR of 89.4% (95% CI = 79.1% to 95.0%). Ever smoking, history of gastric ulcers, nitrite intake above the lowest quartile, and H. pylori infection were responsible for 18.3% (95% CI = 6.5% to 41.8%), 9.7% (95% CI = 5.4% to 16.8%), 40.7% (95% CI = 23.4% to 60.7%), and 10.4% (95% CI = 0.3% to 79.6%) of noncardia gastric adenocarcinomas, respectively, with a combined PAR of 59.0% (95% CI = 16.2% to 91.4%). Conclusion: In this population, a few known risk factors account for a majority of esophageal and gastric cancers. These results suggest that the incidence of these cancers may be decreased by reducing the prevalence of smoking, gastroesophageal reflux, and being overweight and by increasing the consumption of fruits and vegetables. [ABSTRACT FROM AUTHOR]

Background: Orthopedic implants and their fixatives contain materials with carcinogenic potential. Whether these implants are linked to subsequent cancer development remains unknown, mainly because large-scale, long-term follow-up data are scarce.Methods: We conducted a nationwide cohort study in Sweden to examine cancer incidence among 116,727 patients who underwent hip replacement surgery during the period from 1965 through 1994. Through record linkage to the Swedish Cancer Register, we identified all incident cancers through 1995 in this population (693,954 person-years of observation). For each cancer type, the observed number of cases was divided by that expected in the general Swedish population to produce standardized incidence ratios (SIRs).Results: Relative to the general population, the cohort had no overall cancer excess (SIR = 1.01; 95% confidence interval [CI] = 0.99 to 1.03). However, we observed elevated SIRs for prostate cancer (SIR = 1.16; 95% CI = 1.11 to 1.22) and melanoma (SIR = 1.15; 95% CI = 1.01 to 1.30) and a reduction in stomach cancer risk (SIR = 0.83; 95% CI = 0.75 to 0.92). Long-term follow-up (>or=15 years) revealed an excess of multiple myeloma (SIR = 1.86; 95% CI = 1.01 to 3.11) and a statistically nonsignificant increase in bladder cancer (SIR = 1.42; 95% CI = 0.98 to 1.99). There was no material increase in risk for bone or connective tissue cancer for either men or women in any follow-up period.Conclusions: In this, the largest study to date, hip implant patients had similar rates of most types of cancer to those in the general population. Although the excesses of melanoma, multiple myeloma, and prostate and bladder cancers may be due to chance, confounding, or detection bias and should be interpreted cautiously, they warrant further investigation because of the ever-increasing use of hip implants at younger ages. [ABSTRACT FROM AUTHOR]

Background: Incidence rates have risen rapidly for esophageal adenocarcinoma and moderately for gastric cardia adenocarcinoma, while rates have remained stable for esophageal squamous cell carcinoma and have declined steadily for noncardia gastric adenocarcinoma. We examined anthropometric risk factors in a population-based case-control study of esophageal and gastric cancers in Connecticut, New Jersey, and western Washington.Methods: Healthy control subjects (n = 695) and case patients with esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma (n = 589) were frequency-matched to case patients with adenocarcinomas of esophagus or gastric cardia (n = 554) by 5-year age groups, sex, and race (New Jersey only). Classification of cases by tumor site of origin and histology was determined by review of pathology materials and hospital records. Data were collected using in-person structured interviews. Associations with obesity, measured by body mass index (BMI), were estimated by odds ratios (ORs). All ORs were adjusted for geographic location, age, sex, race, cigarette smoking, and proxy response status.Results: The ORs for esophageal adenocarcinoma rose with increasing adult BMI. The magnitude of association with BMI was greater among the younger age groups and among nonsmokers. The ORs for gastric cardia adenocarcinoma rose moderately with increasing BMI. Adult BMI was not associated with risk of esophageal squamous cell carcinoma or noncardia gastric adenocarcinoma.Conclusions: Increasing prevalence of obesity in the United States population may have contributed to the upward trends in esophageal and gastric cardia adenocarcinomas. [ABSTRACT FROM AUTHOR]

Investigates the changes in the incidence and mortality of cancer in the United States. Determinants of temporal patterns; Ranking of cancers according to change in incidence rates; Improvement in cancer detection; Cigarette smoking as the major determinant in the rise of lung cancer cases among women; Influence of acquired immune deficiency syndrome (AIDS) and increased sunlight exposure on cancer incidence.

Evaluates the relation of smoking and alcohol consumption to the development of second cancers among oral and pharyngeal cancer patients. Risk factors for second tumors; Gathering of information on tobacco and alcohol consumption via original and updated interviews; Odds ratios for smoking adjusted for alcohol.

Background: Cervical cancer is the second leading cause of cancer death among Chinese women. Within China, a considerable geographical variation in mortality rates has been observed, but the reasons are not well understood.Methods: Cervical cancer rates were examined in relation to indices of reproductive factors, dietary habits, and selected serum biomedical markers in 65 rural Chinese counties.Results: Cervical cancer mortality rates correlated positively and significantly with antibodies to herpes simplex virus type 2 (HSV-2) (r = 0.40, P < 0.01), serum levels of ferritin (r = 0.33, P < 0.01), body mass index (BMI) (r = 0.42, P < 0.01) and cigarette smoking (r = 0.51, P < 0.05) and negatively and significantly with age at first birth (r = -0.51, P < 0.01), consumption of green vegetables (r = -0.40, P < 0.01) and animal foods (r = -0.40, P < 0.01), and serum levels of selenium (r = -0.26, P < 0.05). When these variables were considered in the multiple regression analysis, early age at first birth and higher BMI were positively associated with cervical cancer mortality, while consumption of green vegetables and animal foods were negatively correlated. In the serum model, infection with HSV-2 and low levels of sex hormone binding globulin (SHBG) were positively related to cervical cancer mortality. No relation was found for consumption of fruits.Conclusions: Although limitations of these ecologic data preclude causal inferences, findings in this study, including associations with HSV-2 infection, early age at first birth, consumption of green vegetables and animal foods, may provide clues to cervical cancer aetiology. [ABSTRACT FROM AUTHOR]

Background: Rates of oesophageal/gastric cardia cancer in Linxian, a rural county in north central China, are among the world's highest, but the risk factors are not well understood.Methods: A nested case-control study of oesophageal and stomach cancers was conducted within a cohort of 29,584 adults who participated in a randomized nutrition intervention trial. Information on participant characteristics collected during interviews before the trial began was compared between individuals who subsequently developed cancers of the oesophagus (N = 640) or stomach (N = 539), mainly cardia, and individually matched controls (control/case ratio = 5). Analyses were performed separately for oesophageal and stomach cancers using conditional logistic regression.Results: For oesophageal cancer, tobacco smoking was associated with a significantly elevated risk, with a twofold increase among long-term smokers. Alcohol consumption was uncommon and not related to risk. High consumption of eggs or fresh vegetables was associated with 20% reductions in risk, and risk significantly declined as pre-trial body mass index (BMI), an indicator of long-term nutritional status, increased. No increases in risk were associated with intake of pickled vegetables or mouldy foods, although consumption levels at the start of the trial were low. Excess risks of 40-80% were found among individuals who had reported a history of cancer, notably of the oesophagus and stomach, in parents or sibs. For stomach cancer, only low BMI was significantly associated with elevated risk.Conclusions: This study indicates that several risk factors for oesophageal and stomach cancers in Linxian, including smoking, nutritional deficiency, and familial cancer occurrence, resemble those in other areas of the world and contribute partly to the remarkably elevated rates in this area of China. [ABSTRACT FROM AUTHOR]

To provide clues to the causes of liver cancer in China, we studied the correlation of certain dietary and biochemical markers with liver cancer mortality across 65 Chinese counties. Mortality rates were significantly linked to the county wide prevalence of hepatitis-B surface antigen positivity. Rates were also higher in counties with high plasma levels of total cholesterol and high consumption of liquor, rapeseed oil, and mouldy corn, while inverse associations were observed for wheat consumption. All of the observed associations, except those with cholesterol and rapeseed oil, were more pronounced in men than in women. No significant correlations with liver cancer mortality were found for consumption of several other foods; plasma levels of retinol, βcarotene, αtocopherol, selenium, zinc and ferritin; or urine levels of aflatoxin B. Although causal inferences cannot be derived, this ecological study suggests that chronic infection with hepatitis-B virus contributes to the substantial variation in liver cancer mortality in China, and provides leads for further studies into the role of dietary and nutritional determinants. [ABSTRACT FROM PUBLISHER]

A case-control study involving interviews with 733 male and 672 female incident lung cancer patients and 1495 population-based controls revealed that cigarette smoking is the dominant cause of lung cancer among men in urban Shanghai. All of the principal cell types were affected, with clear trends of rising risk with increasing intensity and duration of smoking. Far fewer women smoked cigarettes, but the overall risk patterns resembled those among males. Among women, however, smoking accounted for only about one-quarter of all lung cancers and less than 10% of lung adenocarcinomas. The findings lay to rest any doubts about the health hazards of smoking Chinese cigarettes, although smoking is not responsible for the high rates of adenocarcinoma reported among Chinese women. [ABSTRACT FROM PUBLISHER]

Background: A number of vitamins and minerals have been shown to influence carcinogenesis in experimental animals. In humans, epidemiologic evidence suggests that intake of fruits and vegetables may reduce risk of esophageal and other cancers. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian, China, have persistently low intake of multiple nutrients and exhibit one of the world's highest rates of esophageal/gastric cardia cancer, with an exceptionally high risk of esophageal dysplasia.Purpose: To determine whether supplementation with multiple vitamins and minerals may reduce esophageal/gastric cardia cancer among persons with esophageal dysplasia, we conducted a 6-year prospective intervention trial in Linxian.Methods: Mortality and cancer incidence were ascertained from May 1985 through May 1991 for 3318 persons with cytologic evidence of esophageal dysplasia who were randomly assigned to receive, throughout that period, daily supplementation with 14 vitamins and 12 minerals or placebo. Doses were typically two to three times U.S. Recommended Daily Allowances. Compliance was assessed by counting unused pills monthly for all trial participants and by assaying nutrient levels in blood collected from samples of individuals randomly selected without replacement every 3 months throughout the trial. Cancers were identified through routine surveillance and by special cytology and endoscopy screenings after 2 1/2 years and 6 years.Results: A total of 324 deaths occurred during the 6-year intervention period; 167 occurred in the control (placebo) group and 157 occurred in the supplement group. Cancer was the leading cause of death (54% of all deaths); 18% were due to cerebrovascular diseases and 29% to other causes. Cumulative esophageal/gastric cardia death rates were 8% lower (relative risk [RR] = 0.92; 95% confidence interval [CI] = 0.67-1.28) among individuals receiving supplements rather than placebo, a nonsignificant (P > .10) difference. Risk of total mortality was 7% lower (RR = 0.93; 95% CI = 0.75-1.16; P > .10), total cancer 4% lower (RR = 0.96; 95% CI = 0.71-1.29; P > .10), cerebrovascular disease 38% lower (RR = 0.62; 95% CI = 0.37-1.06; P = .08), and other diseases 12% higher (RR = 1.12; 95% CI = 0.74-1.69; P > .10) among the treated group. Cumulative cancer incidence rates were nearly the same in the two groups.Conclusions: No substantial short-term beneficial effect on incidence or mortality for this type of cancer occurred following daily supplementation with multiple vitamins and minerals among adults with precancerous lesions of the esophagus.Implications: Although no statistically significant short-term benefits were observed, longer follow-up should be more informative about the effectiveness of this 6-year supplementation on cancer and other diseases among individuals with esophageal dysplasia. [ABSTRACT FROM AUTHOR]

Background: Epidemiologic evidence indicates that diets high in fruits and vegetables are associated with a reduced risk of several cancers, including cancers of the esophagus and stomach. Vitamins and minerals in these foods may contribute to the reduced cancer risk. The people of Linxian County, China, have one of the world's highest rates of esophageal/gastric cardia cancer and a persistently low intake of several micronutrients.Purpose: We sought to determine if dietary supplementation with specific vitamins and minerals can lower mortality from or incidence of cancer as well as mortality from other diseases in Linxian.Methods: Individuals of ages 40-69 were recruited in 1985 from four Linxian communes. Mortality and cancer incidence during March 1986-May 1991 were ascertained for 29,584 adults who received daily vitamin and mineral supplementation throughout this period. The subjects were randomly assigned to intervention groups according to a one-half replicate of a 2(4) factorial experimental design. This design enabled testing for the effects of four combinations of nutrients: (A) retinol and zinc; (B) riboflavin and niacin; (C) vitamin C and molybdenum; and (D) beta carotene, vitamin E, and selenium. Doses ranged from one to two times U.S. Recommended Daily Allowances.Results: A total of 2127 deaths occurred among trial participants during the intervention period. Cancer was the leading cause of death, with 32% of all deaths due to esophageal or stomach cancer, followed by cerebrovascular disease (25%). Significantly (P = .03) lower total mortality (relative risk [RR] = 0.91; 95% confidence interval [CI] = 0.84-0.99) occurred among those receiving supplementation with beta carotene, vitamin E, and selenium. The reduction was mainly due to lower cancer rates (RR = 0.87; 95% CI = 0.75-1.00), especially stomach cancer (RR = 0.79; 95% CI = 0.64-0.99), with the reduced risk beginning to arise about 1-2 years after the start of supplementation with these vitamins and minerals. No significant effects on mortality rates from all causes were found for supplementation with retinol and zinc, riboflavin and niacin, or vitamin C and molybdenum. Patterns of cancer incidence, on the basis of 1298 cases, generally resembled those for cancer mortality.Conclusions: The findings indicate that vitamin and mineral supplementation of the diet of Linxian adults, particularly with the combination of beta carotene, vitamin E, and selenium, may effect a reduction in cancer risk in this population.Implications: The results on their own are not definitive, but the promising findings should stimulate further research to clarify the potential benefits of micronutrient supplements. [ABSTRACT FROM AUTHOR]

Background: In the United States, Blacks have increasingly higher rates of oral and pharyngeal cancer (oral cancer) than Whites, but determinants of the racial disparity have not been clear.Purpose: The purpose of this study was to explore reasons for the higher incidence of oral cancer among Blacks than Whites.Methods: We used data from a large, population-based case-control study of oral cancer risk factors conducted in four areas of the United States. On the basis of interviews that ascertained characteristics of 1065 oral cancer patients (871 Whites and 194 Blacks) and 1182 controls (979 Whites and 203 Blacks), we examined racial differences in exposure prevalences and relative risks for a number of known etiologic factors, including tobacco and alcohol consumption, diet, and socioeconomic and other variables. To evaluate the extent to which the major risk factors explained the excess risk of oral cancer among Blacks, population-attributable risks were calculated.Results: Differences with respect to alcohol consumption, especially among current smokers, emerged as the most important explanatory variables. After adjusting for smoking, heavy drinking (> or = 30 drinks/week) resulted in a 17-fold increased risk among Blacks and a ninefold increase among Whites. Among drinkers, Blacks tended to drink more than Whites. Also, a higher (P = .01) percentage of Blacks (37%) than Whites (28%) were current smokers, although there were little or no racial differences in relative risks or patterns of use for other smoking variables, including number of cigarettes smoked per day, years of smoking, and age started smoking. From population-attributable risk calculations, we estimated that differences in alcohol and tobacco use account for the bulk of the higher incidence of oral cancer among Blacks in the United States and that, in the absence of alcohol and tobacco, the rates of this cancer according to race (Black, White) and gender would be nearly equal. With regard to other potential etiologic factors, protective effects provided by higher dietary intake of fruits and vitamin C were more pronounced for Whites, while Blacks more often tended to be in sociodemographic and medical or dental health categories associated with increased risk.Conclusions: These analyses provide evidence that various environmental or lifestyle determinants of oral cancer may contribute to the higher oral cancer rates in Blacks than in Whites in the United States, but that patterns and risks associated with alcohol consumption, particularly among current smokers, are the most important contributors to the excess risk in Blacks.Implications: These findings suggest that the key to prevention of oral and pharyngeal cancers among both Blacks and Whites is reduced intake of alcoholic beverages and, because of strong interactive effects, the cessation of smoking. [ABSTRACT FROM AUTHOR]

Background: Stomach cancer is generally thought to evolve through a series of gastric mucosal changes, but the derterminants of the precancerous lesions are not well understood. : Our purpose was to assess risk factors for intestinal metplasia and gastric dysplasia arising from chronicatrophic gastritis in a genral population at high risk for stomach cancer. : A population-based gastroscopic screening of more than 3000 residents was conducted in a county in china eith one of the world's highest rtes of stomach cancer. Information on the lifestyle and other charateristics of the participants was obtained by interview, and responses were compared between those in whom the most advanced gastric lesion was dysplasiaor intestinal metaplasia versus those with chronic atrophic gastritis. : Cigarette smoking was found to nearly double the risk of transition to dysplasia and to be a mild risk factor for intestinal metaplasia. Smoling accounted almost entirely for the 55% higher prevalence of dysplasis among men than among women. Risk of transition to dysplasis had a weak association with several dietary factors and was increased among those participants with a family history of stomach cancer and with blood type A. Conclusions: The findings provide storng evidence for a role of tobacco consumption and offer clues to other enviromental and genetic factord involved in the process of gastric carcinogenesis. (J Natl cancer Inst 84: 1261–1266, 1992] [ABSTRACT FROM PUBLISHER]

Background: Nasopharyngeal carcinoma (NPC) is a relatively uncommon cancer in the United States. Its etiology among White Americans is not well known, but cigarette smoking has been implicated in some epidemiologic studies. Purpose: The purpose of this study was to investigate the roles of cigarette use and alcohol consumption as risk factors for NPC in the United States. Methods: We conducted a case-control study using data from the National Mortality Followback Survey based on information from death certificates. In this study, we compared use of cigarettes and alcohol by 204 White American men and women who died of NPC with that by 408 who died of causes unrelated to cigarette smoking and alcohol use. Results: Risk of NPC increased in proportion to the amount and duration of smoking (with a more than threefold increase among persons smoking heavily) and declined following cessation of smoking. After controlling for smoking, we found an 80% excess risk of NPC among persons whose intake of alcohol was heavy. Conclusion: Use of cigarettes and consumption of alcohol were found to be statistically significant risk factors for NPC. The findings are among the strongest to date indicating that use of cigarettes and perhaps alcohol may contribute to the etiology of these relatively rare cancers among Whites in the United States. [J Natl Cancer Inst 84: 619–622, 1992] [ABSTRACT FROM PUBLISHER]

Radon has long been known to contribute to risk of lung cancer, especially in undergound miners who are exposed to large amounts of the carcinogen. Recently, however, lower amounts of radon present in living areas have been suggested as an important cause of lung cancer. In an effort to clarify the relationship of low amounts of radon with lung cancer risk, we placed alpha-track radon detectors in the homes of 308 women with newly diagnosed lung cancer and 356 randomly selected female control subjects of similar age. Measurements were taken after 1 year. All study participants were part of the general population of Shenyang, People's Republic of China, an industrial city in the northeast part of the country that has one of the world's highest rates of lung cancer in women. The median time of residence in the homes was 24 years. The median household radon level was 2.3 pCi/L of air; 20% of the levels were greater than 4 pCi/L. Radon levels tended to be higher in single-story houses or on the first floor of multiple-story dwellings, and they were also higher in houses with increased levels of indoor air pollution from coal-burning stoves. However, the levels were not higher in homes of women who developed lung cancer than in homes of controls, nor did lung cancer risk increase with increasing radon level. No association between radon and lung cancer was observed regardless of cigarette-smoking status, except for a nonsignificant trend among heavy smokers. No positive associations of lung cancer cell type with radon were observed, except for a nonsignificant excess risk of small cell cancers among the more heavily exposed residents. Our data suggest that projections from surveys of miners exposed to high radon levels may have overestimated the overall risks of lung cancer associated with levels typically seen in homes in this Chinese city. However, further studies in other population groups are needed to clarify the carcinogenic potential of indoor radon. [J Natl Cancer inst 82:1025–1030, 1990] [ABSTRACT FROM PUBLISHER]

A case-control study involving interviews with 1,249 patients with lung cancer and 1,345 population-based controls was conducted in Shenyang, an industrial city in northeastern China, where mortality rates are high among men and women. Cigarette smoking was found to be the principal cause of lung cancer in this population, accounting for 55% of the lung cancers in males and 37% in females. The attributable risk percentage among females is high compared to elsewhere in China, largely because of a higher prevalence of smoking among women. After adjustment for smoking, there were also significant increases in lung cancer risk associated with several measures of exposure to air pollutants. Risks were twice as high among those who reported smoky outdoor environments, and increased in proportion to years of sleeping on beds heated by coal-burning stoves (kang), and to an overall index of indoor air pollution. Threefold increases in lung cancer risk were found among men who worked in the nonferrous smelting industry, where heavy exposures to inorganic arsenic have been reported. The associations with both smoking and indoor air pollution were stronger for squamous cell and small cell carcinomas than for adenocarcinoma of the lung. Risks due to smoking or air pollution were not greatly altered by adjustment for consumption of fresh vegetables or sources of beta carotene or retinol, prior chronic lung diseases, or education level. The findings suggest that smoking and environmental pollution combine to account for the elevated rates of lung cancer mortality in Shenyang. [J Natl Cancer Inst 81:1800–1806, 1989] [ABSTRACT FROM PUBLISHER]

Although overall age-adjusted rates of mortality from lung cancer in the United States continue to rise, rates at ages below 45 years have begun to decline. In this report we show that the decrease is greatest among white men, with a 29% drop between the mid-1970s and mid-1980s, but a decrease also occurred among black men and white and black women. Cohort analyses revealed that the rates of lung cancer peaked among men born around 1925–1930 and among women born around 1935–1940, and have declined thereafter. If these trends continue, overall lung cancer mortality rates will start to decline in the 1990s among men and after the year 2000 among women. [J Natl Cancer Inst 81:1568–1571, 1989] [ABSTRACT FROM PUBLISHER]

A case-control study involving interviews of 207 men with esophageal cancer and 422 control subjects or their next of kin was conducted to identify reasons for the unusually high rates of esophageal cancer among men in coastal South Carolina. Tobacco and alcohol, including moonshine, were identified as the major determinants of esophageal cancer risk. Increased risk was also associated with low intake of fresh fruits but not with drinking of local herbal teas. The findings suggest that efforts aimed at reducing tobacco and alcohol use will help to lower the elevated rates of esophageal cancer in coastal South Carolina. [ABSTRACT FROM PUBLISHER]

A population-based case-control study of oral and pharyn-geal cancer conducted in four areas of the United States provided information on a number of risk factors, including diet. Interviews were obtained from 871 oral cancer patients and 979 controls among whites, frequency matched for age and sex. Consumption frequency of 61 food items was assessed in the questionnaire; attention was given to foods that are sources of vitamins A and C and carotene. The major finding was an inverse relationship between fruit intake and risk of oral and pharyngeal cancer; individuals in the highest quartile of intake had about half the risk of those in the lowest quartile. Vitamin C, carotene, or fiber in fruit did not appear to account completely for this relationship, since these nutrients in vegetables did not provide similar protection. This finding suggests the influence of other constituents in fruits, although it is possible that cooking vegetables may have a nutrient-diminishing effect Dietary intake of other nutrients, such as the B vitamins, vitamin E, folate, and iron, showed no consistent relationship to risk of oral and pharyngeal cancer. Coffee or other hot beverage consumption did not increase risk; intake of nitrite-containing meats or cooking practices, such as smoking, pickling, or charcoal grilling, also did not increase risk. All analyses were adjusted for the effects of tobacco and alcohol, strong risk factors for oral and pharyngeal cancer. Dietary findings among the few subjects who did not use tobacco or alcohol were similar to those for all subjects. [J Natl Cancer Inst 1988:80:1237–1243] [ABSTRACT FROM PUBLISHER]

A total of 3,318 men and women from a region in rural China were randomized to receive daily either a multiple vitamin/mineral supplement or a placebo. Deaths that occurred in the participants were ascertained and classified according to cause over the 6-year period from 1985 to 1991. At the end of supplementation, blood pressure readings were taken, and the prevalence of hypertension was determined. There was a slight reduction in overall mortality in the supplement group (relative risk (RR) = 0.93, 95% confidence interval (Cl) 0.75–1.16), with the decreased relative risk most pronounced for cerebrovascular disease deaths (RR = 0.63, 95% Cl 0.37–1.07). This benefit was greater for men (RR = 0.42, 95% Cl 0.19–0.93) than for women (RR = 0.93, 95% Cl 0.44–1.98). Among the survivors, the presence of elevations in both systolic and diastolic blood pressures was less common in those who received the supplement (RR for men = 0.43, 95% Cl 0.28–0.65; RR for women = 0.92, 95% Cl 0.68–1.24). This study indicates that supplementation with a multivitamin/mineral combination may have reduced mortality from cerebrovascular disease and the prevalence of hypertension in this rural population with a micronutrient-poor diet. [ABSTRACT FROM AUTHOR]