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Numerous studies have reported lower overall cancer mortality rates among immigrants compared to native populations. However, limited information exists regarding cancer mortality among immigrants based on specific birth countries and cancer types. We used population‐based registries and followed 10 million individuals aged 20 years or older in Sweden between 1992 and 2016. The Cox proportional hazard model was used to explore the disparities in cancer mortality by country of birth and cancer type, stratified by gender. Age‐standardized mortality rates were also computed using the world standard population. Hazard ratio (HR) of all‐site cancer was slightly lower among immigrants (males: HRm = 0.97: 95% confidence interval: 0.95, 0.98; females: HRf = 0.93: 0.91, 0.94) than Swedish‐born population. However, the immigrants showed higher mortality for infection‐related cancers, including liver (HRf = 1.10: 1.01, 1.19; HRm = 1.10: 1.02, 1.17), stomach (HRf = 1.39: 1.31, 1.49; HRm = 1.33: 1.26, 1.41) cancers, and tobacco‐related cancers, including lung (HRm = 1.44: 1.40, 1.49), and laryngeal cancers (HRm = 1.47: 1.24, 1.75). The HR of mesothelioma was also significantly higher in immigrants (HRf = 1.44: 1.10, 1.90). Mortality from lung cancer was specifically higher in men from Nordic (HRm = 1.41: 1.27, 1.55) and non‐Nordic Europe (HRm = 1.49: 1.43, 1.55) countries and lower in Asian (HRm = 0.78: 0.66, 0.93) and South American men (HRm = 0.70: 0.57, 0.87). In conclusion, there are large variations in cancer mortality by country of birth, and cancer type and require regular surveillance. Our detailed analyses lead to some novel findings such as excess mortality rate of mesothelioma and laryngeal cancers in Immigrants in Sweden. A targeted cancer prevention program among immigrants in Sweden is needed. [ABSTRACT FROM AUTHOR]

Esophageal cancer (EC), which includes squamous cell carcinoma (ESCC) and adenocarcinoma (EAC), is an important cancer with poor prognosis and high mortality rate. Several occupational exposures have been associated with EC. We aim to investigate the association between occupational asbestos exposure and EC risk, considering types of asbestos and histology of the disease. We included studies mentioned in the list of references in previous reviews and pooled analyses, and we conducted an independent search in PubMed and Scopus. Forest plots of relative risks (RR) were constructed based on the association between occupational asbestos and EC risk. Random‐effects models were used to address heterogeneity between 48 independent cohort and case‐control studies. We found an association between occupational asbestos exposure and EC (meta‐relative risk [RR] = 1.20, 95% confidence interval [CI] = 1.09‐1.32; I2 = 58.8%, p‐heterogeneity [het] <.001). The results of stratification by job (p‐het =.20) indicate an increased RR among asbestos product workers (RR = 1.39, 95% CI = 1.07‐1.81), asbestos applicators (RR = 1.41, 95% CI = 1.20‐1.67), and construction workers (RR = 1.12, 95% CI = 1.02‐1.24). There was no heterogeneity in meta‐RR according to outcome (p =.29), geographic region (p =.69), year of publication (p =.59), quality score (p =.73), asbestos type (p =.93), study design (p =.87), and gender (p =.88), control for potential confounders (p =.20), year of first employment (p =.94) and exposure level (p =.43). The stratification analysis by histology type found an increased RR for both ESCC 1.33(1.03‐1.71) and EAC 1.45(1.03‐2.04) (p‐het =.68). We didn't find evidence of publication bias (p =.07). The results of our study suggest that occupational asbestos exposure is associated with an increased risk of EC in both histology types. [ABSTRACT FROM AUTHOR]

Background: Aspirin intake might be inversely associated with head and neck cancer (HNC). Thus, we investigated this relationship within the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Methods: Four case–control studies within the INHANCE consortium were included (2024 cases, 4196 controls). Study‐specific odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using logistic regression and subsequently pooled with DerSimonian‐Laird random‐effects model. Nonlinearity of the relationship between duration of intake and HNC was modeled with fractional polynomials. Results: Aspirin was inversely associated with HNC overall (OR = 0.48; 95% CI: 0.26, 0.91). Results for laryngeal cancer were similar (OR = 0.54; 95% CI: 0.30, 0.96). Analysis on duration of intake confirmed findings for HNC overall, showing also inverse associations for oropharyngeal and laryngeal cancer. Conclusions: This study suggests that aspirin intake may reduce the risk of HNC, driven mainly by decreases in risk for laryngeal and oropharyngeal cancer. [ABSTRACT FROM AUTHOR]

High‐fat diets have been associated with colorectal cancer (CRC) risk, and the role of polyunsaturated fatty acids (PUFAs) has been reported to vary based on the length of PUFAs. We explored the association between dietary omega‐6 and omega‐3 PUFAs intake and CRC. We analyzed 865 CRC patients and 3206 controls from a case–control study of Iran (IROPICAN study). We used multivariate logistic regression models to calculate the odds ratios (OR) and 95% confidence intervals (CI) for the association between PUFAs intake and CRC risk. Our results showed that gamma‐linolenic acid (18:3 n‐6, GLA), arachidonic acid (20:4n‐6, ARA), a‐linolenic acid (Cis‐18:3n‐3, ALA), eicosapentaenoic acid (20:5n‐3, EPA), docosahexaenoic acid (22:6n‐3, DHA) consumption was not associated with the risk of CRC. However, the OR of linoleic acid (18: 2n‐6, LA) intake was 1.47 (95% CI 1.01–2.14, p = 0.04) for proximal colon and that of docosapentaenoic acid (22:5n‐3, DPA) intake was 1.33 (95% CI 1.05–1.69, p = 0.01) for rectum. This study indicates a high level of LA is associated with an increased risk of proximal colon cancer, and DPA intake was positively associated with rectum cancer risk. Furthermore, our study noted a high intake of n‐6 (from vegetable oils) compared to n‐3 PUFAs (from fish and seafood) in this population. Public awareness and government support is needed to increase fish and seafood production and consumption in Iran. [ABSTRACT FROM AUTHOR]

Background: Cocaine is an illegal recreational drug used worldwide, yet little is known about whether cocaine inhalation (smoking/snorting) increases the risk of head and neck cancer (HNC). Methods: The analyses were conducted by pooling data from three case–control studies with 1639 cases and 2506 controls from the International Head and Neck Cancer Epidemiology Consortium. Epidemiologic data, including cocaine use histories, were obtained in face‐to‐face interviews. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using hierarchical logistic regression models. Results: Controlling for cumulative tobacco and alcohol use, we observed a weak positive association between cocaine use and HNC (ORever vs. never = 1.35, 95% CI: 0.96, 1.90). In stratified analysis, while we did not detect associations among never tobacco or alcohol users due to the limited sample size, the association with cocaine use was observed among tobacco users and alcohol drinkers. ORs for ever and high cumulative use (>18 times) versus never use were 1.40 (95% CI: 0.98, 2.00) and 1.66 (95% CI: 1.03, 2.69) among tobacco users, and 1.34 (95% CI: 0.93, 1.92) and 1.59 (95% CI: 1.00, 2.51) among alcohol drinkers, respectively. Conclusion: In this pooled analysis, we observed a weak positive association between cocaine inhalation and HNC risk. Our findings provide preliminary evidence of the potential carcinogenic effect of cocaine on HNC. Because of study limitations, including limited number of cocaine users, confounding, and heterogeneity across studies, future investigations will require larger studies with more detailed information on cocaine use history. [ABSTRACT FROM AUTHOR]

Introduction: It is unclear whether differences in health outcomes by racial and ethnic groups among World Trade Center (WTC) rescue and recovery workers reflect those of the population of New York State (NYS) or show distinct patterns. We assessed cancer incidence in WTC workers by self‐reported race and ethnicity, and compared it to population figures for NYS. Methods: A total of 61,031 WTC workers enrolled between September 11, 2001 and January 10, 2012 were followed to December 31, 2015. To evaluate the association between race/ethnicity and cancer risk, Poisson regression analysis was used to estimate hazard ratios (HR) adjusted for WTC exposure, age, calendar year, sex and, for lung cancer, cigarette smoking. Results: In comparison to Whites, Black workers had a higher incidence of prostate cancer (HR = 1.99, 95% CI = 1.69−2.34) and multiple myeloma (HR = 3.57, 95% CI = 1.97−6.45), and a lower incidence of thyroid (HR = 0.41, 95% CI = 0.22−0.78) and colorectal cancer (HR = 0.57; 95% CI = 0.33−0.98). Hispanic workers had a higher incidence of liver cancer (HR = 4.03, 95% CI = 2.23−7.28). Compared with NYS population, White workers had significantly higher incidence of prostate cancer (HR = 1.26, 95% CI = 1.18−1.35) and thyroid cancer (HR = 1.80, 95% CI = 1.55−2.08), while Black workers had significantly higher incidence of prostate cancer (HR = 1.22, 95% CI = 1.05−1.40). Conclusion: Cancer incidence in WTC workers generally reflects data from the NYS population, but some differences were identified that merit further investigation. [ABSTRACT FROM AUTHOR]

Background: Gastric cancer (GC) incidence is declining heterogeneously worldwide. We aimed to calculate updated mortality trends for GC. Methods: We investigated time trends for selected countries using the World Health Organization database. We computed age‐standardized mortality rates (ASMR) per 100,000 persons over the 1990–2019 period. We reported rates for the 2010–2014 and 2015–19 calendar periods, and the corresponding percent changes. We used joinpoint regression analysis to identify changes in the slope of mortality trends, and predict the number of deaths and rates for 2025. We also reported 2008–2012 incidence rates of cardia and noncardia GC. Results: Mortality trends from GC have been favorable since 1990 for all countries analyzed and the European Union (EU 27), in both sexes and all ages. GC mortality is predicted to decline in all countries for both sexes, except for French and US women aged 35–64 years, and Canadian men aged 35–64. The highest proportions of cardia GC were observed in Northern and Central Europe while the lowest ones in Southern and Eastern Europe. Elsewhere, the highest proportions were registered in countries with low incidence and mortality rates, whereas high‐mortality countries showed lower proportions of cardia GC. Conclusion: Observed and predicted GC mortality trends declined in most countries in both sexes, with few exceptions, likely due to the control of GC risk factors, in particular Hp infection. [ABSTRACT FROM AUTHOR]

Prior studies have conflicting findings regarding the association between gastroesophageal reflux disease (GERD) and esophageal squamous cell carcinoma (ESCC). We examined this relationship in a prospective cohort in a region of high ESCC incidence. Baseline exposure data were collected from 50 045 individuals using in‐person interviews at the time of cohort entry. Participants were followed until they developed cancer, died, or were lost to follow up. Participants with GERD symptoms were categorized into any GERD (heartburn or regurgitation), mixed symptoms, or heartburn alone. Multivariable Cox regression was used to assess the relationship between GERD symptom group and histologically confirmed ESCC. The model was adjusted for known risk factors for GERD and ESCC. 49 559 individuals were included in this study, of which 9005 had GERD symptoms. Over 13.0 years of median follow up, 290 individuals were diagnosed with ESCC. We found no association between any GERD and risk of ESCC (aHR 0.90, 95% CI: 0.66‐1.24, P =.54). Similar findings were observed for the GERD symptom subtypes. Significant interactions between any GERD and sex (P =.013) as well as tobacco smoking (P =.028) were observed. In post‐hoc analyses, GERD was associated with a decreased risk of ESCC in men (aHR 0.51, 95% CI: 0.27‐0.98 P =.04) and in smokers (aHR 0.26, 95% CI: 0.08‐0.83 P =.02). While there was little evidence for an overall association between GERD symptoms and ESCC risk, significant interactions with sex and smoking were observed. Men and smokers with GERD symptoms had a lower risk of ESCC development. [ABSTRACT FROM AUTHOR]

Background and objective: Chronic obstructive pulmonary disease (COPD) incidence, prevalence, mortality and socioeconomic burden are considerable and vary across countries. The aim of the present study was to update the analysis of COPD mortality worldwide using data from the World Health Organization (WHO) up to 2019. Methods: We obtained COPD mortality and population data for 22 European countries and the European Union (EU) as a whole, 10 American countries and six other countries from the WHO mortality database. We calculated age‐standardized mortality rates in both sexes and examined trends by country with joinpoint analysis between 1994 and 2019. Results: Between 2005–2007 and 2015–2017, overall COPD mortality decreased in EU men (−16.3%) but increased in women (12.7%) to reach rates of 14.0/100,000 in men and of 6.4/100,000 in women. In the United States, mortality declined in men to 21.3/100,000 but rose in women to 18.3/100,000. Mortality declined in most Latin American countries and all Asian countries, while an increase in Australian women was observed. Conclusion: A steady decrease in COPD mortality was observed in most of countries for men, whilst a different trend was observed in women in several countries. These trends are largely explained by changes in smoking habits, with an additional contribution of air pollution and occupational exposures. Despite past and ongoing tobacco control initiatives, this condition still remains a leading cause of death, in particular in countries with lower socio‐demographic indices. [ABSTRACT FROM AUTHOR]

Despite the overall decreasing incidence, nasopharyngeal cancer (NPC) continues to cause a significant health burden among Asian Americans (AAs), who are a fast‐growing but understudied heterogeneous racial group in the United States. We aimed to examine the racial/ethnic disparities in NPC incidence, treatment, and mortality with a specific focus on AA subgroups. NPC patients aged ≥15 years were obtained from the Surveillance, Epidemiology, and End Results (SEER) 18 (1975‐2018). AAs were divided into Chinese, Filipino, Vietnamese, Hawaiian, Japanese, Laotian, Korean, Cambodian, Indian/Pakistani and other Asian/Pacific Islanders (APIs). Age‐adjusted incidence was calculated using the SEER*Stat software. Cox proportional and Fine‐Gray subdistribution hazard models were used to calculate overall and cause‐specific mortalities after adjusting for confounders. Among the total 11 964 NPC cases, 18.4% were Chinese, 7.7% Filipino, 5.0% Vietnamese, 1.2% Hawaiian, 1.0% Japanese, 0.8% Laotian, 0.8% Korean, 0.6% Cambodian, 0.5% Indian/Pakistani and 4.4% other APIs. Laotians had the highest age‐adjusted NPC incidence (9.21 per 100 000), which was 18.04 times higher than it in non‐Hispanic Whites (NHWs). Chinese and Filipinos observed lower overall mortalities, however, Chinese saw increased NPC‐specific mortality than NHWs. Disparities in mortality were also found across different histology subtypes. This is the first and largest study examining the NPC incidence and outcomes in AA subgroups. The significant disparities of NPC within AAs underline the importance of adequate AA‐subgroup sample size in future studies to understand the prognostic role of ethnicity in NPC and advocate more ethnically and culturally tailored cancer prevention and care delivery. [ABSTRACT FROM AUTHOR]

Red meat and processed meat are associated with some gastrointestinal cancers. Our study aims to investigate the association of different meat types with esophageal and gastric cancer (EC, GC) in a high‐risk population. The Golestan Cohort Study (GCS) is a population‐based cohort of 50 045 individuals aged 40 to 75 from northeast Iran. Detailed data on different exposures were collected using validated questionnaires. We considered quintiles of meat consumption, using grams and density (g/1000 kcal/day). We calculated intake of red, processed, organ and white meat, as well as total red meat, including the first three. We used proportional hazards regression models to estimate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) for the association between meat types and cancer. During 12 years of follow‐up, out of 49 585 participants (57.4% women), 369 developed EC (48.2% women) and 368 developed GC (27.5% women), including 309 esophageal squamous cell, 20 esophageal adenocarcinomas, 216 cardia and 95 non‐cardia GC. No association was found for EC except for red meat among females (HR for one quintile increase 1.13, 95% CI = 1.00‐1.27). The risk of GC increased for intake of total red meat (HR 1.08, 95% CI = 1.00‐1.17) and red meat separately (HR 1.09, 95% CI = 1.00‐1.18). The HR for red meat and non‐cardia GC was 1.23 (95% CI = 1.02‐1.48). No associations were observed for other types of meat. In conclusion, in this high‐risk population red meat intake is associated with GC, but not EC, suggesting a substantial role of this modifiable factor in determining the burden of GC. [ABSTRACT FROM AUTHOR]

Twenty years after the September 11th, 2001 terrorist attacks, the association between exposures present at the World Trade Center (WTC) site and the risk of several specific types of cancer has been reported among rescue and recovery workers. The authors' objective was to conduct an updated review of these data. Most studies have found elevated rates of both prostate and thyroid cancers compared with rates in the general population, and some have reported statistically significant differences for the rates of all cancers as well. Studies including a larger combined cohort of WTC‐exposed rescue and recovery workers from 3 main cohorts have since replicated findings for these cancers, with additional years of follow‐up. Among this combined cohort, although a lower‐than‐expected standardized incidence ratio for all cancers was observed, WTC exposure was also related to an increased risk of cutaneous melanoma and tonsil cancer. Importantly, another study found that WTC‐exposed rescue and recovery workers who are enrolled in the federally funded medical monitoring and treatment program experienced improved survival post‐cancer diagnosis compared with New York state patients with cancer. On the basis of these combined cohort studies, the full effect of WTC exposure on cancer risk is becoming clearer. Consequently, the authors believe that surveillance of those with WTC exposure should be continued, and in‐depth analysis of epidemiologic, molecular, and clinical aspects of specific cancers in these workers should be pursued. [ABSTRACT FROM AUTHOR]

Background: Ionizing radiation and mesothelioma have been examined among personnel employed in nuclear power plant and patients treated by external beam radiation therapy (EBRT). The association is still controversial; the purpose of this review is to summarize the scientific evidence published in the literature regarding the relationship between ionizing radiation and incidence of mesothelioma and, if possible, estimating strongness of the association by meta‐analysis of extracted data. Methods: Articles included in the systematic review were retrieved by searching among the three main scientific databases: PubMed, Scopus, and Embase. The literature search was conducted in June 2021. A meta‐analysis of random effects was conducted, stratified by exposure (EBRT, occupational exposure). The heterogeneity of the summary relative risks (RRs) was assessed using I2 statistics. Publication bias was evaluated graphically through the funnel plot. Findings: The exposure to ionizing radiation could be a risk factor for mesothelioma: both for exposure to high doses for short periods (EBRT) (RR of 3.34 [95% confidence interval, CI 1.24–8.99]) and for exposure to low doses for a prolonged duration (exposure working) (RR of 3.57 [95% CI 2.16–5.89]). Conclusions: Despite the low number of mesotheliomas in the general population, the steadily increased risk among individuals exposed to radiation is still worth considering. [ABSTRACT FROM AUTHOR]

Colorectal cancer is a leading cancer worldwide and in Vietnam. Adenomas (adenomatous polyps) is an important precursor of colorectal cancer. There is currently no study to determine the modifiable risk factors for colorectal adenomas, including body mass index (BMI) in Vietnam. We conducted an individually matched case‐control study of 1149 colorectal adenomas and 1145 controls in a large‐scale colorectal screening program involving 103 542 individuals aged 40‐75 years old in Hanoi, Vietnam. Conditional logistic regression was used to evaluate the association between BMI and colorectal adenomas prevalence, after controlling for potential confounders. Overall, comparing to normal weight (ie, 18.5‐22.9 kg/m2), underweight (ie, BMI < 18.5) was associated with a non‐statistically significant increased prevalence of colorectal adenomas (odd ratio [OR] = 1.29 and 95% confident interval [CI]: 0.88‐1.87). This association became significant among male (OR = 1.98, 95% CI: 1.20‐3.27), male who were ever smokers (OR = 2.59, 95% CI: 1.33‐5.03), nonregular exercise (OR = 2.44, 95% CI: 1.26‐4.73) and individuals with cardiometabolic disorders (OR = 3.46, 95% CI: 1.19‐10.00). The association between underweight and colorectal adenomas did not vary by smoking status, drinking status, family history of cancer, adenomas types or cardiometabolic disorders. No association was observed among obese individuals (BMI ≥ 25). In the population with low prevalence of obesity, we found that the association between BMI and colorectal adenomas followed a reversed J‐shape that underweight was associated with increased prevalence. Further studies are, therefore, warranted to replicate our results and to investigate the biologic mechanism the effect of underweight on colorectal adenomas prevalence. What's new? High body mass index (BMI) has been associated with an increased risk of colorectal adenomas in studies including Asian populations. To date, no study has identified modifiable risk factors for colorectal adenomas in Vietnam, a country with a rising colorectal cancer incidence and low obesity prevalence. This case‐control study based on a large‐scale colorectal cancer screening program in Vietnam reports a potential association between underweight and colorectal adenomas prevalence with an inverse J‐shape. The modification of specific factors such as maintaining a normal BMI range, quitting smoking and exercising regularly showed great potential for colorectal cancer prevention and control programs. [ABSTRACT FROM AUTHOR]

Background: World Trade Center (WTC)‐exposed responders may be eligible to receive no‐cost medical monitoring and treatment for certified conditions, including cancer. The survival of responders with cancer has not previously been investigated. Methods: This study compared the estimated relative survival of WTC‐exposed responders who developed cancer while enrolled in two WTC medical monitoring and treatment programs in New York City (WTC‐MMTP responders) and WTC‐exposed responders not enrolled (WTC‐non‐MMTP responders) to non‐responders from New York State (NYS‐non‐responders), all restricted to the 11‐southernmost NYS counties, where most responders resided. Parametric survival models estimated cancer‐specific and all‐cause mortality. Follow‐up ended at death or on December 31, 2016. Results: From January 1, 2005 to December 31, 2016, there were 2,037 cancer cases and 303 deaths (248 cancer‐related deaths) among WTC‐MMTP responders, 564 cancer cases, and 143 deaths (106 cancer‐related deaths) among WTC‐non‐MMTP responders, and 574,075 cancer cases and 224,040 deaths (158,645 cancer‐related deaths) among the NYS‐non‐responder population. Comparing WTC‐MMTP responders with NYS‐non‐responders, the cancer‐specific mortality hazard ratio (HR) was 0.72 (95% confidence interval [CI] = 0.64–0.82), and all‐cause mortality HR was 0.64 (95% CI = 0.58–0.72). The cancer‐specific HR was 0.94 (95% CI = 0.78–1.14), and all‐cause mortality HR was 0.93 (95% CI = 0.79–1.10) comparing WTC‐non‐MMTP responders to the NYS‐non‐responder population. Conclusions: WTC‐MMTP responders had lower mortality compared with NYS‐non‐responders, after controlling for demographic factors and temporal trends. There may be survival benefits from no‐out‐of‐pocket‐cost medical care which could have important implications for healthcare policy, however, other occupational and socioeconomic factors could have contributed to some of the observed survival advantage. [ABSTRACT FROM AUTHOR]

Background: A recent study of World Trade Center (WTC)‐exposed firefighters and emergency medical service workers demonstrated that elevated thyroid cancer incidence may be attributable to frequent medical testing, resulting in the identification of asymptomatic tumors. We expand on that study by comparing the incidence of thyroid cancer among three groups: WTC‐exposed rescue/recovery workers enrolled in a New York State (NYS) WTC‐medical monitoring and treatment program (MMTP); WTC‐exposed rescue/recovery workers not enrolled in an MMTP (non‐MMTP); and the NYS population. Methods: Person‐time began on 9/12/2001 or at enrollment in a WTC cohort and ended at death or on 12/31/2015. Cancer data were obtained through linkages with 13 state cancer registries. We used Poisson regression to estimate rate ratios (RRs) and 95% confidence intervals (CIs) for MMTP and non‐MMTP participants. NYS rates were used as the reference. To estimate potential changes over time in WTC‐associated risk, change points in RRs were estimated using profile likelihood. Results: The thyroid cancer incidence rate among MMTP participants was more than twice that of NYS population rates (RR = 2.31; 95% CI = 2.00–2.68). Non‐MMTP participants had a risk similar to NYS (RR = 0.96; 95% CI = 0.72–1.28). We observed no change points in the follow‐up period. Conclusion: Our findings support the hypothesis that no‐cost screening (a benefit provided by WTC‐MMTPs) is associated with elevated identification of thyroid cancer. Given the high survival rate for thyroid cancer, it is important to weigh the costs and benefits of treatment, as many of these cancers were asymptomatic and may have been detected incidentally. [ABSTRACT FROM AUTHOR]

Helicobacter pylori (Hp) is crucial in gastric carcinogenesis, but infection alone is not a sufficient cause, and the interaction between Hp infection and other risk factors has not been adequately studied. We conducted a pooled analysis of seven case‐control studies from the Stomach cancer Pooling (StoP) Project, comprising 1377 cases and 2470 controls, to explore the interaction among Hp infection and tobacco smoking, alcohol drinking, socioeconomic status (SES) and dietary salt intake on the risk of gastric cancer. We estimated summary odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) by multivariate unconditional logistic regression. The analysis showed no consistent interaction between Hp infection and cigarette smoking, while interaction was more than multiplicative for alcohol drinking (OR = 1.38, 95% CI: 1.07‐1.77, P‐interaction 0.02) and high intake of salt (OR = 2.62, 95% CI: 1.88‐3.65, P‐interaction = 0.04). The interaction with SES followed the multiplicative model (P = 0.49), resulting in a weakening among infected individuals of the protective effect of high SES among observed Hp‐negative individuals. The interactions found were more pronounced in subjects with history of peptic ulcer. The interactions with Hp infection were stronger for cigarette smoking and dietary salt in the case of noncardia cancer, and for alcohol and SES in the case of cardia cancer. No differences were found when stratifying for histologic type. This large‐scale study aimed to quantify the interaction between Hp infection and other modifiable risk factors of gastric cancer revealed that the benefit of combined Hp eradication and lifestyle modification on gastric cancer prevention may be larger than commonly appreciated. What's new? Why do some Helicobacter pylori infections lead to gastric cancer, but not others? In this study, the authors investigated the interaction between H. pylori and other gastric cancer risk factors, including tobacco smoking, alcohol drinking, socioeconomic status (SES) and dietary salt. They combined seven case‐control studies and performed pooled analysis to quantify the interaction between risk factors. They found that the associations with alcohol and salt were more than multiplicative. Smoking and SES, on the other hand, combined with H. pylori infection in a multiplicative fashion. Thus, lifestyle modifications could boost the benefit of eradicating H. pylori. [ABSTRACT FROM AUTHOR]

Background: Marked reductions in childhood cancer mortality occurred over the last decades in high-income countries and, to a lesser degree, in middle-income countries. This study aimed to monitor mortality trends in the Americas and Australasia, focusing on areas showing unsatisfactory trends.Methods: Age-standardized mortality rates per 100,000 children (aged 0-14 years) from 1990 to 2017 (or the last available calendar year) were computed for all neoplasms and 8 leading childhood cancers in countries from the Americas and Australasia, using data from the World Health Organization database. A joinpoint regression was used to identify changes in slope of mortality trends for all neoplasms, leukemia, and neoplasms of the central nervous system (CNS) for major countries.Results: Over the last decades, childhood cancer mortality continued to decrease by approximately 2% to 3% per year in Australasian countries (ie, Japan, Korea, and Australia), by approximately 1.5% to 2% in North America and Chile, and 1% in Argentina. Other Latin American countries did not show any substantial decrease. Leukemia mortality declined in most countries, whereas less favorable trends were registered for CNS neoplasms, particularly in Latin America. Around 2016, death rates from all neoplasms were 4 to 6 per 100,000 boys and 3 to 4 per 100,000 girls in Latin America, and 2 to 3 per 100,000 boys and approximately 2 per 100,000 girls in North America and Australasia.Conclusions: Childhood cancer mortality trends declined steadily in North America and Australasia, whereas they were less favorable in most Latin American countries. Priority must be given to closing the gap by providing high-quality care for all children with cancer worldwide.Lay Summary: Advances in childhood cancer management have substantially improved the burden of these neoplasms over the past 40 years, particularly in high-income countries. This study aimed to monitor recent trends in America and Australasia using mortality data from the World Health Organization. Trends in childhood cancer mortality continued to decline in high-income countries by approximately 2% to 3% per year in Japan, Korea, and Australia, and 1% to 2% in North America. Only a few Latin American countries showed favorable trends, including Argentina, Chile, and Mexico, whereas other countries with limited resources still lagged behind. [ABSTRACT FROM AUTHOR]

Objective: To summarize the latest evidence on head and neck cancer epidemiology from the International Head and Neck Cancer Epidemiology (INHANCE) consortium. Subjects and Methods: INHANCE was established in 2004 to elucidate the etiology of head and neck cancer through pooled analyses of individual‐level data on a large scale. We summarize results from recent INHANCE‐based publications updating our 2015 overview. Results: Seventeen papers were published between 2015 and May 2020. These studies further define the nature of risks associated with tobacco and alcohol, and occupational exposures on head and neck cancer. The beneficial effects on incidence of head and neck cancer were identified for good oral health, endogenous and exogenous hormonal factors, and selected aspects of diet related to fruit and vegetables. INHANCE has begun to develop risk prediction models and to pool follow‐up data on their studies, finding that ~30% of cases had cancer recurrence and 9% second primary cancers, with overall‐ and disease‐specific 5‐year‐survival of 51% and 57%, respectively. Conclusions: The number and importance of INHANCE scientific findings provides further evidence of the advantages of large‐scale internationally collaborative projects and will support the development of prevention strategies. [ABSTRACT FROM AUTHOR]

We estimated mortality figures for 2019 in seven Latin American countries, with focus on breast cancer. We retrieved cancer death certification and population data from the WHO and PAHO databases. We obtained mortality statistics for Argentina, Brazil, Chile, Colombia, Cuba, Mexico and Venezuela for 1970–2015. We predicted current death numbers and age‐standardised (world population) mortality rates using joinpoint regression models. Total cancer mortality is predicted to decline in all countries and both sexes, except Argentinian women. Cuba had the highest all cancer rates for 2019, 136.9/100,000 men and 90.4 women, while Mexico showed the lowest ones, 63.8/100,000 men and 61.9 women. Stomach cancer showed favourable trends over the whole period, while colorectal cancer only recently. Lung cancer rates declined in men, while in women they decreased slightly over the most recent years, only. In Cuban women, lung cancer rates overtook breast cancer ones. Breast cancer showed overall favourable trends, but rates are rising in young women. Prostate and uterine cancer had favourable trends. Pancreas, ovary, bladder and leukaemias showed slightly decreasing trends. Between 1990 and 2019, mortality from all neoplasms is predicted to fall by about 18% in Argentina, 26% in Chile, 14% in Colombia, 17% in Mexico and 13% in Venezuela, corresponding to almost 0.5 million avoided cancer deaths. No decline was observed in Brazil and Cuba. Of concern, the persisting high rates of (cervix) uterus cancer, the high lung cancer rates in Cuba, the possible increases in breast cancer in young women, and the lack of overall declines in Brazil, Cuba and Venezuelan men. What's new? In Latin American countries, overall cancer mortality has declined over the last 3 decades. Still, unfavorable trends continue in certain populations and certain neoplasms. Here, the authors update their earlier work on cancer mortality, looking at trends for several cancer types across 7 Latin American countries. Their analysis predicted a continued decline in total cancer mortality rates among both men and women, with the exception of Argentinian women. Stomach cancer deaths in Chile and Colombia remain particularly high among both sexes, as does lung cancer in Cuba. Breast cancer mortality showed favorable trends overall, but rates are rising among young women. Cervical cancer remains exceedingly high. [ABSTRACT FROM AUTHOR]

Previous studies have reported an association between hot tea drinking and risk of esophageal cancer, but no study has examined this association using prospectively and objectively measured tea drinking temperature. We examined the association of tea drinking temperature, measured both objectively and subjectively at study baseline, with future risk of esophageal squamous cell carcinoma (ESCC) in a prospective study. We measured tea drinking temperature using validated methods and collected data on several other tea drinking habits and potential confounders of interest at baseline in the Golestan Cohort Study, a population‐based prospective study of 50,045 individuals aged 40–75 years, established in 2004–2008 in northeastern Iran. Study participants were followed‐up for a median duration of 10.1 years (505,865 person‐years). During 2004–2017, 317 new cases of ESCC were identified. The objectively measured tea temperature (HR 1.41, 95% CI 1.10–1.81; for ≥60°C vs. <60°C), reported preference for very hot tea drinking (HR 2.41, 95% CI 1.27–4.56; for "very hot" vs. "cold/lukewarm"), and reported shorter time from pouring tea to drinking (HR 1.51, 95% CI 1.01–2.26; for <2 vs. ≥6 min) were all associated with ESCC risk. In analysis of the combined effects of measured temperature and amount, compared to those who drank less than 700 ml of tea/day at <60°C, drinking 700 mL/day or more at a higher‐temperature (≥60°C) was consistently associated with an about 90% increase in ESCC risk. Our results substantially strengthen the existing evidence supporting an association between hot beverage drinking and ESCC. What's new? Previous studies have indicated that hot tea may increase the risk of esophageal cancer. In this large, prospective study, the authors found that drinking hot tea is indeed associated with an increased risk of esophageal squamous cell carcinoma (ESCC). Furthermore, a preference for "very hot" tea more than doubled this risk. It may thus be a reasonable public‐health measure to extrapolate these results to all types of beverages, and to advise the public to wait for beverages to cool to <60°C before consumption. [ABSTRACT FROM AUTHOR]

Background: The smoking prevalence among men in China is high, but the head and neck cancer incidence rates are low. This study's purpose was to investigate the impact of tobacco, betel quid, and alcohol on head and neck cancer risk in East Asia. Methods: A multicenter case‐control study (921 patients with head and neck cancer and 806 controls) in East Asia was conducted. The odds ratio (OR) and 95% confidence interval (CI) were estimated using logistic regression. Results: Head and neck cancer risks were elevated for tobacco (OR = 1.58), betel quid (OR = 8.23), and alcohol (OR = 2.29). The total attributable risk of tobacco and/or alcohol was 47.2%. Tobacco/alcohol appeared to account for a small proportion of head and neck cancer among women (attributable risk of 2.2%). Betel quid chewing alone accounted for 28.7% of head and neck cancer. Conclusions: Betel quid chewing is the strongest risk factor for oral cavity cancer in this Chinese population. Alcohol may play a larger role for head and neck cancer in this population than in European or U.S. populations. [ABSTRACT FROM AUTHOR]

Studies conducted in China linked selenium deficiency to higher risk of esophageal squamous cell carcinoma ( ESCC), but this has not been widely tested outside that selenium-deficient region. The aim of this study was to investigate the association between selenium and other mineral concentrations in toenails and risk of ESCC in a region with high incidence rates. In this nested case-control study, we identified 222 cases of ESCC from the Golestan Cohort Study, Iran, which has followed up 50,045 participants since enrollment (2004-2008). We randomly selected one control for each case matched by age and sex, using incidence density sampling. We used toenail samples collected at baseline to measure the concentration of selenium, zinc, chromium, mercury, and scandium using instrumental neutron activation analysis. Multivariate adjusted logistic regression models were used to estimate odds ratios ( OR) and 95% confidence intervals. Median nail selenium, zinc, chromium, and mercury levels were 1.01, 74.59, 0.77, and 0.018 μg/g in cases and 1.02, 75.71, 0.71, and 0.023 μg/g in controls, respectively. The adjusted odds ratios comparing each fourth quartile of mineral status versus the first quartile were as follows: selenium = 0.78 (95% CI, 0.41-1.49); zinc=0.80 (95% CI, 0.42-1.53); chromium = 0.91 (95% CI, 0.46-1.80); and mercury=0.61 (95% CI, 0.27-1.38), and all trend tests were non-significant. The nail selenium concentration in our controls reflects relatively high selenium status. No evidence of association between selenium or chromium concentrations in toenails and the risk of ESCC was detected in this population. [ABSTRACT FROM AUTHOR]

Background Although the impact of oral hygiene on head and neck cancer risk has been investigated, few studies have been conducted among the Asian population. Methods We conducted a multicenter case-control study to investigate this potential association. We performed unconditional multiple logistic regression models adjusted by potential confounders. Results We observed an inverse association of frequency of dental visits with head and neck cancer risk, with an adjusted odds ratio (OR) of 3.70 (95% CI 2.51-5.45) for never dental visits compared with ≥1 time/year ( Ptrend < .001). We also observed a positive association between the number of missing teeth and head and neck cancer risk, with an adjusted OR for ≥5 missing teeth compared with <5 missing teeth of 1.49 (95% CI 1.08-2.04). Combining multiple oral hygiene indicators, poor oral hygiene scores increased head and neck cancer risk. Conclusion Poor oral hygiene may increase head and neck cancer risk in the Chinese population. Therefore, improving oral hygiene may contribute to reducing the head and neck cancer risk in the Chinese population. [ABSTRACT FROM AUTHOR]

Due to lower female incidence, estimates of exogenous and endogenous hormonal factors in head and neck cancers (HNCs, comprising cancers of the oral cavity, oropharynx, hypopharynx, and larynx) among women have been inconsistent and unable to account for key HNC risk factors. We pooled data from 11 studies from Europe, North America, and Japan. Analysis included 1572 HNC female cases and 4343 controls. Pooled odds ratios (ORs) estimates and their 95% confidence intervals (CIs) were calculated using multivariate logistic regression models adjusting for tobacco smoking and alcohol drinking. Lower risk was observed in women who used hormone replacement therapy (HRT) (OR = 0.58; 95% CI: 0.34-0.77). Pregnancy (OR = 0.61; 95% CI: 0.42-0.90) and giving birth (OR = 0.59; 95% CI: 0.38-0.90) at <35 years of age were inversely associated with HNCs. An inverse association with HNC was observed with age at start of HRT use (OR = 0.59; 95% CI: 0.39-0.90) for each additional 10 years and with duration of use (OR = 0.87; 95% CI: 0.76-0.99 for every 3 years). Exogenous female hormone use is associated with a nearly twofold risk reduction in female HNCs. The lower female HNC incidence may, in part, be explained by endogenous and exogenous estrogen exposures. [ABSTRACT FROM AUTHOR]

It is not clear whether alcohol consumption is associated with lung cancer risk. The relationship is likely confounded by smoking, complicating the interpretation of previous studies. We examined the association of alcohol consumption and lung cancer risk in a large pooled international sample, minimizing potential confounding of tobacco consumption by restricting analyses to never smokers. Our study included 22 case-control and cohort studies with a total of 2548 never-smoking lung cancer patients and 9362 never-smoking controls from North America, Europe and Asia within the International Lung Cancer Consortium (ILCCO) and SYNERGY Consortium. Alcohol consumption was categorized into amounts consumed (grams per day) and also modelled as a continuous variable using restricted cubic splines for potential non-linearity. Analyses by histologic sub-type were included. Associations by type of alcohol consumed (wine, beer and liquor) were also investigated. Alcohol consumption was inversely associated with lung cancer risk with evidence most strongly supporting lower risk for light and moderate drinkers relative to non-drinkers (>0-4.9 g per day: OR = 0.80, 95% CI = 0.70-0.90; 5-9.9 g per day: OR = 0.82, 95% CI = 0.69-0.99; 10-19.9 g per day: OR = 0.79, 95% CI = 0.65-0.96). Inverse associations were found for consumption of wine and liquor, but not beer. The results indicate that alcohol consumption is inversely associated with lung cancer risk, particularly among subjects with low to moderate consumption levels, and among wine and liquor drinkers, but not beer drinkers. Although our results should have no relevant bias from the confounding effect of smoking we cannot preclude that confounding by other factors contributed to the observed associations. Confounding in relation to the non-drinker reference category may be of particular importance. [ABSTRACT FROM AUTHOR]

Burkitt's Lymphoma (BL) has three peaks of occurrence, in children, adults and elderly, at 10, 40 and 70 years respectively. To the best of our knowledge, no study has been conducted to assess predictors of survival in the three age groups. We hypothesized that survival predictors may differ by age group. We, therefore, sought to determine survival predictors for BL in these three groups: children (<15 years of age), adults (40-70 years of age) and elderly (>70 years of age). Using the Surveillance, Epidemiology, and End Results (SEER) database covering the years 2000-2013, we identified 797 children, 1,994 adults and 757 elderly patients newly diagnosed with BL. We used adjusted Cox proportional hazards regression models to determine prognostic factors for survival for each age group. Five-year relative survival in BL for children, adults and elderly were 90.4, 47.8 and 28.9%, respectively. Having at least Stage II disease and multiple primaries were associated with higher mortality in the elderly group. In adults, multiple primaries, Stage III or IV disease, African American race and bone marrow primary were associated with increased mortality whereas Stage IV disease and multiple primaries were associated with worse outcome in children. These findings demonstrate commonalities and differences in predictors of survival that may have implications for management of BL patients. [ABSTRACT FROM AUTHOR]

We aimed at investigating mortality among beryllium-exposed workers, according to solubility of beryllium and beryllium compounds. We conducted an historical cohort study of 16,115 workers employed during 1925-2008 in 15 facilities, including eight entailing exposure to insoluble beryllium and seven entailing exposure to soluble/mixed beryllium compounds, who were followed up for mortality until 2011. Data were analyzed using indirect standardization and Cox regression modeling. Lung cancer standardized mortality ratio ( SMR, national reference rates) was 1.02 (95% confidence interval [ CI]: 0.94-1.10) in the whole cohort, 0.88 (95% CI: 0.75-1.03) in the insoluble beryllium subcohort, and 1.09 (95% CI: 0.99-1.09) in the soluble/mixed beryllium subcohort. For lung cancer, there was an association with period of hire in soluble/mixed beryllium plants but not in insoluble plants, and, conversely, employment in soluble/mixed plants was associated with increased mortality only among workers hired before 1955. There was no trend with duration of employment. Mortality from chronic beryllium disease increased, in particular, among workers hired before 1955 in soluble/mixed beryllium facilities. There was no increase in lung cancer mortality in the entire cohort and lung cancer mortality was not increased among beryllium workers hired in 1955 or later in soluble/mixed beryllium facilities, or at any time among those employed in insoluble beryllium facilities. [ABSTRACT FROM AUTHOR]

Limited information is available on risk of peritoneal mesothelioma after asbestos exposure, and in general on the risk of cancer after cessation of asbestos exposure. We updated to 2013 the follow-up of a cohort of 1083 female and 894 male textile workers with heavy asbestos exposure (up to 100 fb/ mL), often for short periods. A total of 1019 deaths were observed, corresponding to a standardized mortality ratio ( SMR) of 1.68 (95% confidence interval [ CI]: 1.57-1.78). SMRs were 29.1 (95% CI: 21.5-38.6) for peritoneal cancer, 2.96 (95% CI: 2.50-3.49) for lung cancer, 33.7 (95% CI: 25.7-43.4) for pleural cancer, and 3.03 (95% CI: 1.69-4.99) for ovarian cancer. For pleural and peritoneal cancer, there was no consistent pattern of risk in relation to time since last exposure, whereas for lung cancer there was an indication of a decline in risk after 25 years since last exposure. The findings of this unique cohort provide novel data for peritoneal cancer, indicating that - as for pleural cancer - the excess risk does not decline up to several decades after cessation of exposure. [ABSTRACT FROM AUTHOR]

Alcohol consumption is a major cause of disease and death. In a previous study, we reported that in 2002, 3.6% of all cases of cancer and a similar proportion of cancer deaths were attributable to the consumption of alcohol. We aimed to update these figures to 2012 using global estimates of cancer cases and cancer deaths, data on the prevalence of drinkers from the World Health Organization (WHO) global survey on alcohol and health, and relative risks for alcohol-related neoplasms from a recent meta-analysis. Over the 10-year period considered, the total number of alcohol-attributable cancer cases increased to approximately 770,000 worldwide (5.5% of the total number of cancer cases)-540,000 men (7.2%) and 230,000 women (3.5%). Corresponding figures for cancer deaths attributable to alcohol consumption increased to approximately 480,000 (5.8% of the total number of cancer deaths) in both sexes combined-360,000 (7.8%) men and 120,000 (3.3%) women. These proportions were particularly high in the WHO Western Pacific region, the WHO European region and the WHO South-East Asia region. A high burden of cancer mortality and morbidity is attributable to alcohol, and public health measures should be adopted in order to limit excessive alcohol consumption. [ABSTRACT FROM AUTHOR]

Background Three longitudinal studies of cancer incidence in varied populations of World Trade Center responders have been conducted. Methods We compared the design and results of the three studies. Results Separate analyses of these cohorts revealed excess cancer incidence in responders for all cancers combined and for cancers of the thyroid and prostate. Methodological dissimilarities included recruitment strategies, source of cohort members, demographic characteristics, overlap between cohorts, assessment of WTC and other occupational exposures and confounders, methods and duration of follow-up, approaches for statistical analysis, and latency analyses. Conclusions The presence of three cohorts strengthens the effort of identifying and quantifying the cancer risk; the heterogeneity in design might increase sensitivity to the identification of cancers potentially associated with exposure. The presence and magnitude of an increased cancer risk remains to be fully elucidated. Continued long-term follow up with minimal longitudinal dropout is crucial to achieve this goal. Am. J. Ind. Med. 59:96-105, 2015. © 2015 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Evidence of associations between single nutrients and head and neck cancer (HNC) is still more limited and less consistent than that for fruit and vegetables. However, clarification of the protective mechanisms of fruit and vegetables is important to our understanding of HNC etiology. We investigated the association between vitamin C intake from natural sources and cancer of the oral cavity/pharynx and larynx using individual-level pooled data from ten case-control studies (5,959 cases and 12,248 controls) participating in the International Head and Neck Cancer Epidemiology (INHANCE) consortium. After harmonization of study-specific exposure information via the residual method, adjusted odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using unconditional multiple logistic regression models on quintile categories of 'non-alcohol energy-adjusted' vitamin C intake. In the presence of heterogeneity of the estimated ORs among studies, we derived those estimates from generalized linear mixed models. Higher intakes of vitamin C were inversely related to oral and pharyngeal (OR = 0.54, 95% CI: 0.45-0.65, for the fifth quintile category versus the first one, p for trend<0.001) and laryngeal cancers (OR = 0.52, 95% CI: 0.40-0.68, p for trend = 0.006), although in the presence of heterogeneity among studies for both sites. Inverse associations were consistently observed for the anatomical subsites of oral and pharyngeal cancer, and across strata of age, sex, education, body mass index, tobacco, and alcohol, for both cancer sites. The inverse association of vitamin C intake from foods with HNC may reflect a protective effect on these cancers; however, we cannot rule out other explanations. [ABSTRACT FROM AUTHOR]

To develop a quantitative exposure-response relationship between concentrations and durations of inhaled diesel engine exhaust (DEE) and increases in lung cancer risks, we examined the role of temporal factors in modifying the estimated effects of exposure to DEE on lung cancer mortality and characterized risk by mine type in the Diesel Exhaust in Miners Study (DEMS) cohort, which followed 12,315 workers through December 1997. We analyzed the data using parametric functions based on concepts of multistage carcinogenesis to directly estimate the hazard functions associated with estimated exposure to a surrogate marker of DEE, respirable elemental carbon (REC). The REC-associated risk of lung cancer mortality in DEMS is driven by increased risk in only one of four mine types (limestone), with statistically significant heterogeneity by mine type and no significant exposure-response relationship after removal of the limestone mine workers. Temporal factors, such as duration of exposure, play an important role in determining the risk of lung cancer mortality following exposure to REC, and the relative risk declines after exposure to REC stops. There is evidence of effect modification of risk by attained age. The modifying impact of temporal factors and effect modification by age should be addressed in any quantitative risk assessment (QRA) of DEE. Until there is a better understanding of why the risk appears to be confined to a single mine type, data from DEMS cannot reliably be used for QRA. [ABSTRACT FROM AUTHOR]

The etiology of esophageal squamous cell carcinoma (ESCC) in the high risk area of northern Iran is only partially known. We aimed to investigate prolonged animal contact as a risk factor for ESCC in this population. From 2003 to 2007, we administered a validated questionnaire to 300 ESCC cases and 571 randomly selected controls matched for neighborhood of residence, age (±2 years) and sex. Questions on lifelong exposure to equines, ruminants, canines, and poultry, including duration and level of contact, were asked in a face-to-face interviews. Conditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs) adjusted for potential confounders. A total of 94.7% of cases and 68.7% of controls reported lifelong history of contact with ruminants. After controlling for potential confounders, contact with ruminants was associated with an eightfold increase (95% CI: 3.92-14.86) in risk of ESCC, and increments in duration of contact raised the risk estimates in a dose-dependent manner. Contact with equines and poultry did not significantly change associated OR for ESCC risk and contact with ruminants. OR (95% CI) for contact with canines was 1.99 (1.35-2.93) which after exclusion of contact with ruminants was not significant (OR for contact only with canine: 3.18, 95% CI: 0.73-13.17). These results add to the evidence that contact with ruminants may increase the risk of ESCC. [ABSTRACT FROM AUTHOR]

Salt tea is the most commonly used beverage in Kashmir, India, where esophageal squamous cell carcinoma (ESCC) is the most common cancer. Salt tea is brewed in a unique way in Kashmir, usually with addition of sodium bicarbonate, which makes salt tea alkaline. As little information about the association between salt tea drinking and ESCC was available, we conducted a large-scale case-control study to investigate this association in Kashmir. We recruited 703 histologically confirmed cases of ESCC and 1664 controls individually matched to cases for age, sex, and district of residence. Conditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (95% CIs). Participants who consumed >1,250 ml day−1 showed an increased risk of ESCC (OR = 2.60, 95% CIs = 1.68-4.02). Samovar (a special vessel for the beverage preparation) users (OR = 1.77, 95% CIs 1.25-2.50) and those who ate cereal paste with salt tea (OR = 2.14, 95% CIs = 1.55-2.94) or added bicarbonate sodium to salt tea (OR = 2.12, 95% CIs = 1.33-3.39) were at higher risk of ESCC than others. When analysis was limited to alkaline tea drinkers only, those who both consumed cereal paste with salt tea and used samovar vessel were at the highest risk (OR = 4.58, 95% CIs = 2.04-10.28). This study shows significant associations of salt tea drinking and some related habits with ESCC risk. [ABSTRACT FROM AUTHOR]

There are suggestions of an inverse association between folate intake and serum folate levels and the risk of oral cavity and pharyngeal cancers (OPCs), but most studies are limited in sample size, with only few reporting information on the source of dietary folate. Our study aims to investigate the association between folate intake and the risk of OPC within the International Head and Neck Cancer Epidemiology (INHANCE) Consortium. We analyzed pooled individual-level data from ten case-control studies participating in the INHANCE consortium, including 5,127 cases and 13,249 controls. Odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were estimated for the associations between total folate intake (natural, fortification and supplementation) and natural folate only, and OPC risk. We found an inverse association between total folate intake and overall OPC risk (the adjusted OR for the highest vs. the lowest quintile was 0.65, 95% CI: 0.43-0.99), with a stronger association for oral cavity (OR = 0.57, 95% CI: 0.43-0.75). A similar inverse association, though somewhat weaker, was observed for folate intake from natural sources only in oral cavity cancer (OR = 0.64, 95% CI: 0.45-0.91). The highest OPC risk was observed in heavy alcohol drinkers with low folate intake as compared to never/light drinkers with high folate (OR = 4.05, 95% CI: 3.43-4.79); the attributable proportion (AP) owing to interaction was 11.1% (95% CI: 1.4-20.8%). Lastly, we reported an OR of 2.73 (95% CI:2.34-3.19) for those ever tobacco users with low folate intake, compared with nevere tobacco users and high folate intake (AP of interaction =10.6%, 95% CI: 0.41-20.8%). Our project of a large pool of case-control studies supports a protective effect of total folate intake on OPC risk. [ABSTRACT FROM AUTHOR]

Intake of dairy products has been associated with risk of some cancers, but findings are often inconsistent and information on hepatocellular carcinoma (HCC) risk is limited, particularly from prospective settings. The aim of our study was to investigate the association between consumption of total and specific dairy products (milk/cheese/yogurt) and their components (calcium/vitamin D/fats/protein), with first incident HCC ( Ncases = 191) in the European Prospective Investigation into Cancer and Nutrition cohort, including a nested case-control subset ( Ncases = 122) with the assessment of hepatitis B virus/hepatitis C virus infections status, liver damage and circulating insulin-like growth factor (IGF)-I levels. For cohort analyses, multivariable-adjusted Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CI). For nested case-control analyses, conditional logistic regression was used to calculate odds ratios and 95% CI. A total of 477,206 participants were followed-up for an average of 11 years (person-years follow-up = 5,415,385). In the cohort study, a significant positive HCC risk association was observed for total dairy products (highest vs. lowest tertile, HR = 1.66, 95% CI: 1.13-2.43; ptrend = 0.012), milk (HR = 1.51, 95% CI: 1.02-2.24; ptrend = 0.049), and cheese (HR = 1.56, 95% CI: 1.02-2.38; ptrend = 0.101), but not yogurt (HR = 0.94, 95% CI: 0.65-1.35). Dietary calcium, vitamin D, fat and protein from dairy sources were associated with increased HCC risk, whereas the same nutrients from nondairy sources showed inverse or null associations. In the nested case-control study, similar results were observed among hepatitis-free individuals. Results from this large prospective cohort study suggest that higher consumption of dairy products, particularly milk and cheese, may be associated with increased HCC risk. Validation of these findings in other populations is necessary. Potential biologic mechanisms require further exploration. [ABSTRACT FROM AUTHOR]

The article presents a response from Paolo Boffetta to the commentary on their paper on the causation of malignant mesothelioma published in the "American Journal of Industrial Medicine." Topics covered include errors and change in authorship of the document, effect of time since last exposure to asbestos and questions on the integrity of the document since the authors of the document are involved in asbestos litigation.

This study tests the hypothesis that prediagnostic serum levels of 20 cancer-associated inflammatory biomarkers correlate directly with future development of head and neck, esophageal, and lung cancers in a high-risk prospective cohort. This is a nested case-control pilot study of subjects enrolled in the Golestan Cohort Study, an ongoing epidemiologic project assessing cancer trends in Golestan, Iran. We measured a panel of 20 21cytokines, chemokines, and inflammatory molecules using Luminex technology in serum samples collected 2 or more years before cancer diagnosis in 78 aerodigestive cancer cases and 81 controls. Data was analyzed using Wilcoxon rank sum test, odds ratios, receiver operating characteristic areas of discrimination, and multivariate analysis. Biomarkers were profoundly and globally elevated in future esophageal and lung cancer patients compared to controls. Odds ratios were significant for association between several biomarkers and future development of esophageal cancer, including interleukin-1Rα (IL-1Ra; 35.9), interferon α2 (IFN-a2; 34.0), fibroblast growth factor-2 (FGF-2; 17.4), and granulocyte/macrophage colony-stimulating factor ( GM- CSF; 17.4). The same pattern was observed among future lung cancer cases for G- CSF (27.7), GM- CSF (13.3), and tumor necrosis factor-α (TNF-a; 8.6). By contrast, the majority of biomarkers studied showed no significant correlation with future head and neck cancer development. This study provides the first direct evidence that multiple inflammatory biomarkers are coordinately elevated in future lung and esophageal cancer patients 2 or more years before cancer diagnosis. [ABSTRACT FROM AUTHOR]

Background: The current study was conducted to analyze the association between cigarette smoking and metastasis (the primary outcome) as well as time to biochemical disease recurrence (BCR), metastasis, castration-resistant prostate cancer (CRPC), and prostate cancer-specific and overall mortality (secondary outcomes) after radical prostatectomy among men from the Shared Equal Access Regional Cancer Hospital cohort.Methods: A retrospective analysis was performed of 1450 subjects for whom smoking status was available from preoperative notes. Analysis of baseline characteristics by smoking status was performed using the chi-square and rank sum tests. The association between smoking status and time to the event was analyzed using Kaplan-Meier plots, the log-rank test, and Cox and competing risk models.Results: A total of 549 men (33%) men were active smokers and 1121 (67%) were nonsmokers at the time of surgery. Current smokers were younger and had a lower body mass index, higher prostate-specific antigen level, and more extracapsular extension and seminal vesicle invasion (all P<.05). A total of 509 patients, 26 patients, 30 patients, 18 patients, and 217 patients, respectively, experienced BCR, metastasis, CRPC, prostate cancer-related death, and any-cause death over a median follow-up of 62 months, 75 months, 61 months, 78 months, and 78 months, respectively. After adjusting for preoperative features, active smoking was found to be associated with an increased risk of BCR (hazards ratio [HR], 1.25; P=.024), metastasis (HR, 2.64; P=.026), CRPC (HR, 2.62; P=.021), and overall mortality (HR, 2.14; P<.001). Similar results were noted after further adjustment for postoperative features, with the exception of BCR (HR, 1.10; P=.335), metastasis (HR, 2.51; P=.044), CRPC (HR, 2.67; P=.015), and death (HR, 2.03; P<.001).Conclusions: Among patients undergoing radical prostatectomy, cigarette smoking was associated with an increased risk of metastasis. In addition, smoking was associated with a higher risk of BCR, CRPC, and overall mortality. If confirmed, these data suggest that smoking is a modifiable risk factor in patients with aggressive prostate cancer. [ABSTRACT FROM AUTHOR]

Studies have persistently associated esophageal squamous cell carcinoma ( ESCC) risk with low socioeconomic status ( SES), but this association is unexplored in Kashmir, an area with a high incidence of ESCC in the northernmost part of India. We carried out a case-control study to assess the association of multiple indicators of SES and ESCC risk in the Kashmir valley. A total number of 703 histologically confirmed ESCC cases and 1664 controls matched to the cases for age, sex, and district of residence were recruited from October 2008 to January 2012. Conditional logistic regression models were used to calculate unadjusted and adjusted odds ratios and 95% confidence intervals. Composite wealth scores were constructed based on the ownership of several appliances using multiple correspondence analyses. Higher education, living in a kiln brick or concrete house, use of liquefied petroleum gas and electricity for cooking, and higher wealth scores all showed an inverse association with ESCC risk. Compared to farmers, individuals who had government jobs or worked in the business sector were at lower risk of ESCC, but this association disappeared in fully adjusted models. Occupational strenuous physical activity was strongly associated with ESCC risk. In summary, we found a strong relationship of low SES and ESCC in Kashmir. The findings need to be studied further to understand the mechanisms through which such SES parameters increase ESCC risk. [ABSTRACT FROM AUTHOR]

Background In the period 1990 to 2001, a case-control study on oral cancer and maté consumption was conducted at the Cancer Institute of Uruguay. Methods The study included 696 newly diagnosed cases with squamous cell carcinoma and 696 controls afflicted with nonneoplastic conditions not related to tobacco smoking and alcohol drinking. The participants were matched on age and residence and the study was restricted to men. Results In order to control confounding for tobacco and alcohol, we fitted 2 models. According to model 1, the odds ratio (OR) for maté consumption was 1.15 (95% confidence interval [CI], 0.76-1.73), whereas the results for model 2 showed an OR of 3.47 (95% CI, 1.60-7.52). Conclusions The inclusion of a term for the interaction between maté and smoking (or drinking) was rewarding and the ORs were even higher than those observed with the crude estimates. Head Neck, 2013 [ABSTRACT FROM AUTHOR]

Opium use has been associated with higher risk of cancers of the esophagus, bladder, larynx, and lung; however, no previous study has examined its association with gastric cancer. There is also little information on the associations between hookah (water pipe) smoking or the chewing of tobacco products and the risk of gastric cancer. In a case-control study in Golestan Province of Iran, we enrolled 309 cases of gastric adenocarcinoma (118 noncardia, 161 cardia and 30 mixed-location adenocarcinomas) and 613 matched controls. Detailed information on long-term use of opium, tobacco products and other covariates were collected using structured and validated lifestyle and food frequency questionnaires. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were obtained using conditional logistic regression models. Opium use was associated with an increased risk of gastric adenocarcinoma, with an adjusted OR (95% CI) of 3.1 (1.9-5.1), and this increased risk was apparent for both anatomic subsites (cardia and noncardia). There was a dose-response effect, and individuals with the highest cumulative opium use had the strongest association (OR: 4.5; 95% CI: 2.3-8.5). We did not find a statistically significant association between the use of any of the tobacco products and risk of gastric adenocarcinoma, overall or by anatomic subsite. We showed, for the first time, an association between opium use and gastric adenocarcinoma. Given that opium use is a traditional practice in many parts of the world, these results are of public health significance. [ABSTRACT FROM AUTHOR]

Interindividual variation in DNA adduct levels in individuals exposed to similar amounts of environmental carcinogens may be due to genetic variability. We analysed the influence of genes involved in determining/modifying DNA damage, including microsomal epoxide hydrolase1 (EPHX1) His139Arg, N-acetyl-transferase, NAD(P)H:quinone oxidoreductase1 (NQO1) Pro187Ser, manganese superoxide dismutase2 (MnSOD2) Val16Ala, and apurinic/apyrimidinic endonuclease1 (APE1) Asp148Glu polymorphisms in blood of 120 smokers. Subsequently, we examined the effects of the combinations of the variant alleles of EPHX, NQO1 and MnSOD2 together with the wild type allele of APE1 on DNA damage by calculating the 'sum of at-risk alleles.' We reviewed the studies examining the relationships of DNA adducts with at-risk alleles in environmentally exposed subjects. Our findings showed that smokers carrying the EPHX1-139Arg and the NQO1-187Ser variants were significantly more likely to have higher adduct levels. Null associations were found with the other variants. Nevertheless, DNA adduct levels in smokers with ≥5 at-risk alleles were significantly different from those with fewer than two alleles. A similar picture emerged from studies of DNA adducts and at-risk alleles in environmentally exposed and smoking subjects. Certain at-risk allele combinations may confer a greater likelihood of increased levels of adducts after environmental insults. The increase in DNA adduct levels in susceptible subjects exposed to environmental carcinogens may reflect changes in the mechanisms that protect cells from the accumulation of genetic damage. Alterations of the physiological processes designed to maintain homeostasis may reduce the individual 'genotoxic tolerance' to environmental challenges and result in phenotypes characterized by high levels of DNA adducts. Environ. Mol. Mutagen. 54:375-383, 2013. © 2013 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs) likely play a role in many cancers even in never-smokers. We tried to find a model to explain the relationship between variation in PAH-related DNA adduct levels among people with similar exposures, multiple genetic polymorphisms in genes related to metabolic and repair pathways, and nucleotide excision repair (NER) capacity. In 111 randomly selected female never-smokers from the Golestan Cohort Study in Iran, we evaluated 21 SNPs in 14 genes related to xenobiotic metabolism and 12 SNPs in eight DNA repair genes. NER capacity was evaluated by a modified comet assay, and aromatic DNA adduct levels were measured in blood by32P-postlabeling. Multivariable regression models were compared by Akaike's information criterion (AIC). Aromatic DNA adduct levels ranged between 1.7 and 18.6 per 108 nucleotides (mean: 5.8 ± 3.1). DNA adduct level was significantly lower in homozygotes for NAT2 slow alleles and ERCC5 non-risk-allele genotype, and was higher in the MPO homozygote risk-allele genotype. The sum of risk alleles in these genes significantly correlated with the log-adduct level ( r = 0.4, p < 0.001). Compared with the environmental model, adding Phase I SNPs and NER capacity provided the best fit, and could explain 17% more of the variation in adduct levels. NER capacity was affected by polymorphisms in the MTHFR and ERCC1 genes. Female non-smokers in this population had PAH-related DNA adduct levels three to four times higher than smokers and occupationally-exposed groups in previous studies, with large inter-individual variation which could best be explained by a combination of Phase I genes and NER capacity. [ABSTRACT FROM AUTHOR]

To investigate whether renal cell carcinoma (RCC) histologic subtypes possess different etiologies, we conducted analyses of established RCC risk factors by subtype (clear cell, papillary and chromophobe) in two case-control studies conducted in the United States (1,217 cases, 1,235 controls) and Europe (1,097 cases, 1,476 controls). Histology was ascertained for 706 U.S. cases (58% of total) and 917 European cases (84%) through a central slide review conducted by a single pathologist. For the remaining cases, histology was abstracted from the original diagnostic pathology report. Case-only analyses were performed to compute odds ratios (ORs) and 95% confidence intervals (CI) summarizing subtype differences by age, sex and race. Case-control analyses were performed to compute subtype-specific ORs for other risk factors using polytomous regression. In case-only analyses, papillary cases ( N = 237) were older (OR = 1.2, 95% CI = 1.1-1.4 per 10-year increase), less likely to be female (OR = 0.5, 95% CI = 0.4-0.8) and more likely to be black (OR = 2.6, 95% CI = 1.8-3.9) as compared to clear cell cases ( N = 1,524). In case-control analyses, BMI was associated with clear cell (OR = 1.2, 95% CI = 1.1-1.3 per 5 kg/m2 increase) and chromophobe RCC ( N = 80; OR = 1.2, 95% CI = 1.1-1.4), but not papillary RCC (OR = 1.1, 95% CI = 1.0-1.2; test versus clear cell, p = 0.006). No subtype differences were observed for associations with smoking, hypertension or family history of kidney cancer. Our findings support the existence of distinct age, sex and racial distributions for RCC subtypes, and suggest that the obesity-RCC association differs by histology. [ABSTRACT FROM AUTHOR]