The protective effect of dietary folate intake on gastric cancer is modified by alcohol consumption: A pooled analysis of the StoP Consortium.

Dietary folate intake has been identified as a potentially modifiable factor of gastric cancer (GC) risk, although the evidence is still inconsistent. We evaluate the association between dietary folate intake and the risk of GC as well as the potential modification effect of alcohol consumption. We pooled data for 2829 histologically confirmed GC cases and 8141 controls from 11 case-control studies from the international Stomach Cancer Pooling Consortium. Dietary folate intake was estimated using food frequency questionnaires. We used linear mixed models with random intercepts for each study to calculate adjusted odds ratios (OR) and 95% confidence interval (CI). Higher folate intake was associated with a lower risk of GC, although this association was not observed among participants who consumed >2.0 alcoholic drinks/day. The OR for the highest quartile of folate intake, compared with the lowest quartile, was 0.78 (95% CI, 0.67-0.90, P-trend = 0.0002). The OR per each quartile increment was 0.92 (95% CI, 0.87-0.96) and, per every 100 µg/day of folate intake, was 0.89 (95% CI, 0.84-0.95). There was a significant interaction between folate intake and alcohol consumption (P-interaction = 0.02). The lower risk of GC associated with higher folate intake was not observed in participants who consumed >2.0 drinks per day, ORQ4v Q1 = 1.15 (95% CI, 0.85-1.56), and the OR100 µg/day = 1.02 (95% CI, 0.92-1.15). Our study supports a beneficial effect of folate intake on GC risk, although the consumption of >2.0 alcoholic drinks/day counteracts this beneficial effect.

Occupational benzene exposure and colorectal cancer: a systematic review and meta-analysis.

Recent reports suggest that benzene exposure may be associated with solid cancers, such as lung and bladder cancers. Instead, evidence on the association between benzene and colorectal cancer (CRC) is sparse. Thus, we aimed to summarize current literature on the association between occupational benzene exposure and CRC. We searched Pubmed, Embase (through Ovid), and Scopus to retrieve cohort and nested case-control studies on the association between occupational benzene exposure and solid cancers. The search was initially completed in December 2022 and later updated in April 2024. We assessed quality of included studies using a modified version of Newcastle-Ottawa Scale. We computed pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) of CRC according to occupational benzene exposure, using the Paule-Mandel method. Twenty-eight studies were included in the meta-analysis. Most of them were conducted in Europe or North America (82.1%) and were industry-based (89.3%). Pooled RRs comparing workers exposed to benzene with those who were unexposed for incidence and mortality were 1.10 (95% CI: 1.06, 1.15) and 1.04 (95% CI: 0.97, 1.11) for CRC, 1.12 (95% CI: 1.01, 1.24) and 1.08 (95% CI: 0.99, 1.19) for colon cancer, and 1.04 (95% CI: 0.94, 1.14) and 1.05 (95% CI: 0.92, 1.19) for rectal cancer, respectively. Only one study supported the occurrence of a dose-response relationship between occupational benzene exposure and CRC, while others found no increase in risk according to dose of exposure or duration of employment. Our findings suggest that occupational benzene exposure may be associated with CRC. Further research with detailed assessment of individual-level exposure is warranted to confirm our results.

Diabetes and gastric cancer incidence and mortality in the Asia Cohort Consortium: A pooled analysis of more than a half million participants.

BACKGROUND: Evidence suggests a possible link between diabetes and gastric cancer risk, but the findings remain inconclusive, with limited studies in the Asian population. We aimed to assess the impact of diabetes and diabetes duration on the development of gastric cancer overall, by anatomical and histological subtypes. METHODS: A pooled analysis was conducted using 12 prospective studies included in the Asia Cohort Consortium. Among 558 981 participants (median age 52), after a median follow-up of 14.9 years and 10.5 years, 8556 incident primary gastric cancers and 8058 gastric cancer deaths occurred, respectively. Cox proportional hazard regression models were used to estimate study-specific hazard ratios (HRs) and 95% confidence intervals (CIs) and pooled using random-effects meta-analyses. RESULTS: Diabetes was associated with an increased incidence of overall gastric cancer (HR 1.15, 95% CI 1.06-1.25). The risk association did not differ significantly by sex (women vs men: HR 1.31, 95% CI 1.07-1.60 vs 1.12, 1.01-1.23), anatomical subsites (noncardia vs cardia: 1.14, 1.02-1.28 vs 1.17, 0.77-1.78) and histological subtypes (intestinal vs diffuse: 1.22, 1.02-1.46 vs 1.00, 0.62-1.61). Gastric cancer risk increased significantly during the first decade following diabetes diagnosis (HR 4.70, 95% CI 3.77-5.86), and decreased with time (nonlinear p < .01). Positive associations between diabetes and gastric cancer mortality were observed (HR 1.15, 95% CI 1.03-1.28) but attenuated after a 2-year time lag. CONCLUSION: Diabetes was associated with an increased gastric cancer incidence regardless of sex, anatomical subsite, or subtypes of gastric cancer. The risk of gastric cancer was particularly high during the first decade following diabetes diagnosis.

Family history and gastric cancer incidence and mortality in Asia: a pooled analysis of more than half a million participants.

BACKGROUND: The family history of gastric cancer holds important implications for cancer surveillance and prevention, yet existing evidence predominantly comes from case-control studies. We aimed to investigate the association between family history of gastric cancer and gastric cancer risk overall and by various subtypes in Asians in a prospective study. METHODS: We included 12 prospective cohorts with 550,508 participants in the Asia Cohort Consortium. Cox proportional hazard regression was used to estimate study-specific adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between family history of gastric cancer and gastric cancer incidence and mortality, then pooled using random-effects meta-analyses. Stratified analyses were performed for the anatomical subsites and histological subtypes. RESULTS: During the mean follow-up of 15.6 years, 2258 incident gastric cancers and 5194 gastric cancer deaths occurred. The risk of incident gastric cancer was higher in individuals with a family history of gastric cancer (HR 1.44, 95% CI 1.32-1.58), similarly in males (1.44, 1.31-1.59) and females (1.45, 1.23-1.70). Family history of gastric cancer was associated with both cardia (HR 1.26, 95% CI 1.00-1.60) and non-cardia subsites (1.49, 1.35-1.65), and with intestinal- (1.48, 1.30-1.70) and diffuse-type (1.59, 1.35-1.87) gastric cancer incidence. Positive associations were also found for gastric cancer mortality (HR 1.30, 95% CI 1.19-1.41). CONCLUSIONS: In this largest prospective study to date on family history and gastric cancer, a familial background of gastric cancer increased the risk of gastric cancer in the Asian population. Targeted education, screening, and intervention in these high-risk groups may reduce the burden of gastric cancer.

Dietary intake of copper and gastric cancer: a pooled analysis within the Stomach cancer Pooling (StoP) Project.

BACKGROUND: Evidence on the potential association between dietary copper intake and gastric cancer (GC) is lacking. Thus, we aimed to evaluate this association within the Stomach cancer Pooling (StoP) Project-an international consortium of epidemiological studies on GC. METHODS: Data from five case-control studies within the StoP Project were included (2448 cases, 4350 controls). We estimated adjusted odds ratios (ORs) and 95% CIs for the association between dietary copper intake and GC using multivariable mixed-effects logistic regression models. We also modelled the dose-response relationship between copper intake and GC using a logistic mixed-effects model with fractional polynomial. RESULTS: The OR for the highest quartile of copper intake compared with the lowest one was 0.78 (95% CI: 0.63-0.95; P for trend = 0.013). Results were similar for non-cardia-type (OR: 0.72; 95% CI: 0.57-0.91), intestinal-type (OR: 0.75; 95% CI: 0.56-0.99) and other histological-type GC (OR: 0.65; 95% CI: 0.44-0.96). The dose-response analysis showed a steep decrease in ORs for modest intakes (<1 mg/day), which were subsequently steady for ≤3 mg/day (OR: 0.09; 95% CI: 0.02-0.41) and slowly increased for higher intakes. CONCLUSIONS: The findings of our large study suggest that copper intake might be inversely associated with GC, although their confirmation by prospective studies is required.

Determinants of early-onset colorectal cancer: a multicenter case-control study in Iran.

BACKGROUND: We aimed to study the risk factors of early-onset colorectal cancer (CRC) incidence in the Iranian population. Early onset CRC in Iran is a relevant health issue that deserves further epidemiological efforts to be defined and controlled as far as possible. Early age screening of low-tract of the intestine would be particularly useful in families of colorectal cancer patients. METHODS: We analyzed data from a multicenter hospital-based case-control study in Iran (The Iranian Study of Opium and Cancer). Sociodemographic and lifestyle information was collected using validated questionnaires. Multivariate logistic regressions estimated the odds ratios (OR) and 95% confidence intervals (CIs) for the association of early-onset CRC in individuals under the age of 50 and potential risk factors, including physical activity, socioeconomic status, body shape at age 15, dietary factors, vitamin D, cigarettes and waterpipe smoking, opium use and family history of CRC. Additionally, a subgroup analysis was conducted for individuals with a very young age of CRC onset (i.e. <35 years). RESULTS: We analyzed data of 189 developed CRC below age 50 (99 colon and 90 rectum), and 66 patients under the age 35 (13 colon and 21 rectum). Early CRC was inversely associated with vegetables (OR, 0.59; 95% CI, 0.38-0.92 for 422-576 g/day) and vitamin D (OR, 0.49; 95% CI, 0.26-0.94), and positively associated with red meat intake (OR, 1.80; 1.15-2.83 per 25.65 g/day). Vegetables (OR, 0.51; 95% CI, 0.27-0.98 for 576 g/day), red meat (OR, 2.05; 95% CI, 1.11-3.79 for 25.65 g/day), vitamin D (OR, 0.29; 95% CI, 0.10-0.86) and opium use (OR, 2.61; 95% CI, 1.01-6.74) were associated with early rectum cancer. Results were heterogeneous by cancer site for high fruit and vegetables intakes and cigarette smoking. Family history was associated with CRC (OR, 3.16; 95% CI, 1.29-10.9) and rectum cancer (OR, 3.22; 95% CI, 1.24-14.4) in subjects younger than 35, and, to a lesser extent, with CRC and rectum cancer before age 50. CONCLUSION: Early-onset CRC was related to the intake of vegetables, vitamin D and red meat in Iran. Early-onset rectum cancer was associated with regular opium use. Family history was associated with early CRC and early rectum cancer, particularly below the age of 35.

The association between dietary fiber intake and gastric cancer: a pooled analysis of 11 case-control studies.

PURPOSE: Gastric cancer (GC) is among the leading causes of cancer mortality worldwide. The objective of this study was to investigate the association between dietary fiber intake and GC. METHODS: We pooled data from 11 population or hospital-based case-control studies included in the Stomach Cancer Pooling (StoP) Project, for a total of 4865 histologically confirmed cases and 10,626 controls. Intake of dietary fibers and other dietary factors was collected using food frequency questionnaires. We calculated the odds ratios (OR) and 95% confidence intervals (CI) of the association between dietary fiber intake and GC by using a multivariable logistic regression model adjusted for study site, sex, age, caloric intake, smoking, fruit and vegetable intake, and socioeconomic status. We conducted stratified analyses by these factors, as well as GC anatomical site and histological type. RESULTS: The OR of GC for an increase of one quartile of fiber intake was 0.91 (95% CI: 0.85, 0.97), that for the highest compared to the lowest quartile of dietary fiber intake was 0.72 (95% CI: 0.59, 0.88). Results were similar irrespective of anatomical site and histological type. CONCLUSION: Our analysis supports the hypothesis that dietary fiber intake may exert a protective effect on GC.

Diabetes is associated with increased liver cancer incidence and mortality in adults: A report from Asia Cohort Consortium.

There has been growing evidence suggesting that diabetes may be associated with increased liver cancer risk. However, studies conducted in Asian countries are limited. This project considered data of 968,738 adults pooled from 20 cohort studies of Asia Cohort Consortium to examine the association between baseline diabetes and liver cancer incidence and mortality. Cox proportional hazard model and competing risk approach was used for pooled data. Two-stage meta-analysis across studies was also done. There were 839,194 subjects with valid data regarding liver cancer incidence (5654 liver cancer cases [48.29/100,000 person-years]), follow-up time and baseline diabetes (44,781 with diabetes [5.3%]). There were 747,198 subjects with valid data regarding liver cancer mortality (5020 liver cancer deaths [44.03/100,000 person-years]), follow-up time and baseline diabetes (43,243 with diabetes [5.8%]). Hazard ratio (HR) (95% confidence interval [95%CI]) of liver cancer diagnosis in those with vs. without baseline diabetes was 1.97 (1.79, 2.16) (p < .0001) after adjusting for baseline age, gender, body mass index, tobacco smoking, alcohol use, and heterogeneity across studies (n = 586,072; events = 4620). Baseline diabetes was associated with increased cumulative incidence of death due to liver cancer (adjusted HR (95%CI) = 1.97 (1.79, 2.18); p < .0001) (n = 595,193; events = 4110). A two-stage meta-analytic approach showed similar results. This paper adds important population-based evidence to current literature regarding the increased incidence and mortality of liver cancer in adults with diabetes. The analysis of data pooled from 20 studies of different Asian countries and the meta-analysis across studies with large number of subjects makes the results robust.

Risk of Skin Cancer in Workers Exposed to Diesel Exhaust: A Systematic Review and Meta-Analysis of Cohort Studies.

BACKGROUND: Our objective was to study the association between occupational exposure to diesel exhaust (DE) and skin cancer. METHODS: A systematic review following STROBE guidelines and PECOS criteria was conducted to identify cohort studies describing the association between occupational DE exposure and the risk of skin cancer. We extracted 12 independent risk estimates for melanoma skin cancer (MSC), 8 for non-melanoma skin cancer (NMSC), and 3 for skin cancer not otherwise specified (SC-NOS). Random effects meta-analyses were performed, site-specific and stratified by geographic region and quality score. 95% confidence intervals (CI) were reported. Between-study heterogeneity and potential publication bias were investigated. RESULTS: There was no overall evidence of an increased risk of MSC [RR=0.90, 95% CI: 0.73-1.11; I2=92.86%, 95% CI: 82.83-97.03%], NMSC [RR=1.04, 95% CI: 0.88-1.23; I2=60.79%, 95% CI: 0-87.34%] or SC-NOS [RR=0.72, 95% CI: 0.54-0.97; I2=26.60%, 95% CI: 0-94.87%] in workers exposed to DE. No difference between low-quality and high-quality studies was found. A stratified analysis by geographical region did not reveal any significant differences. There was no evidence of publication bias. CONCLUSIONS: No evidence of an association between skin cancer and occupational DE exposure was found. Residual confounding and other sources of bias cannot be ruled out.

Occupational exposure to diesel exhaust and head and neck cancer: a systematic review and meta-analysis of cohort studies.

Exposure to diesel exhaust (DE) and other fossil fuels in the workplace can cause several health effects including cancer. We conducted a systematic review and meta-analysis of cohort studies examining the association between occupational DE exposure and the risk of head and neck cancer (HNC), including cancer of the oral cavity, pharynx and larynx. We included cohort studies mentioned in the Monograph of the International Agency for Research on Cancer, 2014, on DE. Forest plots of relative risk (RR) were constructed for HNC overall and its anatomical subtypes. A random-effects model was used to address heterogeneity between studies. Fifteen articles were included after removing duplicates and irrelevant reports. The summary RR for DE exposure was 1.08 [95% confidence interval (CI) = 1.01-1.17, P heterogeneity = <0.001] for HNC overall, 0.98 (95% CI = 0.87-1.11) for oral cavity, 1.05 (95% CI = 0.77-1.43) for pharyngeal, 1.15 (95% CI = 0.96-1.38) for oral cavity and pharyngeal combined, and 1.13 (95% CI = 1.03-1.24) for laryngeal cancer. There were elevated RRs for incidence studies of HNC (RR = 1.13; 95% CI = 1.05-1.22, P = 0.001), European studies (RR = 1.13; 95% CI = 1.05-1.23, P = 0.001), and female studies (RR = 1.77; 95% CI = 1.31-2.39, P = 0.003). Our study suggested an association between occupational DE exposure and the risk of HNC, particularly laryngeal cancer. Although residual confounding cannot be ruled out, our results support the importance of controlling occupational DE exposure.

Dietary intake of vitamin C and gastric cancer: a pooled analysis within the Stomach cancer Pooling (StoP) Project.

BACKGROUND: Previous studies suggest that dietary vitamin C is inversely associated with gastric cancer (GC), but most of them did not consider intake of fruit and vegetables. Thus, we aimed to evaluate this association within the Stomach cancer Pooling (StoP) Project, a consortium of epidemiological studies on GC. METHODS: Fourteen case-control studies were included in the analysis (5362 cases, 11,497 controls). We estimated odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the association between dietary intake of vitamin C and GC, adjusted for relevant confounders and for intake of fruit and vegetables. The dose-response relationship was evaluated using mixed-effects logistic models with second-order fractional polynomials. RESULTS: Individuals in the highest quartile of dietary vitamin C intake had reduced odds of GC compared with those in the lowest quartile (OR: 0.64; 95% CI: 0.58, 0.72). Additional adjustment for fruit and vegetables intake led to an OR of 0.85 (95% CI: 0.73, 0.98). A significant inverse association was observed for noncardia GC, as well as for both intestinal and diffuse types of the disease. The results of the dose-response analysis showed decreasing ORs of GC up to 150-200 mg/day of vitamin C (OR: 0.54; 95% CI: 0.41, 0.71), whereas ORs for higher intakes were close to 1.0. CONCLUSIONS: The findings of our pooled study suggest that vitamin C is inversely associated with GC, with a potentially beneficial effect also for intakes above the currently recommended daily intake (90 mg for men and 75 mg for women).

Systematic review of studies on exposure to arsenic in drinking water and cognitive and neurobehavioral effects.

An association between exposure to arsenic (As) and neurologic and behavioral effects has been reported in some studies, but no systematic review is available of the evidence linking As in drinking water and neurobehavioral effects after consideration of study quality and potential confounding, with focus on low-level circumstances of exposure. We conducted a systematic review and reported it in compliance with the Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines, through a search of the databases PubMed, Web of Science, Scopus, and Embase. We included in the review the studies reporting results based on exposure from drinking water in humans. Endpoints were heterogeneous across studies, so we classified them into eight broad domains and developed an ad-hoc system to evaluate their methodological quality, based on three tiers. It was not possible to conduct meta-analysis because of the heterogeneity in exposure assessment and in the definition and assessment of outcomes. The search identified 18,518 articles. After elimination of duplicates and irrelevant articles, we retained 106 articles which reported results on As exposure and neurobehavioral effects, of which 22 reported risk estimates from exposure in drinking water (six among adults and 16 among children). None of the studies was conducted blindly. Among the studies in adults, two, which were conducted in highly exposed populations, were classified as high quality. These two studies were broadly consistent in reporting an association between exposure to As and decline in cognitive function; however, they provide no evidence of an association for exposure below 75 µg/L. The four lower-quality studies were based on populations with low exposure; these studies reported associations with inconsistent outcomes, few of which remained statistically significant after adjustment for multiple comparisons. Among the five high-quality studies of children, one reported an association between As in drinking water and intellectual function, whereas none of the other studies reported an association with different neurobehavioral indicators, after adjusting for potential confounders and multiple comparisons. Out of seven intermediate-quality studies, three reported an association with cognitive function or other outcomes; but sources of bias were not adequately controlled. The remaining studies were negative. The four low-quality studies did not contribute to the overall evidence because of methodological limitations. Our assessment of the available literature showed a lack of evidence for a causal association between exposure to As in drinking water and neurobehavioral effects. To clarify whether such an association exists, further studies prospectively evaluating changes in both the concentration of As in drinking water during the life course, and neurobehavioral outcomes, as well as appropriately controlling for potential confounders, are needed.

Association of female reproductive and hormonal factors with gallbladder cancer risk in Asia: A pooled analysis of the Asia Cohort Consortium.

The female predominance of gallbladder cancer (GBC) has led to a hypothesis regarding the hormone-related aetiology of GBC. We aimed to investigate the association between female reproductive factors and GBC risk, considering birth cohorts of Asian women. We conducted a pooled analysis of 331,323 women from 12 cohorts across 4 countries (China, Japan, Korea, and Singapore) in the Asia Cohort Consortium. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) to assess the association between reproductive factors (age at menarche, parity, age at first delivery, breastfeeding, and age at menopause) and GBC risk. We observed that a later age at menarche was associated with an increased risk of GBC (HR 1.4, 95% CI 1.16-1.70 for 17 years and older vs. 13-14 years), especially among the cohort born in 1940 and later (HR 2.5, 95% CI 1.50-4.35). Among the cohort born before 1940, women with a later age at first delivery showed an increased risk of GBC (HR 1.56, 95% CI 1.08-2.24 for 31 years of age and older vs. 20 years of age and younger). Other reproductive factors did not show a clear association with GBC risk. Later ages at menarche and at first delivery were associated with a higher risk of GBC, and these associations varied by birth cohort.

Association between reproductive factors with lung cancer incidence and mortality: A pooled analysis of over 308,000 females in the Asia cohort consortium.

Previous studies have investigated the association between reproductive factors and lung cancer risk; however, findings have been inconsistent. In order to assess this association among Asian women, a total of 308,949 female participants from 11 prospective cohorts and four Asian countries (Japan, Korea, China, and Singapore) were included. Cox proportional hazards regression models were used to estimate the hazard ratios (HR) and 95% confidence intervals (CIs). A total of 3,119 primary lung cancer cases and 2247 lung cancer deaths were identified with a mean follow-up of 16.4 years. Parous women had a lower risk of lung cancer incidence and mortality as compared with nulliparous women, with HRs of 0.82 (95% CI = 0.70-0.96) and 0.78 (95% CI = 0.65-0.94). The protective association of parity and lung cancer incidence was greater among ever-smokers (HR = 0.66, 95% CI = 0.49-0.87) than in never-smokers (HR = 0.90, 95% CI = 0.74-1.09) (P-interaction = 0.029). Compared with age at first delivery ≤20 years, older age at first delivery (21-25, ≥26 years) was associated with a lower risk of lung cancer incidence and mortality. Women who ever used hormone replacements had a higher likelihood of developing non-small cell lung cancer (HR = 1.31, 95% CI = 1.02-1.68), compared to those who never used hormone replacements. Future studies are needed to assess the underlying mechanisms, the relationships within these female reproductive factors, and the potential changes in smoking habits over time.

Mineral Intake and Cardiovascular Disease, Cancer, and All-Cause Mortality: Findings from the Golestan Cohort Study.

Associations between mineral intake and mortality in non-Western countries have not been studied adequately. This study evaluated these associations in the Golestan Cohort Study, featuring a Middle Eastern population. The mineral intake was estimated from the baseline food frequency questionnaire, adjusted by using the nutrient density method, and divided into quintiles. We used Cox proportional hazards models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for the mortality. We analyzed 41,863 subjects with a mean age of 51.46 ± 8.73 years at the baseline. During 578,694 person-years of follow-up (median: 14.1 Years), 7217 deaths were recorded. Dietary calcium intake was inversely associated with the all-cause mortality (HRQ5 vs. Q1 = 0.91, 95%CI = 0.85-0.99). We observed significant associations between calcium (HRQ5 vs. Q1 = 0.82, 95% CI = 0.73-0.93), copper (HRQ5 vs. Q1 = 1.11, 95% CI = 0.99-1.26), and selenium intake (HRQ5 vs. Q1 = 1.14, 95% CI = 1.01-1.29) and CVD mortality. Dietary phosphorus (HRQ5 vs. Q1 = 0.81, 95%CI = 0.69-0.96) and copper intake (HRQ5 vs. Q1 = 0.84, 95%CI = 0.71-0.99) were inversely associated with cancer mortality. In this study within a Middle Eastern population, a higher dietary intake of calcium exhibited an inverse association with all-cause mortality. Furthermore, nuanced associations were observed in the cause-specific mortality, suggesting potential avenues for dietary interventions and emphasizing the importance of considering dietary factors in public health strategies.

Occupational asbestos exposure and risk of esophageal cancer: A systematic review and meta-analysis.

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.

The global gastric cancer consortium: an update from the Stomach cancer Pooling (StoP) project.

We updated to December 2023 the main findings of the stomach cancer pooling (StoP) project including about 13 000 cases and 31 000 controls from 29 case-control and 5 nested studies. The StoP project quantified more precisely than previously available the positive associations of tobacco smoking, high alcohol consumption, meat intake, selected occupations (e.g. agricultural and miners), gastric ulcer and family history with gastric cancer and the inverse associations with socioeconomic status and selected aspects of diet (fruits, including citrus fruits, vegetables, including allium and mushrooms, and polyphenols). No consistent associations were found with coffee, yoghurt and leisure-time physical activity, metformin or proton pump inhibitors use.

Cocaine use and head and neck cancer risk: A pooled analysis in the International Head and Neck Cancer Epidemiology Consortium.

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.

An immunogenetic basis for lung cancer risk.

Cancer risk is influenced by inherited mutations, DNA replication errors, and environmental factors. However, the influence of genetic variation in immunosurveillance on cancer risk is not well understood. Leveraging population-level data from the UK Biobank and FinnGen, we show that heterozygosity at the human leukocyte antigen (HLA)-II loci is associated with reduced lung cancer risk in smokers. Fine-mapping implicated amino acid heterozygosity in the HLA-II peptide binding groove in reduced lung cancer risk, and single-cell analyses showed that smoking drives enrichment of proinflammatory lung macrophages and HLA-II+ epithelial cells. In lung cancer, widespread loss of HLA-II heterozygosity (LOH) favored loss of alleles with larger neopeptide repertoires. Thus, our findings nominate genetic variation in immunosurveillance as a critical risk factor for lung cancer.