RESUMO
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.
Assuntos
Melanoma , Exposição Ocupacional , Ataques Terroristas de 11 de Setembro , Neoplasias Cutâneas , Estudos de Coortes , Humanos , Masculino , Exposição Ocupacional/efeitos adversos , Trabalho de ResgateRESUMO
Rationale: Benzene has been classified as carcinogenic to humans, but there is limited evidence linking benzene exposure to lung cancer. Objectives: We aimed to examine the relationship between occupational benzene exposure and lung cancer. Methods: Subjects from 14 case-control studies across Europe and Canada were pooled. We used a quantitative job-exposure matrix to estimate benzene exposure. Logistic regression models assessed lung cancer risk across different exposure indices. We adjusted for smoking and five main occupational lung carcinogens and stratified analyses by smoking status and lung cancer subtypes. Measurements and Main Results: Analyses included 28,048 subjects (12,329 cases, 15,719 control subjects). Lung cancer odds ratios ranged from 1.12 (95% confidence interval, 1.03-1.22) to 1.32 (95% confidence interval, 1.18-1.48) (Ptrend = 0.002) for groups with the lowest and highest cumulative occupational exposures, respectively, compared with unexposed subjects. We observed an increasing trend of lung cancer with longer duration of exposure (Ptrend < 0.001) and a decreasing trend with longer time since last exposure (Ptrend = 0.02). These effects were seen for all lung cancer subtypes, regardless of smoking status, and were not influenced by specific occupational groups, exposures, or studies. Conclusions: We found consistent and robust associations between different dimensions of occupational benzene exposure and lung cancer after adjusting for smoking and main occupational lung carcinogens. These associations were observed across different subgroups, including nonsmokers. Our findings support the hypothesis that occupational benzene exposure increases the risk of developing lung cancer. Consequently, there is a need to revisit published epidemiological and molecular data on the pulmonary carcinogenicity of benzene.
Assuntos
Neoplasias Pulmonares , Doenças Profissionais , Exposição Ocupacional , Humanos , Neoplasias Pulmonares/induzido quimicamente , Neoplasias Pulmonares/epidemiologia , Benzeno/toxicidade , Exposição Ocupacional/efeitos adversos , Carcinógenos , Pulmão , Estudos de Casos e Controles , Doenças Profissionais/induzido quimicamente , Doenças Profissionais/epidemiologiaRESUMO
BACKGROUND: The birth cohort effect has been suggested to influence the rate of breast cancer incidence and the trends of associated reproductive and lifestyle factors. We conducted a cohort study to determine whether a differential pattern of associations exists between certain factors and breast cancer risk based on birth cohorts. METHODS: This was a cohort study using pooled data from 12 cohort studies. We analysed associations between reproductive (menarche age, menopause age, parity and age at first delivery) and lifestyle (smoking and alcohol consumption) factors and breast cancer risk. We obtained hazard ratios (HRs) with 95% confidence intervals (CIs) using the Cox proportional hazard regression analysis on the 1920s, 1930s, 1940s and 1950s birth cohorts. RESULTS: Parity was found to lower the risk of breast cancer in the older but not in the younger birth cohort, whereas lifestyle factors showed associations with breast cancer risk only among the participants born in the 1950s. In the younger birth cohort group, the effect size was lower for parous women compared to the other cohort groups (HR [95% CI] 0.86 [0.66-1.13] compared to 0.60 [0.49-0.73], 0.46 [0.38-0.56] and 0.62 [0.51-0.77]). Meanwhile, a higher effect size was found for smoking (1.45 [1.14-1.84] compared to 1.25 [0.99-1.58], 1.06 [0.85-1.32] and 0.86 [0.69-1.08]) and alcohol consumption (1.22 [1.01-1.48] compared to 1.10 [0.90-1.33], 1.15 [0.96-1.38], and 1.07 [0.91-1.26]). CONCLUSION: We observed different associations of parity, smoking and alcohol consumption with breast cancer risk across various birth cohorts.
Assuntos
Neoplasias da Mama , Gravidez , Feminino , Humanos , Neoplasias da Mama/epidemiologia , Neoplasias da Mama/etiologia , Coorte de Nascimento , Estudos de Coortes , Japão , Fatores de Risco , Estilo de Vida , China , República da CoreiaRESUMO
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.
Assuntos
Amianto , Neoplasias Esofágicas , Exposição Ocupacional , Humanos , Exposição Ocupacional/efeitos adversos , Neoplasias Esofágicas/etiologia , Neoplasias Esofágicas/epidemiologia , Amianto/efeitos adversos , Fatores de Risco , Estudos de Casos e Controles , Masculino , Adenocarcinoma/etiologia , Adenocarcinoma/epidemiologia , FemininoRESUMO
Incidence of esophageal and gastric cancer has been linked to low B-vitamin status. We conducted matched nested case-control studies of incident esophageal squamous cell carcinoma (ESCC; 340 case-control pairs) and gastric cancer (GC; 352 case-control pairs) within the Golestan Cohort Study. The primary exposure was plasma biomarkers: riboflavin and flavin mononucleotide (FMN) (vitamin B2), pyridoxal phosphate (PLP) (B6), cobalamin (B12), para-aminobenzoylglutamate (pABG) (folate), and total homocysteine (tHcy); and indicators for deficiency: 3-hydroxykyurenine-ratio (HK-r for vitamin B6) and methylmalonic acid (MMA for B12). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression adjusting for matching factors and potential confounders. High proportions of participants had low B-vitamin and high tHcy levels. None of the measured vitamin B levels was associated with the risk of ESCC and GC, but elevated level of MMA was marginally associated with ESCC (OR = 1.42, 95% CI = 0.99-2.04) and associated with GC (OR = 1.53, 95% CI = 1.05-2.22). Risk of GC was higher for the highest versus lowest quartile of HK-r (OR = 1.95, 95%CI = 1.19-3.21) and for elevated versus non-elevated HK-r level (OR = 1.59, 95% CI = 1.13-2.25). Risk of ESCC (OR = 2.81, 95% CI = 1.54-5.13) and gastric cancer (OR = 2.09, 95%CI = 1.17-3.73) was higher for the highest versus lowest quartile of tHcy. In conclusion, insufficient vitamin B12 was associated with higher risk of ESCC and GC, and insufficient vitamin B6 status was associated with higher risk of GC in this population with prevalent low plasma B-vitamin status. Higher level of tHcy, a global indicator of OCM function, was associated with higher risk of ESCC and GC.
RESUMO
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.
Assuntos
Carcinoma Pulmonar de Células não Pequenas , Neoplasias Pulmonares , Gravidez , Feminino , Humanos , Incidência , Estudos Prospectivos , Neoplasias Pulmonares/epidemiologia , Ásia/epidemiologia , Hormônios , Fatores de Risco , Modelos de Riscos ProporcionaisRESUMO
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.
Assuntos
Neoplasias da Vesícula Biliar , Menarca , Humanos , Feminino , Neoplasias da Vesícula Biliar/epidemiologia , Neoplasias da Vesícula Biliar/etiologia , Pessoa de Meia-Idade , Fatores de Risco , Adulto , Ásia/epidemiologia , Idoso , Estudos de Coortes , História Reprodutiva , Modelos de Riscos Proporcionais , Menopausa , Fatores Etários , Adolescente , ParidadeRESUMO
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.
Assuntos
Consumo de Bebidas Alcoólicas , Ácido Fólico , Neoplasias Gástricas , Humanos , Neoplasias Gástricas/prevenção & controle , Neoplasias Gástricas/epidemiologia , Ácido Fólico/administração & dosagem , Consumo de Bebidas Alcoólicas/efeitos adversos , Feminino , Masculino , Estudos de Casos e Controles , Pessoa de Meia-Idade , Idoso , Dieta , Adulto , Fatores de Risco , Inquéritos e QuestionáriosRESUMO
Body fatness is considered a probable risk factor for biliary tract cancer (BTC), whereas cholelithiasis is an established factor. Nevertheless, although obesity is an established risk factor for cholelithiasis, previous studies of the association of body mass index (BMI) and BTC did not take the effect of cholelithiasis fully into account. To better understand the effect of BMI on BTC, we conducted a pooled analysis using population-based cohort studies in Asians. In total, 905 530 subjects from 21 cohort studies participating in the Asia Cohort Consortium were included. BMI was categorized into four groups: underweight (<18.5 kg/m2 ); normal (18.5-22.9 kg/m2 ); overweight (23-24.9 kg/m2 ); and obese (25+ kg/m2 ). The association between BMI and BTC incidence and mortality was assessed using hazard ratios (HR) and 95% confidence intervals (CIs) by Cox regression models with shared frailty. Mediation analysis was used to decompose the association into a direct and an indirect (mediated) effect. Compared to normal BMI, high BMI was associated with BTC mortality (HR 1.19 [CI 1.02-1.38] for males, HR 1.30 [1.14-1.49] for females). Cholelithiasis had significant interaction with BMI on BTC risk. BMI was associated with BTC risk directly and through cholelithiasis in females, whereas the association was unclear in males. When cholelithiasis was present, BMI was not associated with BTC death in either males or females. BMI was associated with BTC death among females without cholelithiasis. This study suggests BMI is associated with BTC mortality in Asians. Cholelithiasis appears to contribute to the association; and moreover, obesity appears to increase BTC risk without cholelithiasis.
Assuntos
Neoplasias do Sistema Biliar , Colelitíase , Masculino , Feminino , Humanos , Obesidade/complicações , Obesidade/epidemiologia , Sobrepeso/epidemiologia , Fatores de Risco , Estudos de Coortes , Ásia/epidemiologia , Neoplasias do Sistema Biliar/epidemiologia , Colelitíase/complicações , Colelitíase/epidemiologia , Índice de Massa CorporalRESUMO
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.
Assuntos
Neoplasias Hepáticas , Humanos , Neoplasias Hepáticas/epidemiologia , Neoplasias Hepáticas/mortalidade , Incidência , Ásia/epidemiologia , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Estudos de Coortes , Diabetes Mellitus/epidemiologia , Diabetes Mellitus/mortalidade , Fatores de Risco , Modelos de Riscos Proporcionais , IdosoRESUMO
BACKGROUND: Gastric cancer incidence is higher in men, and a protective hormone-related effect in women is postulated. We aimed to investigate and quantify the relationship in the Stomach cancer Pooling (StoP) Project consortium. METHODS: A total of 2,084 cases and 7,102 controls from 11 studies in seven countries were included. Summary odds ratios (ORs) and 95% confidence intervals (CIs) assessing associations of key reproductive factors and menopausal hormone therapy (MHT) with gastric cancer were estimated by pooling study-specific ORs using random-effects meta-analysis. RESULTS: A duration of fertility of ≥ 40 years (vs. < 20), was associated with a 25% lower risk of gastric cancer (OR = 0.75; 95% CI: 0.58-0.96). Compared with never use, ever, 5-9 years and ≥ 10 years use of MHT in postmenopausal women, showed ORs of 0.73 (95% CI: 0.58-0.92), 0.53 (95% CI: 0.34-0.84) and 0.71 (95% CI: 0.50-1.00), respectively. The associations were generally similar for anatomical and histologic subtypes. CONCLUSION: Our results support the hypothesis that reproductive factors and MHT use may lower the risk of gastric cancer in women, regardless of anatomical or histologic subtypes. Given the variation in hormones over the lifespan, studies should address their effects in premenopausal and postmenopausal women. Furthermore, mechanistic studies may inform potential biological processes.
Assuntos
Neoplasias Gástricas , Masculino , Humanos , Feminino , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Fatores de Risco , Pré-Menopausa , IncidênciaRESUMO
BACKGROUND: Poor oral health has been linked to various systemic diseases, including multiple cancer types, but studies of its association with lung cancer have been inconclusive. METHODS: We examined the relationship between dental status and lung cancer incidence and mortality in the Golestan Cohort Study, a large, prospective cohort of 50,045 adults in northeastern Iran. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between three dental health measures (i.e., number of missing teeth; the sum of decayed, missing, or filled teeth (DMFT); and toothbrushing frequency) and lung cancer incidence or mortality with adjustment for multiple potential confounders, including cigarette smoking and opium use. We created tertiles of the number of lost teeth/DMFT score in excess of the loess adjusted, age- and sex-specific predicted numbers, with subjects with the expected number of lost teeth/DMFT or fewer as the reference group. RESULTS: During a median follow-up of 14 years, there were 119 incident lung cancer cases and 98 lung cancer deaths. Higher DMFT scores were associated with a progressively increased risk of lung cancer (linear trend, p = 0.011). Compared with individuals with the expected DMFT score or less, the HRs were 1.27 (95% CI: 0.73, 2.22), 2.15 (95% CI: 1.34, 3.43), and 1.52 (95% CI: 0.81, 2.84) for the first to the third tertiles of DMFT, respectively. The highest tertile of tooth loss also had an increased risk of lung cancer, with a HR of 1.68 (95% CI: 1.04, 2.70) compared with subjects with the expected number of lost teeth or fewer (linear trend, p = 0.043). The results were similar for lung cancer mortality and did not change substantially when the analysis was restricted to never users of cigarettes or opium. We found no associations between toothbrushing frequency and lung cancer incidence or mortality. CONCLUSION: Poor dental health indicated by tooth loss or DMFT, but not lack of toothbrushing, was associated with increased lung cancer incidence and mortality in this rural Middle Eastern population.
Assuntos
Neoplasias Pulmonares , Perda de Dente , Masculino , Adulto , Feminino , Humanos , Estudos de Coortes , Perda de Dente/epidemiologia , Neoplasias Pulmonares/epidemiologia , Neoplasias Pulmonares/etiologia , Estudos Prospectivos , Escovação DentáriaRESUMO
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.
Assuntos
Arsênio , Cognição , Água Potável , Exposição Ambiental , Poluentes Químicos da Água , Humanos , Água Potável/química , Arsênio/toxicidade , Poluentes Químicos da Água/toxicidade , Cognição/efeitos dos fármacosRESUMO
PURPOSE: Anti SARS-CoV-2 vaccination initially showed high effectiveness in preventing COVID-19. However, after the surge of variants of concern, the effectiveness dropped. Several studies investigated if this was related to the decrease of the humoral response over time; however, this issue is still unclear. The aim of this study was to understand whether SARS-CoV-2 anti-S IgG levels can be used to predict breakthrough infection risk and define the timing for further booster doses administration. METHOD: Within the framework of the ORCHESTRA Project, over 20,000 health workers from 11 European centers were enrolled since December 2020. We performed two Cox proportional hazards survival analyses regarding pre-Omicron (from January to July 2021) and Omicron (December 2021-May 2022) periods. The serological response was classified as high (above the 75th percentile), medium (25th-75th), or low (< 25th). RESULTS: Seventy-four (0.33%) and 2122 (20%) health workers were infected during the first and second periods, respectively. Both Cox analyses showed that having high anti-S titer was linked to a significantly lower risk of infection as compared to having medium serological response [HR of high vs medium anti-S titer = 0.27 (95% CI 0.11-0.66) during the first phase, HR = 0.76 (95% CI 0.62-0.93) during the second phase]. CONCLUSION: Vaccine effectiveness wanes significantly after new variants surge, making anti-S titer unsuitable to predict optimal timing for further booster dose administration. Studies on other immunological indicators, such as cellular immunity, are therefore needed to better understand the mechanisms and duration of protection against breakthrough infection risk.
Assuntos
Anticorpos Antivirais , Vacinas contra COVID-19 , COVID-19 , Pessoal de Saúde , Imunoglobulina G , SARS-CoV-2 , Humanos , COVID-19/prevenção & controle , COVID-19/imunologia , Pessoal de Saúde/estatística & dados numéricos , SARS-CoV-2/imunologia , Europa (Continente)/epidemiologia , Imunoglobulina G/sangue , Anticorpos Antivirais/sangue , Feminino , Adulto , Masculino , Vacinas contra COVID-19/imunologia , Vacinas contra COVID-19/administração & dosagem , Pessoa de Meia-Idade , Imunização Secundária , Glicoproteína da Espícula de Coronavírus/imunologia , Infecções IrruptivasRESUMO
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).
Assuntos
Ácido Ascórbico , Neoplasias Gástricas , Masculino , Humanos , Feminino , Neoplasias Gástricas/prevenção & controle , Dieta , Frutas , Verduras , Estudos de Casos e Controles , Ingestão de Alimentos , Fatores de RiscoRESUMO
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.
Assuntos
Neoplasias Gástricas , Humanos , Neoplasias Gástricas/mortalidade , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/genética , Masculino , Feminino , Incidência , Ásia/epidemiologia , Estudos Prospectivos , Pessoa de Meia-Idade , Fatores de Risco , Idoso , Adulto , Seguimentos , Predisposição Genética para DoençaRESUMO
BACKGROUND: Diesel exhaust (DE) is human carcinogen with sufficient evidence only for lung cancer. Systematic evidence on other cancer types is scarce, thus we aimed to systematically review current literature on the association between occupational DE exposure and risk of liver and pancreatic cancers. METHODS: We performed a systematic literature review to identify cohort studies on occupational DE exposure and risk of cancers other than lung. We computed pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) for liver and pancreatic cancers using DerSimonian and Laird random-effects model. RESULTS: Fifteen studies reporting results on pancreatic cancer and fourteen on liver cancer were included. We found a weakly increased risk of pancreatic cancer in workers exposed to DE (RR: 1.07, 95% CI: 1.00, 1.14), mainly driven by results on incidence (RR: 1.11, 95% CI: 1.02, 1.22). As for liver cancer, results were suggestive of a positive association (RR: 1.09; 95% CI: 0.99, 1.19), although a significant estimate was present in studies published before 2000 (RR: 1.41; 95% CI: 1.09, 1.82). We found no compelling evidence of publication bias. CONCLUSIONS: Our findings suggest an association between occupational DE exposure and liver and pancreatic cancer. Further studies with detailed exposure assessment, environmental monitoring data, and appropriate control for confounders are warranted.
Assuntos
Neoplasias Hepáticas , Exposição Ocupacional , Neoplasias Pancreáticas , Emissões de Veículos , Humanos , Neoplasias Pancreáticas/epidemiologia , Neoplasias Pancreáticas/etiologia , Exposição Ocupacional/efeitos adversos , Exposição Ocupacional/estatística & dados numéricos , Neoplasias Hepáticas/epidemiologia , Doenças Profissionais/epidemiologia , Doenças Profissionais/etiologiaRESUMO
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.
RESUMO
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.
Assuntos
Benzeno , Neoplasias Colorretais , Exposição Ocupacional , Exposição Ocupacional/efeitos adversos , Benzeno/toxicidade , Neoplasias Colorretais/epidemiologia , Neoplasias Colorretais/induzido quimicamente , Humanos , Doenças Profissionais/induzido quimicamente , Doenças Profissionais/epidemiologiaRESUMO
Arsenic is a known carcinogen for the lungs, the bladder, and the skin, while systematic evidence on other cancer types is lacking, especially for occupational exposure. Thus, we aimed to systematically summarize current evidence on the association between occupational arsenic exposure and digestive cancers, including head and neck cancer (HNC). We conducted a systematic review on Pubmed, Web of Science, and Embase search engines. We computed pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) using DerSimonian and Laird random-effects model. Occurrence of publication bias was assessed using contour-enhanced funnel plots and Egger's test. Twenty-two studies on digestive cancers and 11 on HNC were included in the meta-analysis. RRs for the association with occupational exposure to arsenic of 1.23 (95% CI: 1.07-1.40; I2=72.3%, p<0.001) and 1.08 (95% CI: 0.76-1.53; I2=76.6%, p<0.001) for digestive cancer and HNC, respectively, were observed. As for specific cancer types, arsenic was associated with rectal cancer (RR: 1.51; 95% CI: 1.003-2.28; I2=37.0%, p=0.174), but not with other investigated cancer types. No clear evidence of publication bias was found. The results of our study suggest that the observed association between occupational arsenic exposure and digestive cancer might be mainly driven by a positive association for rectal cancer, while arsenic exposure did not appear to be associated with HNC. However, further high-quality studies with detailed assessment of arsenic exposure are warranted to clarify the potential association of arsenic with digestive cancers and HNC.