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BMC Cancer Nov 2023RAS mutations affect prognosis in patients with metastatic colorectal cancer (mCRC) and have been identified as strong negative predictive markers for anti-epidermal... (Meta-Analysis)
Meta-Analysis
BACKGROUND
RAS mutations affect prognosis in patients with metastatic colorectal cancer (mCRC) and have been identified as strong negative predictive markers for anti-epidermal growth factor receptor monoclonal antibody (anti-EGFR mAb) therapy, but many tumors containing wild-type RAS genes still do not respond to these therapies. Some additional biomarkers may have prognostic or predictive roles, but conclusions remain controversial.
METHODS
We performed a meta-analysis and systematic review of randomized controlled trials comparing anti-EGFR mAb therapy with alternative therapy that investigated the prognostic and predictive impact of additional biomarkers in RAS wild-type (wt) mCRC patients. Hazard ratios (HRs) and 95% confidence intervals (CIs) for progression-free survival (PFS) and overall survival (OS) and odds ratios (ORs) for objective response rate (ORR) were calculated. The prognostic value of biomarkers was investigated by separately pooling HR and OR for different treatment groups in an individual study. The predictive value was assessed by pooling study interactions between treatment effects and biomarker subgroups.
RESULTS
Thirty publications reporting on eighteen trials were selected, including a total of 13,507 patients. In prognostic analysis, BRAF mutations were associated with poorer PFS [HRs = 3.76 (2.47-5.73) and 2.69 (1.82-3.98)] and OS [HRs = 2.66 (1.95-3.65) and 2.45 (1.55-3.88)] in both the experimental and control arms; low miR-31-3p expression appeared to have longer PFS and OS. In terms of predictive effect, a lack of response to anti-EGFR therapy was observed in patients with BRAF mutant tumors (P < 0.01 for PFS). Patients with tumors with any mutation in the KRAS/NRAS/BRAF/PIK3CA gene also showed similar results compared with all wild-type tumors (P for PFS, OS, and ORR were < 0.01, < 0.01 and 0.01, respectively). While low miR-31-3p expression could predict PFS (P = 0.01) and OS (P = 0.04) benefit. The prognostic and predictive value regarding PIK3CA mutations, PTEN mutations or deletions, EGFR, EREG/AREG, HER2, HER3, and HER4 expression remains uncertain.
CONCLUSIONS
In RAS wt mCRC patients receiving EGFR-targeted therapy, BRAF mutation is a powerful prognostic and therapy-predictive biomarker, with no effect found for PIK3CA mutation, PTEN mutation or deletion, but the combined biomarker KRAS/NRAS/BRAF/PIK3CA mutations predict resistance to anti-EGFR therapy. Low miR-31-3p expression may have positive prognostic and therapy predictive effects. Evidence on the prognostic and predictive roles of EGFR and its ligands, and HER2/3/4 is insufficient.
Topics: Humans; Prognosis; Proto-Oncogene Proteins B-raf; Colorectal Neoplasms; Proto-Oncogene Proteins p21(ras); ErbB Receptors; Antibodies, Monoclonal; Colonic Neoplasms; Rectal Neoplasms; Biomarkers; Class I Phosphatidylinositol 3-Kinases; Mutation; MicroRNAs; Biomarkers, Tumor
PubMed: 37974093
DOI: 10.1186/s12885-023-11600-z -
Environment International Aug 2023The World Health Organization (WHO) and the International Labour Organization (ILO) are developing joint estimates of the work-related burden of disease and injury... (Meta-Analysis)
Meta-Analysis
The prevalences and levels of occupational exposure to dusts and/or fibres (silica, asbestos and coal): A systematic review and meta-analysis from the WHO/ILO Joint Estimates of the Work-related Burden of Disease and Injury.
BACKGROUND
The World Health Organization (WHO) and the International Labour Organization (ILO) are developing joint estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large number of individual experts. Evidence from human, animal and mechanistic data suggests that occupational exposure to dusts and/or fibres (silica, asbestos and coal dust) causes pneumoconiosis. In this paper, we present a systematic review and meta-analysis of the prevalences and levels of occupational exposure to silica, asbestos and coal dust. These estimates of prevalences and levels will serve as input data for estimating (if feasible) the number of deaths and disability-adjusted life years that are attributable to occupational exposure to silica, asbestos and coal dust, for the development of the WHO/ILO Joint Estimates.
OBJECTIVES
We aimed to systematically review and meta-analyse estimates of the prevalences and levels of occupational exposure to silica, asbestos and coal dust among working-age (≥ 15 years) workers.
DATA SOURCES
We searched electronic academic databases for potentially relevant records from published and unpublished studies, including Ovid Medline, PubMed, EMBASE, and CISDOC. We also searched electronic grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews and included study records; and consulted additional experts.
STUDY ELIGIBILITY AND CRITERIA
We included working-age (≥ 15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (< 15 years) and unpaid domestic workers. We included all study types with objective dust or fibre measurements, published between 1960 and 2018, that directly or indirectly reported an estimate of the prevalence and/or level of occupational exposure to silica, asbestos and/or coal dust.
STUDY APPRAISAL AND SYNTHESIS METHODS
At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, then data were extracted from qualifying studies. We combined prevalence estimates by industrial sector (ISIC-4 2-digit level with additional merging within Mining, Manufacturing and Construction) using random-effects meta-analysis. Two or more review authors assessed the risk of bias and all available authors assessed the quality of evidence, using the ROB-SPEO tool and QoE-SPEO approach developed specifically for the WHO/ILO Joint Estimates.
RESULTS
Eighty-eight studies (82 cross-sectional studies and 6 longitudinal studies) met the inclusion criteria, comprising > 2.4 million measurements covering 23 countries from all WHO regions (Africa, Americas, Eastern Mediterranean, South-East Asia, Europe, and Western Pacific). The target population in all 88 included studies was from major ISCO groups 3 (Technicians and Associate Professionals), 6 (Skilled Agricultural, Forestry and Fishery Workers), 7 (Craft and Related Trades Workers), 8 (Plant and Machine Operators and Assemblers), and 9 (Elementary Occupations), hereafter called manual workers. Most studies were performed in Construction, Manufacturing and Mining. For occupational exposure to silica, 65 studies (61 cross-sectional studies and 4 longitudinal studies) were included with > 2.3 million measurements collected in 22 countries in all six WHO regions. For occupational exposure to asbestos, 18 studies (17 cross-sectional studies and 1 longitudinal) were included with > 20,000 measurements collected in eight countries in five WHO regions (no data for Africa). For occupational exposure to coal dust, eight studies (all cross-sectional) were included comprising > 100,000 samples in six countries in five WHO regions (no data for Eastern Mediterranean). Occupational exposure to silica, asbestos and coal dust was assessed with personal or stationary active filter sampling; for silica and asbestos, gravimetric assessment was followed by technical analysis. Risk of bias profiles varied between the bodies of evidence looking at asbestos, silica and coal dust, as well as between industrial sectors. However, risk of bias was generally highest for the domain of selection of participants into the studies. The largest bodies of evidence for silica related to the industrial sectors of Construction (ISIC 41-43), Manufacturing (ISIC 20, 23-25, 27, 31-32) and Mining (ISIC 05, 07, 08). For Construction, the pooled prevalence estimate was 0.89 (95% CI 0.84 to 0.93, 17 studies, I 91%, moderate quality of evidence) and the level estimate was rated as of very low quality of evidence. For Manufacturing, the pooled prevalence estimate was 0.85 (95% CI 0.78 to 0.91, 24 studies, I 100%, moderate quality of evidence) and the pooled level estimate was rated as of very low quality of evidence. The pooled prevalence estimate for Mining was 0.75 (95% CI 0.68 to 0.82, 20 studies, I 100%, moderate quality of evidence) and the pooled level estimate was 0.04 mg/m (95% CI 0.03 to 0.05, 17 studies, I 100%, low quality of evidence). Smaller bodies of evidence were identified for Crop and animal production (ISIC 01; very low quality of evidence for both prevalence and level); Professional, scientific and technical activities (ISIC 71, 74; very low quality of evidence for both prevalence and level); and Electricity, gas, steam and air conditioning supply (ISIC 35; very low quality of evidence for both prevalence and level). For asbestos, the pooled prevalence estimate for Construction (ISIC 41, 43, 45,) was 0.77 (95% CI 0.65 to 0.87, six studies, I 99%, low quality of evidence) and the level estimate was rated as of very low quality of evidence. For Manufacturing (ISIC 13, 23-24, 29-30), the pooled prevalence and level estimates were rated as being of very low quality of evidence. Smaller bodies of evidence were identified for Other mining and quarrying (ISIC 08; very low quality of evidence for both prevalence and level); Electricity, gas, steam and air conditioning supply (ISIC 35; very low quality of evidence for both prevalence and level); and Water supply, sewerage, waste management and remediation (ISIC 37; very low quality of evidence for levels). For coal dust, the pooled prevalence estimate for Mining of coal and lignite (ISIC 05), was 1.00 (95% CI 1.00 to 1.00, six studies, I 16%, moderate quality of evidence) and the pooled level estimate was 0.77 mg/m (95% CI 0.68 to 0.86, three studies, I 100%, low quality of evidence). A small body of evidence was identified for Electricity, gas, steam and air conditioning supply (ISIC 35); with very low quality of evidence for prevalence, and the pooled level estimate being 0.60 mg/m (95% CI -6.95 to 8.14, one study, low quality of evidence).
CONCLUSIONS
Overall, we judged the bodies of evidence for occupational exposure to silica to vary by industrial sector between very low and moderate quality of evidence for prevalence, and very low and low for level. For occupational exposure to asbestos, the bodies of evidence varied by industrial sector between very low and low quality of evidence for prevalence and were of very low quality of evidence for level. For occupational exposure to coal dust, the bodies of evidence were of very low or moderate quality of evidence for prevalence, and low for level. None of the included studies were population-based studies (i.e., covered the entire workers' population in the industrial sector), which we judged to present serious concern for indirectness, except for occupational exposure to coal dust within the industrial sector of mining of coal and lignite. Selected estimates of the prevalences and levels of occupational exposure to silica by industrial sector are considered suitable as input data for the WHO/ILO Joint Estimates, and selected estimates of the prevalences and levels of occupational exposure to asbestos and coal dust may perhaps also be suitable for estimation purposes. Protocol identifier: https://doi.org/10.1016/j.envint.2018.06.005. PROSPERO registration number: CRD42018084131.
Topics: Humans; Adolescent; Occupational Diseases; Dust; Prevalence; Silicon Dioxide; Cross-Sectional Studies; Coal; Steam; Asbestos; Occupational Exposure; World Health Organization; Cost of Illness
PubMed: 37487377
DOI: 10.1016/j.envint.2023.107980 -
Cancers Nov 2022The discovery that ameloblastoma has a high mutation incidence of V600E may enable a better investigation of pathophysiology. However, there is inconsistent evidence... (Review)
Review
The discovery that ameloblastoma has a high mutation incidence of V600E may enable a better investigation of pathophysiology. However, there is inconsistent evidence regarding this mutation occurrence and its association with clinical information. This systematic review and meta-analysis aim to pool the overall mutation prevalence of V600E in reported ameloblastoma cases and to determine its association with patient demographic and clinicopathological features. Following the PRISMA guidelines, a comprehensive article search was conducted through four databases (Scopus, Google Scholar, PubMed, and Web of Science). Seventeen articles between 2014 and 2022 met the inclusion criteria with 833 ameloblastoma cases. For each included study, the significance of V600E on the outcome parameters was determined using odd ratios and 95% confidence intervals. Meta-analysis prevalence of V600E in ameloblastoma was 70.49%, and a significant meta-analysis association was reported for those younger than 54 years old and in the mandible. On the contrary, other factors, such as sex, histological variants, and recurrence, were insignificant. As a result of the significant outcome of V600E mutation in ameloblastoma pathogenesis, targeted therapy formulation can be developed with this handful of evidence.
PubMed: 36428683
DOI: 10.3390/cancers14225593 -
European Respiratory Review : An... Jan 2024Molecular pathways found to be important in pulmonary fibrosis are also involved in cancer pathogenesis, suggesting common pathways in the development of pulmonary... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Molecular pathways found to be important in pulmonary fibrosis are also involved in cancer pathogenesis, suggesting common pathways in the development of pulmonary fibrosis and lung cancer.
RESEARCH QUESTION
Is pulmonary fibrosis from exposure to occupational carcinogens an independent risk factor for lung cancer?
STUDY DESIGN AND METHODS
A comprehensive search of PubMed, Embase, Web of Science and Cochrane databases with over 100 search terms regarding occupational hazards causing pulmonary fibrosis was conducted. After screening and extraction, quality of evidence and eligibility criteria for meta-analysis were assessed. Meta-analysis was performed using a random-effects model.
RESULTS
52 studies were identified for systematic review. Meta-analysis of subgroups identified silicosis as a risk factor for lung cancer when investigating odds ratios for silicosis in autopsy studies (OR 1.47, 95% CI 1.13-1.90) and for lung cancer mortality in patients with silicosis (OR 3.21, 95% CI 2.67-3.87). Only considering studies with an adjustment for smoking as a confounder identified a significant increase in lung cancer risk (OR 1.58, 95% CI 1.34-1.87). However, due to a lack of studies including cumulative exposure, no adjustments could be included. In a qualitative review, no definitive conclusion could be reached for asbestosis and silicosis as independent risk factors for lung cancer, partly because the studies did not take cumulative exposure into account.
INTERPRETATION
This systematic review confirms the current knowledge regarding asbestosis and silicosis, indicating a higher risk of lung cancer in exposed individuals compared to exposed workers without fibrosis. These individuals should be monitored for lung cancer, especially when asbestosis or silicosis is present.
Topics: Humans; Silicon Dioxide; Lung Neoplasms; Pulmonary Fibrosis; Asbestosis; Silicosis; Occupational Exposure
PubMed: 38355151
DOI: 10.1183/16000617.0224-2023 -
Biomedical and Environmental Sciences :... Nov 2018To evaluate the possible association between radon exposure and kidney cancer. (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
To evaluate the possible association between radon exposure and kidney cancer.
METHODS
We performed a systematic review and a meta-analysis based on random effect models to provide a pooled association measure.
RESULTS
We subjected 8 studies (overall relative risks and 95% confidence intervals: 1.01, 0.72 to 1.43, I2 = 64.4%) to meta-analysis. Subgroup analysis revealed a marginally significant association between radon exposure and kidney cancer in studies conducted in Europe. Two population-based studies provided no evidence for the increased risk of kidney cancer in the general population.
CONCLUSION
The association between radon and kidney cancer remains unclear but cannot be excluded because of its biological plausibility and the limited number and quality of existing studies. Additional data from the general population and well-designed miner cohort studies are needed to reveal the real relationship between radon exposure and kidney cancer.
Topics: Cohort Studies; Environmental Exposure; Humans; Kidney Neoplasms; Radon
PubMed: 30558701
DOI: 10.3967/bes2018.108 -
Cells Apr 2023Betel quid and areca nut are complex mixture carcinogens, but little is known about whether their derived single-agent arecoline or arecoline -oxide (ANO) is...
Betel quid and areca nut are complex mixture carcinogens, but little is known about whether their derived single-agent arecoline or arecoline -oxide (ANO) is carcinogenic, and the underlying mechanisms remain unclear. In this systematic review, we analyzed recent studies on the roles of arecoline and ANO in cancer and strategies to block carcinogenesis. In the oral cavity, flavin-containing monooxygenase 3 oxidizes arecoline to ANO, and both alkaloids conjugate with -acetylcysteine to form mercapturic acid compounds, which are excreted in urine, reducing arecoline and ANO toxicity. However, detoxification may not be complete. Arecoline and ANO upregulated protein expression in oral cancer tissue from areca nut users compared to expression levels in adjacent normal tissue, suggesting a causal relationship between these compounds and oral cancer. Sublingual fibrosis, hyperplasia, and oral leukoplakia were diagnosed in mice subjected to oral mucosal smearing of ANO. ANO is more cytotoxic and genotoxic than arecoline. During carcinogenesis and metastasis, these compounds increase the expression of epithelial-mesenchymal transition (EMT) inducers such as reactive oxygen species, transforming growth factor-β1, Notch receptor-1, and inflammatory cytokines, and they activate EMT-related proteins. Arecoline-induced epigenetic markers such as sirtuin-1 hypermethylation, low protein expression of miR-22, and miR-886-3-p accelerate oral cancer progression. Antioxidants and targeted inhibitors of the EMT inducers used reduce the risk of oral cancer development and progression. Our review findings substantiate the association of arecoline and ANO with oral cancer. Both of these single compounds are likely carcinogenic to humans, and their mechanisms and pathways of carcinogenesis are useful indicators for cancer therapy and prognosis.
Topics: Arecoline; Cyclic N-Oxides; Mouth Neoplasms; Carcinogenesis; Humans; Animals; Mice; Areca; Oxygenases; Oxidation-Reduction; Acetylcysteine; Epigenesis, Genetic; Carcinogens
PubMed: 37190117
DOI: 10.3390/cells12081208 -
BMC Cancer Feb 2015Sinonasal cancer (SNC) has been related to occupational exposures, but the relative risk associated to specific jobs and/or carcinogen exposures other than wood and... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Sinonasal cancer (SNC) has been related to occupational exposures, but the relative risk associated to specific jobs and/or carcinogen exposures other than wood and leather dust is generally based on small or inadequate sample sizes and the range of observed estimates is large. This paper is aimed at investigating such relationship through a systematic review of the literature followed by a meta-analysis of studies meeting specific inclusion criteria.
METHODS
Systematic search was made with PubMed, Google Scholar and Scopus engines using related keywords. Occupational exposures include wood and leather dust, formaldehyde, nickel and chromium compounds, textile industry, farming and construction. Meta-analysis of published studies after 1985 with a case-control or cohort design was performed, firstly using the fixed-effect model. Heterogeneity was assessed with the Q statistical test and quantified by the I(2) index. When the heterogeneity hypothesis appeared relevant, the random-effect model was chosen. Sources of heterogeneity were explored using subgroup analyses.
RESULTS
Out of 63 reviewed articles, 28 (11 cohort, 17 case-control) were used in the meta-analysis. Heterogeneity among studies was observed and random-effects models were used. Exposure to wood dust results associated with SNC (RRpooled = 5.91, 95% CI: 4.31-8.11 for the case-control studies and 1.61, 95% CI: 1.10-2.37 for the cohort studies), as well as to leather dust (11.89, 95% CI: 7.69-18.36). The strongest associations are with adenocarcinomas (29.43, 95% CI: 16.46-52.61 and 35.26, 95% CI: 20.62-60.28 respectively). An increased risk of SNC for exposures to formaldehyde (1.68, 95% CI: 1.37-2.06 for the case control and 1.09, 95% CI: 0.66-1.79 for the cohort studies), textile industry (2.03, 95% CI: 1.47-2.8), construction (1.62, 95% CI: 1.11-2.36) and nickel and chromium compounds (18.0, 95% CI: 14.55-22.27) was found. Subset analyses identified several sources of heterogeneity and an exposure-response relationship was suggested for wood dust (p = 0.001).
CONCLUSIONS
By confirming the strength of association between occupational exposure to causal carcinogens and SNC risk, our results may provide indications to the occupational etiology of SNC (not only wood and leather dusts). Future studies could be focused on specific occupational groups to confirm causative agents and to define appropriate preventive measures.
Topics: Agriculture; Dust; Formaldehyde; Humans; Metals, Heavy; Occupational Exposure; Odds Ratio; Paranasal Sinus Neoplasms; Publication Bias; Risk; Textile Industry
PubMed: 25885319
DOI: 10.1186/s12885-015-1042-2 -
Toxics Feb 2023N-nitroso compounds (NOCs) are a class of chemical carcinogens found in various environmental sources such as food, drinking water, cigarette smoke, the work... (Review)
Review
N-nitroso compounds (NOCs) are a class of chemical carcinogens found in various environmental sources such as food, drinking water, cigarette smoke, the work environment, and the indoor air population. We conducted a systematic review and meta-analysis to investigate the links between nitrate, nitrite, and NOCs in food and water and the risk of gastrointestinal (GI) cancers, including esophageal cancer (EC), gastric cancer (GC), colorectal cancer (CRC), and pancreatic cancer (PC). A systematic search of the literature in Scopus, PubMed, Google Scholar, Web of Science, ScienceDirect, and Embase was performed for studies on the association between NOCs in drinking water and food sources and GI cancers. Forest plots of relative risk (RR) were constructed for all the cancer sites and the intake sources. The random-effects model was used to assess the heterogeneity between studies. Forty articles were included after removing duplicate and irrelevant articles. The meta-analysis indicated that the intake of high dose vs. low dose of these compounds was significantly associated with the overall GI cancer risk and nitrite (RR = 1.18, 95% CI = 1.07-1.29), and N-nitrosodimethylamine (NDMA) (RR = 1.32, 95% CI = 1.06-1.65). We found that dietary nitrite intake increased GC (RR = 1.33, 95% CI = 1.02-1.73), and EC (RR = 1.38, 95% CI = 1.01-1.89). Additionally, dietary NDMA intake increased the risk of CRC (RR = 1.36, 95% CI = 1.18-1.58). This meta-analysis provides some evidence that the intake of dietary and water nitrate, nitrite, and NOCs may be associated with GI cancers. In particular, dietary nitrite is linked to GC and EC risks and dietary NDMA intake is associated with CRC.
PubMed: 36851064
DOI: 10.3390/toxics11020190 -
European Respiratory Review : An... Mar 2021Globally, radon is the leading risk factor for lung cancer in never-smokers (LCINS). In this study, we systematically reviewed and meta-analysed the evidence of the risk... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Globally, radon is the leading risk factor for lung cancer in never-smokers (LCINS). In this study, we systematically reviewed and meta-analysed the evidence of the risk of LCINS associated with residential radon exposure.
METHODS
Medline and Embase databases were searched using predefined inclusion and exclusion criteria to identify relevant studies published from 1 January 1990 to 5 March 2020 focused on never-smokers. We identified four pooled collaborative studies (incorporating data from 24 case-control studies), one case-control study and one cohort study for systematic review. Meta-analysis was performed on the results of the four pooled studies due to different measures of effect and outcome reported in the cohort study and insufficient information reported for the case-control study. In a analysis, the corresponding risk for ever-smokers was also examined.
RESULTS
Risk estimates of lung cancer from residential radon exposure were pooled in the meta-analysis for 2341 never-smoker cases, 8967 never-smoker controls, 9937 ever-smoker cases and 12 463 ever-smoker controls. Adjusted excess relative risks (aERRs) per 100 Bq·m of radon level were 0.15 (95% CI 0.06-0.25) for never-smokers and 0.09 (95% CI 0.03-0.16) for ever-smokers, and the difference between them was statistically insignificant (p=0.32). The aERR per 100 Bq·mwas higher for men (0.46; 95% CI 0.15-0.76) than for women (0.09; 95% CI -0.02-0.20) among never-smokers (p=0.027).
CONCLUSION
This study provided quantified risk estimates for lung cancer from residential radon exposure among both never-smokers and ever-smokers. Among never-smokers in radon-prone areas, men were at higher risk of lung cancer than women.
Topics: Case-Control Studies; Cohort Studies; Environmental Exposure; Female; Humans; Lung Neoplasms; Male; Radon; Risk Factors; Smokers
PubMed: 33536262
DOI: 10.1183/16000617.0230-2020 -
World Journal of Urology Apr 2023There is conflicting evidence on the association between asbestos exposure and bladder cancer. We performed a systematic review and meta-analysis to provide evidence on... (Meta-Analysis)
Meta-Analysis
PURPOSE
There is conflicting evidence on the association between asbestos exposure and bladder cancer. We performed a systematic review and meta-analysis to provide evidence on occupational asbestos exposure and the risk of mortality and incidence of bladder cancer.
METHODS
We searched three relevant electronic databases (Pubmed, Scopus, and Embase) from inception to October 2021. The methodological quality of included articles was evaluated using the US National Institutes of Health tool. Standardized incidence ratios (SIRs) and standardized mortality ratios (SMRs) for bladder cancer, as well as respective 95% confidence intervals (CIs), were extracted or calculated for each included cohort. Main and subgroup meta-analyses according to first year of employment, industry, sex, asbestos type, and geographic region were performed.
RESULTS
Fifty-nine publications comprising 60 cohorts were included. Bladder cancer incidence and mortality were not significantly associated with occupational asbestos exposure (pooled SIR: 1.04, 95% CI: 0.95-1.13, P = 0.000; pooled SMR: 1.06, 95% CI: 0.96-1.17, P = 0.031). Bladder cancer incidence was higher among workers employed between 1908 and 1940 (SIR: 1.15, 95% CI: 1.01-1.31). Mortality was elevated in asbestos workers cohorts (SMR: 1.12, 95% CI: 1.06-1.30) and in the subgroup analysis for women (SMR: 1.83, 95% CI: 1.22-2.75). No association was found between asbestos types and bladder cancer incidence or mortality. We observed no difference in the subgroup analysis for countries and no direct publication bias evidence.
CONCLUSION
There is evidence that workers with occupational asbestos exposure have a bladder cancer incidence and mortality similar to the general population.
Topics: Humans; Female; Occupational Diseases; Asbestos; Occupational Exposure; Urinary Bladder Neoplasms; Incidence; Lung Neoplasms
PubMed: 36847813
DOI: 10.1007/s00345-023-04327-w