Occupational exposure to polycyclic aromatic hydrocarbons and the risk of upper gastrointestinal cancers: a systematic review and meta-analysis of cohort studies.
Jul 2026· European Journal of Cancer Prevention· 0 citations· 65 references
Medicine
TL;DR
Occupational PAH exposure is modestly associated with upper gastrointestinal cancer risk, particularly esophageal cancer, with higher risk estimates observed in high-exposure occupations.
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are environmental and occupational risk factors for some cancers. We conducted a systematic review and meta-analysis on the risk of upper gastrointestinal cancers, including esophageal and gastric cancers, among workers exposed to PAHs. We searched PubMed, EMBASE, and SCOPUS through December 2024, as well as International Agency for Research on Cancer Monographs and reference lists, for cohort and nested case-control studies. Relative risks (RRs) and odds ratios were pooled using random-effects models. Heterogeneity was assessed with the I2 statistic. Subgroup analyses were conducted by sex, region, industry type, study quality, and publication year. Duration of exposure-response was evaluated using meta-regression. Twenty-seven studies met the inclusion criteria, comprising diverse high-exposure occupations including coke production, aluminum production, metalworking, and chimney sweeping. Overall, occupational PAH exposure was associated with an increased risk of upper gastrointestinal cancers [relative risk (RR) = 1.23, 95% confidence interval (CI): 1.10-1.38]. For esophageal cancer, the pooled RR was 1.31 (95% CI: 1.05-1.63), with higher risk estimates observed in high-exposure occupations. Gastric cancer showed a modestly elevated risk (RR = 1.19, 95% CI: 1.05-1.35). Meta-regression indicated a positive association between duration of exposure and esophageal cancer risk (RR per year = 1.03, 95% CI: 1.01-1.06), but not for gastric cancer. No evidence of publication bias was detected (P = 0.66 for esophageal and P = 0.33 for gastric cancer). Occupational PAH exposure is modestly associated with upper gastrointestinal cancer risk, particularly esophageal cancer. Residual confounding and other sources of bias cannot be excluded, preventing conclusions in terms of causality.
Lung cancer is a major global health issue, especially among men. While smoking and occupational or environmental exposures are known risks, the role of benzene remains under investigation. We aimed to conduct a systematic review and meta-analysis to evaluate the association between occupational benzene exposure and lung cancer incidence and mortality. We included cohort and case-control studies mentioned in the 2018 IARC Monograph on benzene and performed a systematic literature review to identify studies published up to 2024 by using PubMed, SCOPUS, and EMBASE databases. We constructed forest plots of relative risk (RR) to visualize and analyze the data. A random-effects model was used to address heterogeneity between studies. Stratified analyses were conducted to explore effect modification. We included 44 independent studies in our meta-analysis. The findings didn't reveal an association between total occupational benzene exposure and lung cancer overall (RR = 1.00, 95% CI 0.93-1.07, p-het ≤ 0.001, 45 risk estimates) or in major industries. Stratified analyses suggested an association in case controls studies (RR = 1.16, 95% CI 1.10-1.22: 7 risk estimates, p-het = 0.001), and in studies with results adjusted for smoking (RR = 1.17, 95% CI 1.11-1.24: 6 risk estimates, p-het = 0.001). There was also an association between high-level benzene exposure and lung cancer (p-trend = 0.03). Publication bias was excluded (p = 0.16). The increased risk after adjustment for smoking and the suggestion of a dose-response, are consistent with the hypothesis of an association between benzene exposure and lung cancer risk.
M. S. Seyyedsalehi, Mattia Bonetti, Darshi Shah et al.· European Journal of Epidemio...· 0 citations
Nitrogen dioxide (NO₂) is a major air pollutant generated from fossil fuel combustion in transportation and industrial activities and is associated with adverse health effects. Prolonged exposure to NO₂ may induce chronic inflammation and endothelial dysfunction, which contribute to the development of hypertension. This study aimed to systematically review the association between NO₂ exposure and the incidence of hypertension among workers. The review was conducted in accordance with PRISMA guidelines, with literature searches performed in Google Scholar, PubMed, and ScienceDirect for publications from 2020 to 2025. Inclusion criteria comprised full-text articles in English or Indonesian employing observational study designs (cross-sectional, cohort, case-control, or ecological) and involving workers in both formal and informal sectors. Eligible studies examined NO₂ exposure as the independent variable and hypertension as the outcome. Of 2,051 records identified, five studies met the inclusion criteria, originating from China and Nigeria. Risk of bias was assessed using the office of health assessment and translation (OHAT) risk of bias tool. The findings demonstrated a consistent association between NO₂ exposure and an increased risk of hypertension, particularly in poorly ventilated work environments. These results underscore the importance of improving workplace air quality management, strengthening exposure monitoring, and implementing preventive occupational health strategies.
A. Rachmawati, Morrin Choirunnisa Thohira, M. Fitrah et al.· International Journal of Pub...· 0 citations
Background Ultra-processed food (UPF) intake has been associated with digestive system cancer risk, but evidence remains scattered across cancer sites, study designs, and exposure metrics. This systematic review and meta-analysis evaluated associations between UPF intake and digestive system cancer risk overall and by cancer site. We further examined UPF subcategories and dose–response relationships. Methods We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library for English-language cohort and case–control studies published from database inception to May 1, 2026. Hazard ratios (HRs) from cohort studies and odds ratios (ORs) from case–control studies were pooled separately with their corresponding 95% confidence intervals (CIs) using random-effects models. Additional analyses were conducted to investigate site-specific digestive system cancers, UPF subcategories, and dose–response relationships, alongside subgroup, sensitivity, meta-regression, and publication bias assessments. The study protocol was registered in PROSPERO (CRD420261404299). Results A total of nine prospective cohort studies and five case–control studies were included. The main pooled estimates showed a 12% higher risk in cohort studies (HR = 1.12, 95% CI: 1.05–1.20; I2 = 37.6%) and 42% higher odds in case–control studies (OR = 1.42, 95% CI: 1.25–1.60; I2 = 26.7%). Site-specific analyses showed relatively consistent positive associations for colorectal and colon cancer outcomes. Among UPF subcategories, ultra-processed meat/protein products were associated with higher digestive system cancer risk (HR = 1.33, 95% CI: 1.15–1.53). In dose–response analyses using UPF weight share as the primary exposure metric, each 10-percentage-point increase in UPF intake was associated with a 6% higher risk (HR = 1.06, 95% CI: 1.01–1.10), with evidence of non-linearity, although no reliable threshold could be identified. Supplementary analyses based on g/day showed a consistent direction of association. Sensitivity analyses supported the stability of the main findings, and no clear evidence of publication bias was observed. Conclusion Higher UPF intake was associated with increased digestive system cancer risk, with relatively consistent evidence for colorectal and colon cancers. Ultra-processed meat/protein products may be a relevant contributing subcategory, and dose–response analyses suggested an exposure–response gradient. Because evidence came mainly from observational studies and dose–response data were limited, findings require confirmation in high-quality prospective studies. Systematic Review Registration https://www.crd.york.ac.uk/PROSPERO/view/CRD420261404299, identifier PROSPERO (CRD420261404299).
Yanjie Jiang, Shipeng Zhang, Hanyu Wang et al.· Frontiers in Nutrition· 0 citations
High-molecular-weight carcinogens significantly accumulate in human lungs in Northern Thailand, reflecting substantial environmental exposure, while tissue lipid content modulates toxin bioaccumulation, underscores an urgent need for targeted public health strategies addressing both environmental pollution and tobacco use.
BACKGROUND
The incidence of thyroid cancer (TC) has risen in recent decades, prompting investigation of environmental contributors beyond traditional risk factors.
SUMMARY
This narrative review examines the association between TC and chemical exposures including per- and polyfluoroalkyl substance (PFAS), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs), phthalates, phenols, nitrates, and polycyclic aromatic hydrocarbons (PAHs). Several studies have shown a link between PFAS and PCB exposure and TC, particularly papillary thyroid cancer. Nitrates, even at currently accepted safe exposure levels have also been shown to have an association with TC. Findings for phthalates, PBDEs, phenols, and PAHs are inconsistent and less studied.
CONCLUSION
Current evidence supports that an association exists between select chemical exposures and TC development, but study limitations prevent any direct link to causation. Further research is needed to guide clinical practice and public health policy.
Rachael Caretti, H. Arain, Herbert Chen· The Oncologist· 0 citations
BACKGROUND
Ambient air pollution is associated with cardiovascular morbidity and mortality, but its relationship with venous thromboembolism (VTE) remains uncertain. We performed an updated systematic review and meta-analysis evaluating particulate matter exposure and VTE risk.
METHODS
PubMed, Embase, Web of Science, and the Cochrane Library were searched for observational studies evaluating PM2.5 or PM10 exposure and venous thrombotic outcomes. Studies were stratified by pollutants, exposure duration, and effect measure. Estimates were harmonized to 10 μg/m³, and random-effects models using restricted maximum-likelihood estimation and Hartung-Knapp adjustment were applied.
RESULTS
Nineteen studies representing >4.5 million participants met the inclusion criteria. Overall long-term analyses showed no significant association for PM2.5 (HR 1.42, 95% CI 0.88-2.28; I²=97.0%) or PM10 (HR 1.18, 95% CI 0.85-1.64; I²=96.2%). However, sensitivity analyses restricted to studies natively reporting effects per 10 μg/m³ showed an association between PM2.5 and VTE (HR 1.070, 95% CI 1.010-1.135; I²=0%), while PM10 showed a borderline association (HR 1.023, 95% CI 1.000-1.047; I²=0%). Short-term PM2.5 and PM10 exposures were not significantly associated with venous thrombotic risk.
CONCLUSIONS
Evidence suggests a possible modest association between long-term PM2.5 exposure and VTE; however, considerable between-study variability and sensitivity to exposure harmonization limit definitive conclusions. Standardized exposure metrics and consistent VTE definitions are needed to clarify this association.
Maximiliano Víctor Manuel Correa Lara, J. G. Chávez, E. Hernández· Thrombosis and Haemostasis· 0 citations