Formaldehyde in pathology services: from molecular toxicity to histopathological change and occupational risk.

Hematological changes in formaldehyde-exposed workers: A critical review and meta-analysis.

Formaldehyde (FA) is a widely used chemical with known carcinogenic properties, particularly for the upper respiratory tract. Concerns about probable FA-induced hematotoxicity and leukemia have sparked investigations into its health risks. This review scrutinized the quality of exposure evaluations in studies exploring the hematotoxicity of FA and assessed the association between FA exposure and blood dyscrasias. A total of 22 studies were included in the systematic review; among them, 10 provided sufficient data for meta-analysis. FA exposure was significantly associated with changes in blood parameters, including white blood cells (standardized mean difference [SMD] = -1.450 ± 0.636), T cytotoxic cells (SMD = 2.813 ± 1.013), and natural killer (NK) cells (SMD = 1.911 ± 0.775). None of the other blood parameters were significantly affected. However, because of inconsistencies and limitations in exposure assessment methods across the reviewed studies, a clear dose-response relationship could not be established. Overall, changes in some blood parameters were possibly a response to the sensory irritation of FA in the upper respiratory tract. Based on the available scientific evidence, inhaled FA is not distributed beyond portal-of-entry to distal tissues or organs. It is recommended that the exposure of workers to FA be evaluated in a more comprehensive way by following well-validated FA sampling and analysis methods in future studies to better elucidate the association between FA exposure and hematotoxicity. Also, biological monitoring is recommended to estimate overall worker exposure to formaldehyde and to assess the association between FA exposure and its probable hematotoxicity.

Biomarkers and detection techniques for genotoxic damage in workers exposed to benzene, toluene, and xylene: a narrative review

Occupational Medicine In The Prevention And Management Of Workplace Related Cancer: Mechanisms, Strategies And Emerging Challenges

The role of occupational medicine in identifying, managing, and preventing cancers linked to workplace exposures, while addressing diagnostic advances, regulatory frameworks, and preventive strategies is examined.

Environmental Genotoxins and Human Health Risks: Exposure Pathways, Mechanisms, Biomarkers and Challenges for Causal Risk Assessment

This critical narrative review integrates evidence on major environmental genotoxin classes, exposure routes, molecular mechanisms, human biomonitoring, disease associations and risk-assessment practice for well-established and less mature evidence domains.

Occupational Hazards, Injuries, and Health Outcomes Among Water and Wastewater Workers: A Systematic Review

Water and wastewater workers encounter complex occupational exposures, but evidence on related injuries and adverse health outcomes remains fragmented. We systematically searched PubMed/MEDLINE, Scopus, Web of Science Core Collection, and Embase on 23 April 2026 and synthesized evidence using a Population–Exposure–Outcome framework and PRISMA 2020. Two reviewers independently screened and extracted data. Methodological quality was evaluated with design-specific Joanna Briggs Institute tools, and certainty for prevention measures was assessed using a GRADE-informed narrative approach. Seventy studies published from 1940 to 2025 were included; most were cross-sectional. The most reproducible findings concerned respiratory effects from bioaerosols, endotoxins, and hydrogen sulfide, musculoskeletal morbidity (12-month low-back-pain prevalence up to 72.8%), and severe acute hazards during chemical handling and confined-space entry. Infectious findings, including hepatitis A/E, Helicobacter pylori, and intestinal parasites, were heterogeneous and particularly vulnerable to confounding by community background prevalence. Employment duration, inadequate personal protective equipment, insufficient training, and unsafe facility design amplified risk. Meta-analysis was precluded by heterogeneity, and confidence was limited by cross-sectional designs and inconsistent adjustment. The review was not registered and received no external funding. Engineering controls, confined-space safeguards, and task-specific protective equipment are priority measures, although intervention-effectiveness evidence remains low or very low certainty.

Genotoxic, Cytotoxic, and Inflammatory Alterations of the Oral Mucosa Caused by the Use of Electronic Cigarettes: Literature Systematic Review

Introduction: The increased use of electronic cigarettes (vapes) has been identified as a new public health problem. Objective: To find evidence on the effects of vaping on the establishment of cellular and tissue damage and to identify carcinogenic pathways related to head and neck cancer and oral cancer. Method: Systematic review research in the PubMed, LILACS, SciELO, and Cochrane databases, with a ten-year time frame (2014-2024). Descriptors: e-cigarettes, vaping, oral cancer, squamous carcinoma, and head & neck cancer. Fourteen original in vitro and in vivo studies that investigated alterations at the molecular and clinical level resulting from exposure to and consumption of vapes were included and analyzed. The studies were classified according to the risk of bias using the OHAT and ROBINS-E tools. Results: Findings were grouped by the predominance of genotoxic and cytotoxic effects, as well as alterations in inflammatory pathways and cell progression and tissue lesions in the oral mucosa. In vitro and in vivo results showed DNA damage, micronucleus formation, reduced cell viability, increased LDH and ROS, activation of oncogenic pathways such as NF-κB and STAT3, and inflammatory pathways (increased interleukins) and progression pathways (epithelial-mesenchymal transition phenotype). Conclusion: Together, the findings demonstrate that vapes are capable of activating carcinogenic pathways in head and neck cells and oral mucosa. In addition, we consider activating and accelerating inflammatory processes, creating a microenvironment favorable to neoplastic initiation, promotion, and progression. These findings highlight the need for more robust clinical studies and mechanistic investigations focused on agent-speciftradic pathways.