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

Occupational cancer: global burden, major carcinogens, diagnostic challenges, and prevention prospects

Occupational cancer remains one of the most important challenges in occupational health and public health. This review summarizes current evidence on the global burden of occupational malignancies, major workplace carcinogens, occupational respiratory cancer and international registration systems. Particular attention is paid to mining workers and the under-recognition of occupational cancer in Kazakhstan. The article discusses criteria for establishing occupational causality, latency periods, oxidetive stress, immune disturbances and molecular biomarkers. The need for a national occupational cancer registry and risk-based surveillance of workers exposed to occupational carcinogens is substantiated.

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

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

BACKGROUND AND OBJECTIVE Formaldehyde (FA), classified as a Group 1 human carcinogen by the International Agency for Research on Cancer (IARC), constitutes a significant occupational hazard within hospital pathology service, where it remains the "gold standard" fixative for tissue preservation. Despite widespread recognition of its toxicological properties, the specific carcinogenic and non-carcinogenic health risks confronting pathology personnel subjected to chronic, low-level, and intermittent exposures remain incompletely characterized. This review synthesizes the current body of evidence regarding the cellular and molecular mechanisms of FA toxicity, histopathological (HP) alterations in target tissues, and associated occupational health risks among pathology staff. Study selection for review: A comprehensive literature search was conducted across PubMed∕MEDLINE, Web of Science, and Scopus databases, encompassing publications through December 2025. Studies were selected based on relevance to FA toxicity mechanisms, HP effects, and occupational exposure in pathology settings. Given the heterogeneity of study designs and outcomes, a narrative synthesis approach was adopted. EVIDENCE SYNTHESIS The synthesized evidence demonstrates that pathology personnel are routinely exposed to FA concentrations exceeding recommended occupational exposure limits (OELs). At the cellular level, FA exerts toxicity through deoxyribonucleic acid (DNA)-protein crosslink formation, oxidative stress induction, and inflammatory pathway activation. HP examination of exposed individuals reveals a characteristic progression from ciliary loss and goblet cell hyperplasia through squamous metaplasia to epithelial dysplasia in the nasal mucosa. Non-carcinogenic health effects, including respiratory symptoms and genotoxicity biomarker elevation, are highly prevalent. However, direct epidemiological evidence substantiating elevated cancer risk within this specific occupational cohort remains limited, mainly due to improper (occupational medicine) reporting. CONCLUSIONS This review confirms substantial non-carcinogenic health effects among pathology personnel, with documented HP alterations representing preneoplastic changes at the portal of entry. The mechanistic evidence supports biological plausibility for carcinogenic risk, though epidemiological confirmation specific to this workforce remains lacking, highlighting a critical research gap.

Occupational benzene exposure and risk of lung cancer: a systematic review and meta-analysis.

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.

The Role of Pesticide Exposure and Chronic Physical Exertion in Rheumatoid Arthritis Development - Mechanisms and Clinical Implications - A Narrative Review

Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease influenced by both genetic and environmental factors. Increasing evidence suggests that exposure to pesticides and excessive physical activity resulting in physiological overload may influence the risk of developing RA. Aim: To summarize current knowledge on the impact of pesticide exposure and physical activity on the risk of developing RA. Material and methods: A narrative literature review was conducted using publications from PubMed and Google Scholar, supplemented with studies from major scientific publishers and medical databases. Epidemiological studies, systematic reviews, meta-analyses, and selected experimental studies on RA risk factors were analyzed. Results: Exposure to pesticides, including insecticides, herbicides, and fungicides, as well as other occupational hazards such as organic solvents, silica, asbestos, animal dust, and engine exhaust emissions, was associated with an increased risk of RA. In contrast, studies on per- and polyfluoroalkyl substances (PFAS) suggested a possible protective effect in women. Regular moderate physical activity was linked to a reduced risk of RA development. Conclusions: Environmental and occupational exposures may contribute to RA development, whereas moderate physical activity may have a protective effect. Further research is needed to clarify these relationships and support effective prevention strategies.

Pesticide Exposure and Gynecological Cancers: A Review of Epidemiological Evidence and Mechanistic Pathways

Environmental exposure to pesticides is considered a risk factor for gynecological cancers, contributing to their onset and progression through various mechanisms. This narrative review investigates the role of different pesticides in the development and progression of ovarian, endometrial, and cervical cancers, and provides a comprehensive synthesis of epidemiological findings along with molecular mechanisms, highlighting carcinogenic pathways, conflicting findings, and potential therapeutic implications. Relevant epidemiological and experimental studies published between 2000 and 2025 were identified through searches of major scientific databases. Various pesticides, particularly organochlorines, contribute to gynecological cancers through mechanisms such as estrogen mimicry, DNA damage, oxidative stress, increased pro-inflammatory cytokines, and disruption of cellular signaling pathways. However, most studies found no significant association between certain pesticides, such as Triazines and Atrazine, and gynecological cancers. Furthermore, some pesticides, like Carbendazim, exhibit a dual role; while carcinogenic, they can also serve therapeutic purposes in cancer treatment when utilized with nanotechnology. Overall, pesticide exposure is a significant factor in the development and progression of women’s cancers, although the strength of the evidence varies across pesticide classes. Despite numerous studies, contradictory findings necessitate further research to clarify causal relationships.