Occupational exposure in industrial and artisanal tanneries has been reported in several studies. Tannery workers are exposed to chemical, biological, ergonomic and work-related hazards that may lead to adverse health disorders. The aim of this study was to evaluate systematically the available data on Chromium (Cr) exposure among workers in industrial and artisanal tanneries, as well as the associated clinical manifestations and risk factors in in both settings. A systematic literature search was conducted across major databases, including PubMed, Scopus, Web of Science and Google Scholar, covering studies published between 2010 and 2025. Eligible studies included human observational investigations among workers reporting biomonitoring data on Cr exposure (total Cr, Cr(III)-trivalent, and/or Cr(VI)-hexavalent and evaluating at least one health effect. Studies from all geographical regions were considered. Of 1040 records, 34 studies from eight countries (n = 6565; predominantly male) met the inclusion criteria. Elevated Cr concentrations were detected in the blood of TWs (3.84 ± 0.21-269.7 ± 211.1 µg/L), with substantially higher levels observed in toenails (124.0-298.8 µg/g). Urinary Cr concentrations (8.39-19.1 µg/L) were also elevated but remained below the ACGIH BEI (25 µg/L). Dermatological and respiratory disorders were the most frequently reported occupational health outcomes in industrial tanneries, with comparable effects reported in artisanal settings despite limited Cr exposure. While occupational exposure to Cr(VI) has been consistently associated with oxidative stress (increased MDA levels and decreased GSH and SOD activities) and cytogenetic damage (Increased micronuclei frequency, chromosomal aberrations, and DNA strand breaks), the findings regarding hematological and biochemical changes remained inconsistent across both settings. However, co-exposure to multiple chemical and biological hazards further complicates the specific attribution of observed health effects to Cr(VI). The findings highlight a strong association between occupational Cr exposure and adverse health effects affecting multiple biological systems. Despite existing urinary Cr biomonitoring guidelines, an officially recognized occupational biological limit value for blood Cr in TWs remains lacking. These results underscore the need for improved occupational safety measures, stricter regulatory policies and region-specific biomonitoring studies to establish appropriate reference values, particularly for blood Cr, and improve the interpretation of exposure data.
Benzo[a]pyrene (B[a]P), a widespread environmental carcinogen, exerts multifaceted toxicity beyond direct DNA damage. Recent studies highlight the profound capacity of B[a]P to disrupt epigenetic landscapes, particular histone modifications, across diverse biological systems. This review synthesizes both in vitro and in vivo experimental findings to elucidate the mechanisms and consequences of B[a]P-induced histone modifications. In vitro studies demonstrate that B[a]P and its ultimate metabolite, BPDE, significantly alter key histone marks, including phosphorylation (γH2AX), acetylation (H3K9/14/18/27ac, H4K5/12/16ac), methylation (H3K4/9/27/36/79 me), lactylation (H4K12la), and ubiquitination (uH2A), in epithelial and connective cells. These changes are driven through multiple interconnected pathways: (1) Direct interference, where BPDE-dG adducts physically widen the DNA minor groove, entrapping histone tails and sterically blocking modifying enzymes; (2) Regulation of epigenetic enzymes, via modulating the expression/activity of HDACs, HATs, HMTs, and ubiquitin ligases; and (3) Oxidative stress and receptor signaling, primarily through AhR activation and ROS generation, altering metabolite pools and downstream kinase cascades. In vivo evidence from animal models and occupational human exposure confirms these alterations, linking specific histone code disruptions (e.g. decreased H3K36me3, H3K79me2; increased H3K9me2) to functional outcomes such as genomic instability, impaired DNA repair, aberrant gene expression, stemness promotion, and ultimately carcinogenicity in lung, liver, and reproductive tissues. Notably, B[a]P toxicity exhibits tissue, cell-type, and species specificity, and can be transgenerational. Emerging as potential biomarkers and therapeutic targets, these B[a]P-driven epigenetic alterations represent a critical, non-mutational axis of its toxicity. This mechanistic understanding bridges genetic and epigenetic carcinogenesis, offering novel insights for its risk assessment and intervention strategies.
Statins are the main medications prescribed to improve lipid profiles and avoid cardiovascular risks in humans. Preclinical studies have shown that statins may impair male reproduction; however, their effects on female reproduction remain unclear. This study conducted a systematic review of the literature regarding preclinical primary studies that assessed female reproductive outcomes in rodent models after exposure to statins. The studies were searched in the databases PubMed, Scopus, Embase, Web of Science, LILACS, and SciELO, using distinct combinations of the search terms "statins", "ovary", "uterus", "female reproduction", "mice", "rats", followed by the Boolean operators AND or OR. Subsequently, duplicities and studies that did not meet the eligibility criteria were excluded from this review. Afterward, the risk of bias was evaluated through the 10 points of the SYRCLE's risk of bias tool. Extraction and qualitative analysis of the data were carried out, and whenever possible, a meta-analysis was applied to assess the data quantitatively. The results indicated that normocholesterolemic female rodents exposed to statins showed ovarian morphological changes, such as impaired follicular dynamics. Additionally, when rodents were induced with endometriosis or reproductive-related cancer, there was a reduction in the volume of endometriotic implants and a complementary action on the reduction of tumor proliferation, respectively. As a limitation, there were no studies assessing the effects of statins in hyperlipidemic rodents, which may make it difficult to translate the adverse effects of statins observed in normolipidemic rodents to humans.
