Jul 2026· Frontiers in Cell and Developmental Biology· Vol 14· 0 citations· 151 references
Medicine
TL;DR
Current evidence supports a biologically plausible framework in which AH exposure may contribute to PCa initiation and progression and may intersect with pathways implicated in therapy resistance, although causal inference remains constrained by exposure misclassification, mixture complexity, and limited longitudinal biomarker data.
Abstract
Prostate cancer (PCa) remains one of the most common malignancies in men worldwide, yet modifiable environmental contributors remain incompletely defined. Aromatic hydrocarbons (AHs), particularly benzene and polycyclic aromatic hydrocarbons (PAHs), are widespread pollutants in ambient air, occupational settings, tobacco smoke, and high-temperature cooking emissions. In this review, we synthesize evidence from population-based and occupational epidemiology, dietary exposure proxies, animal carcinogenesis models, organoid systems, and cell-based mechanistic studies to assess the biological plausibility of AH-related prostate carcinogenesis. Human studies support modest but recurrent associations between long-term exposure to traffic-related mixtures, benzene-containing emissions, PAH-generating cooking practices, and increased PCa risk, with stronger duration–response signals in occupational settings. Experimental evidence further indicates that benzo[a]pyrene and related PAHs can induce prostatic mutagenesis, oxidative and genotoxic stress, endocrine perturbation, epigenetic remodeling, and immunosuppressive changes in the tumor microenvironment. The most coherent mechanisms involve AhR–AR crosstalk, CYP1A1/1B1-mediated bioactivation, ROS generation, DNA-adduct formation, DNMT1/HDAC6-associated epigenetic regulation, JAK2/STAT3-linked survival signaling, epithelial–mesenchymal transition, and IDO/TDO–kynurenine–AhR-mediated immune suppression. Collectively, current evidence supports a biologically plausible framework in which AH exposure may contribute to PCa initiation and progression and may intersect with pathways implicated in therapy resistance, although causal inference remains constrained by exposure misclassification, mixture complexity, and limited longitudinal biomarker data. Future studies should integrate precise exposure assessment with prostate-specific molecular studies, organoid systems, animal models, and prospective human cohorts.
Puberty is a sensitive period of endocrine development with lifelong implications for cardiometabolic and reproductive health. This review evaluates evidence linking ambient air pollution and polycyclic aromatic hydrocarbons (PAHs) to pubertal development. Studies suggest that associations between air pollution and pubertal timing depend on pollutant composition, exposure timing, and exposure intensity. Component-level analyses of PM2.5 implicate organic matter (OM) and sulfate fractions in associations with earlier menarche and precocious puberty, with OM enriched in combustion-derived PAHs. In contrast, high chronic PM2.5 exposure has also been associated with delayed menarche in heavily polluted settings. Biomarker studies further support biological plausibility, associating PAH exposure to earlier breast development and disruption of hypothalamic kisspeptin–GnRH signaling. Evidence suggests that air pollution may alter pubertal timing through endocrine-disrupting mechanisms, with PAHs representing a plausible mechanistic pathway. Future studies should prioritize longitudinal cohorts, pollutant mixture analyses, and male populations.
Alicia K. Peterson· Current Environmental Health...· 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.
Outdoor air pollution (OAP) is a major global environmental health threat associated with respiratory disease and solid tumors, with growing evidence linking it to hematologic malignancies. This review summarizes the molecular mechanisms and epidemiologic evidence connecting OAP exposure to acute and chronic leukemias, lymphomas, myelodysplastic syndromes (MDS), clonal hematopoiesis of indeterminate potential (CHIP), and multiple myeloma (MM). Pollutants implicated in hematologic carcinogenesis include particulate matter (PM), benzene, nitrogen dioxide (NO₂), sulfur dioxide (SO₂), arsenic, and ethylene oxide. Molecular mechanisms include oxidative stress, DNA damage, epigenetic dysregulation, chronic inflammation, and hematopoietic stem cell dysfunction. Epidemiologic evidence is strongest for acute myeloid leukemia (AML), particularly with benzene exposure. Acute lymphoblastic leukemia (ALL) has also been associated with traffic-related pollution, NO₂, and PM exposure, though findings are less consistent. Certain lymphoma subtypes demonstrate pollutant-specific associations, while emerging evidence suggests possible links between OAP exposure and MDS and CHIP. In contrast, evidence for chronic leukemias and MM remains limited. Despite limitations, including exposure misclassification and residual confounding, cumulative molecular and epidemiologic evidence supports OAP as an important and potentially modifiable risk factor for hematologic malignancies. OAP exposure disproportionately affects racial and ethnic minorities, low-income communities, and rapidly industrializing regions, magnifying existing health disparities. Further research, environmental policy reform, and public health interventions are needed to reduce exposure and disease burden. HSC: hematopoietic stem cell. Created in BioRender. Murli, H. (2026) https://BioRender.com/tkhy5k7
Hamsa Murli, Sadia Alam, Evelyn B Mesler et al.· Current Hematologic Malignan...· 0 citations
INTRODUCTION
Chronic obstructive pulmonary disease (COPD) progression may be influenced by non-smoking environmental exposures, especially among never-smokers and environmentally exposed populations. Semi-volatile organic compounds (SVOCs) are relevant because they persist in air, particles, dust, surfaces and biological matrices and can enter the body through inhalation, dust ingestion, diet and dermal uptake. This review aimed to synthesize evidence on SVOC exposure assessment, respiratory and COPD-related outcomes, and candidate metabolomic pathways related to COPD progression.
METHODS
We conducted a critical narrative review with structured evidence mapping. PubMed and Web of Science searches identified 4535 records; 3087 remained after DOI- and title-based deduplication, and 1251 unique studies were included in the primary evidence map after screening and manual classification.
RESULTS
Polycyclic aromatic hydrocarbons (PAHs) and phthalates showed the most developed evidence across respiratory and lung-function outcomes and the closest, although still limited, evidence related to COPD progression. Evidence from asthma, airway inflammation, general lung function and cross-sectional COPD occurrence was interpreted as supportive but indirect. Direct progression evidence in diagnosed COPD cohorts remains sparse. Metabolomic evidence suggested candidate pathways involving glycerophospholipid-sphingolipid remodeling, amino-acid metabolism, arginine-nitric oxide signaling, acylcarnitine-tricarboxylic acid cycle activity and redox balance, but these pathways have not been validated as mediators.
CONCLUSION
Current evidence supports respiratory relevance of several SVOC classes but is insufficient to establish SVOCs as causal drivers of COPD progression. Future longitudinal COPD cohorts should integrate repeated environmental sampling, human biomonitoring, source attribution, mixture modeling and targeted metabolomics to clarify preventable exposure-progression pathways.
Yi Fan, Hao Zhou, Xikang Fan et al.· Ecotoxicology and Environmen...· 0 citations
Environmental genotoxins are exogenous chemical agents or complex particulate mixtures capable of damaging DNA, chromosomes or genome-maintenance systems. Their public-health importance extends beyond cancer because persistent or poorly repaired lesions may contribute to reproductive impairment, developmental disturbance, haematological toxicity and other chronic disease pathways. This critical narrative review integrates evidence on major environmental genotoxin classes, exposure routes, molecular mechanisms, human biomonitoring, disease associations and risk-assessment practice. Literature published from 1 January 2000 to 31 May 2026 was examined through accessible scholarly indexes and authoritative sources, with earlier foundational studies retained where necessary. The evidence is strongest when exposure characterisation, mechanistic plausibility, internal-dose biomarkers and prospective health outcomes converge. Such convergence is clearest for aflatoxin B1 and hepatocellular carcinoma, benzene and haematological malignancy, inorganic arsenic and several cancers, inhaled hexavalent chromium and respiratory cancer, and ambient particulate pollution and lung cancer. For many pesticides, drinking-water by-products, metals and emerging particulate contaminants, genotoxic signals are credible but heterogeneous because exposure mixtures, assay protocols, tissue choice, confounding and dose relevance differ markedly. Comet, micronucleus, chromosome-aberration and DNA-adduct assays provide complementary information, yet none independently quantifies disease risk. Mutational signatures and adductomics offer stronger source attribution, but translation from experimental systems to population-level causation remains incomplete. Current single-chemical regulation also underrepresents cumulative exposure, susceptibility, co-exposures and environmental inequity. More defensible risk assessment requires harmonised longitudinal biomonitoring, repeated personal exposure measurement, mechanistically anchored dose-response analysis, transparent mixture methods and explicit separation of hazard identification from exposure-specific risk. Prevention should prioritise source control for well-established hazards while uncertainty is reduced for less mature evidence domains.
Omoighele F. Akhigbe, O. Abutu, N. Y. Wike et al.· Asian Journal of Research in...· 0 citations
Polycyclic aromatic hydrocarbon (PAH) derivatives, including nitrated, oxygenated, halogenated, and alkylated PAHs, have attracted growing concern because of their wide environmental distribution and enhanced toxicity compared with parent PAHs. They are generated through combustion, industrial emissions, and secondary atmospheric or microbial transformations, and have been detected across multiple environmental media and even in remote regions. Compared with parent PAHs, these derivatives often show greater persistence, mobility, bioavailability, and toxicity, thereby increasing ecological and human health risks. Human exposure occurs through inhalation, ingestion, and dermal contact, but the dominant exposure route depends on the exposure setting. Toxicological studies further show that PAH derivatives impair growth, development, reproduction, and cellular function through oxidative stress, DNA damage, mitochondrial dysfunction, endocrine disruption, and metabolic disturbance. However, current evidence remains fragmented because monitoring systems, exposure models, and toxicity assessments often focus on parent PAHs or single compounds. This review therefore integrates emission sources, multimedia fate, different exposure routes, mixture toxicity, and management limitations of PAH derivatives. It also examines differences among exposure scenarios and populations, identifies regulatory and monitoring gaps, and evaluates control and remediation strategies. The resulting synthesis provides a basis for improving risk assessment and environmental management of PAH derivatives.
Chenglong Wu, Xian Zhou, Pengfei Li et al.· Journal of Environmental Man...· 0 citations