This narrative review examines the potential health impacts of environmental exposure to rare earth elements (REEs) within mining and industrial settings. The scope encompasses a broad range of conditions, including bronchitis, interstitial lung disease, and other chronic lung diseases in human populations. The authors synthesize available data to describe the spectrum of potential adverse effects, ranging from oxidative stress and immune dysregulation to fibrosis and tumorigenesis.
The review indicates that elevated internal REE burdens are associated with increased prevalence of respiratory symptoms and chronic lung diseases. Furthermore, the synthesis suggests that tissue injury and remodeling are promoted by mechanisms such as oxidative stress, inflammatory dysregulation, and calcium homeostasis imbalance. It is important to note that these findings are largely derived from experimental models, and current knowledge does not yet fully integrate into population-based risk assessments.
The authors highlight significant limitations, including a lack of validated biomarkers of effect and unclear long-term dose–response relationships. Consequently, the practice relevance centers on the urgent need for improved exposure assessment and biomonitoring strategies. Until more robust evidence is available, clinicians and public health officials should interpret these associations cautiously while considering the need for evidence-based interventions to address this emerging concern.
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Rare earth elements (REEs) are increasingly released into the environment due to intensive mining, industrial processing, and expanding technological applications, resulting in widespread human exposure. Within the respiratory exposome framework, REEs have increasingly been recognized as a potentially important class of airborne contaminants. Fine and ultrafine REE-containing particles can penetrate deeply into the distal lung, where they exhibit high biopersistence and limited clearance. Epidemiological evidence from mining and industrial regions suggests that elevated internal REE burdens may be associated with increased prevalence of respiratory symptoms and chronic lung diseases, including bronchitis and interstitial lung disease. Toxicokinetic and experimental studies provide mechanistic support, demonstrating that inhaled REEs preferentially deposit in the alveolar region, interact with epithelial and immune cells, and may translocate into systemic circulation. At the molecular level, REEs have been shown to induce oxidative stress, immune and inflammatory dysregulation, and calcium homeostasis imbalance in experimental models, thereby promoting tissue injury and remodeling. These processes may contribute to a progressive pathological continuum from persistent inflammation to fibrosis and, potentially, tumorigenesis. Notably, exposure characteristics—including particle physicochemical properties, dose, co-exposure scenarios, and host susceptibility—critically shape health outcomes in real-world settings. Despite accumulating evidence, key uncertainties remain regarding human-relevant exposure thresholds, long-term dose–response relationships, and validated biomarkers of effect. Current knowledge is still largely derived from experimental models, with limited integration into population-based risk assessment. Overall, this review uses a structured literature search and narrative synthesis approach to integrate environmental exposure pathways, toxicokinetic characteristics, and mechanistic evidence within an exposome-oriented framework. It highlights that REEs represent emerging inhalation hazards with the potential to contribute to the burden of chronic respiratory diseases, underscoring the need for improved exposure assessment, biomonitoring strategies, and evidence-based public health interventions.