Plastic pollution has emerged as a global environmental and public health crisis, with micro- and nanoplastics (MNPs) representing a pervasive component of the human exposome. Generated through the continuous fragmentation of larger plastic materials, MNPs exhibit physicochemical properties that influence their environmental fate, biological interactions, and toxic potential. Human exposure occurs primarily through ingestion and inhalation, facilitating particle translocation across biological barriers and systemic distribution. Experimental studies have shown that MNP exposure can disrupt mitochondrial and lysosomal function, induce oxidative stress and DNA damage, and modulate inflammatory, apoptotic, and fibrotic pathways. Although evidence supports their multiorgan toxicity, the kidney has emerged as a critical target organ due to its role in filtration and excretion. Experimental studies, often conducted at concentrations exceeding estimated environmentally relevant exposure levels, have associated renal MNP exposure with oxidative injury, apoptosis, and fibrotic remodeling, while emerging mechanistic findings suggest potential links to pro-oncogenic cellular alterations; however, these effects have not been established in humans, and their clinical relevance remains uncertain. Furthermore, the detection of plastic particles in human blood, tissues, and urine underscores the translational relevance of MNP exposure while highlighting important gaps in exposure assessment, dose–response characterization, and mechanistic understanding. In this narrative review, we integrate current evidence regarding environmental exposure pathways, biodistribution, and molecular mechanisms of MNP-induced toxicity, emphasizing the need for integrated exposome-based approaches, omics technologies, advanced experimental models, and longitudinal studies to improve human health risk assessment and guide regulatory policies.
Mariana Abrantes Do Amaral, O. Foresto-Neto, M. D. de Oliveira et al.· International Journal of Mol...· 0 citations
Climate change has reshaped global health in unprecedented ways, with CKD increasingly recognized as a major climate-sensitive condition. Kidney diseases affect an estimated 850 million people worldwide, and countries with the highest incidence are often facing rapid social and economic vulnerability alongside sustained rises in annual temperatures. A growing body of evidence has demonstrated that recurrent heat exposure, failures in heat dissipation, and associated environmental stressors markedly increase the risk of acute kidney injury and accelerate its progression to CKD. On the other hand, epidemiological indicators reinforce this relationship, showing approximately a 30% increase in kidney disease morbidity in regions exposed to high heat, as well as heat-associated CKD epidemics in Central America, Mexico, India, and Sri Lanka, even in the absence of traditional risk factors. These patterns suggested that chronic heat stress and repeated dehydration during manual labor may act as catalysts that unmask metabolic vulnerabilities or enhance susceptibility to nephrotoxic exposures. In this review, we integrated robust population-level data with mechanistic biological insights to explain how these climatic trends disproportionately affect vulnerable populations. We examined historical and contemporary temperature trajectories, identified countries with the greatest climatic and epidemiological burden, and presented key indicators such as incidence, mortality, and clinically relevant population metrics. At the molecular level, we connected these findings to heat-sensitive pathways involving dehydration, mitochondrial dysfunction, tubular injury, inflammation, renal hypoperfusion, and uric acid stone formation. Finally, we situated these processes within the ecological and evolutionary context of human thermoregulation, highlighting a growing adaptation lag between accelerating global warming and the limits of human physiological resilience. Thus, we argued that a comprehensive understanding of these multilevel interactions, from environmental conditions to cellular metabolism, is crucial for shaping effective prevention efforts, early diagnostic strategies, and evidence-based policies capable of mitigating the global rise of heat-associated kidney disease.
S. Yamada, Marcella Cipelli, P. S. Chagas et al.· Kidney360· 0 citations
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