Search Results (299)

Spray cosmetics couple formulation composition with actuator design and biological targets, so their performance is governed by rapid, nonequilibrium interfacial processes that cannot be predicted from in-bottle stability or equilibrium surface tension alone. This targeted narrative review integrates evidence across storage stability, atomization, droplet flight and evaporation, deposition, film formation, active delivery, inhalation safety and environmental fate. It examines how surfactant molecular structure, micellar replenishment, dynamic surface tension, interfacial viscoelasticity and extensional rheology influence droplet-size distributions, wetting, spreading and deposition. Particular attention is given to competing effects: enhanced breakup may increase airborne fine fractions; stronger interfacial films may impair sprayability; enhanced penetration may reduce barrier tolerance; and bio-based origin does not necessarily imply a lower life-cycle burden. Across moisturizing, sunscreen, hair- and scalp-care, makeup-setting, cleansing-foam and emerging functional sprays, this review develops an interface-to-outcome framework and a multiobjective operating-window concept linking formulation and device variables to efficacy, manufacturability, safety and sustainability. The available evidence supports product-specific, whole-process validation rather than optimization against any single equilibrium property, while highlighting the need for spray-relevant dynamic measurements, realistic exposure assessment and validated formulation–device co-design. Full article

Cannabis use has increased substantially in the United States, driven by broader legalization, decriminalization, and expanding medical and recreational availability. For facial plastic surgeons, the clinical implications remain difficult to define because “cannabis use” encompasses heterogeneous products and routes, including smoked flower, vaping, concentrates, edibles, pharmaceutical cannabinoids, topical cannabidiol (CBD), and frequent co-use with tobacco or nicotine. Current evidence suggests that systemic cannabis use, particularly inhaled or heavy perioperative use, may be associated with increased surgical complications in selected populations; however, existing studies are limited by retrospective design, inconsistent exposure definitions, inadequate dose and route characterization, and confounding by tobacco use and comorbidities. Cannabinoids exert biologic effects through the endocannabinoid system, particularly CB1 and CB2 receptors, which are expressed in the central nervous system, immune cells, vasculature, and skin. These pathways influence inflammation, keratinocyte proliferation, fibroblast activity, angiogenesis, immune surveillance, pain signaling, and tissue remodeling. The net effect of cannabinoid exposure on wound healing is likely context dependent, varying based on receptor expression, wound-healing phase, route of administration, cannabinoid composition, local tissue environment, and patient-specific risk factors. Preclinical and early dermatologic literature suggests potential therapeutic roles for topical cannabinoids, especially CBD, in modulating inflammation and epithelial repair. In contrast, systemic perioperative cannabis use has been associated in several surgical cohorts with infection, delayed healing, hematoma, nonunion, and reoperation. Evidence specific to facial plastic surgery remains sparse. The most directly relevant study evaluated cannabis and tobacco use in patients undergoing operative mandibular fracture repair. Cannabis-only use was not associated with increased complications, although the cohort was small; concurrent cannabis and tobacco use was associated with higher rates of surgical site infection, facial nonunion, abscess, debridement, and malocclusion. To date, no published studies address cannabis-associated outcomes in rhinoplasty, rhytidectomy, blepharoplasty, browlift, or facial rejuvenation. This review summarizes the biologic rationale, available surgical evidence, and clinical considerations for incorporating cannabis use into individualized perioperative risk assessment in facial plastic surgery. Full article

Background/Objectives: Microplastics (MPs) and nanoplastics (NPs) have emerged as ubiquitous environmental contaminants resulting from the extensive production, use, and degradation of plastic materials. Human exposure occurs primarily through contaminated food and drinking water, with inhalation representing an additional important route. Growing concern has focused on the ability of these particles, particularly NPs, to cross biological barriers, enter the systemic circulation, and reach human tissues. The aim of this review was to summarize current evidence on dietary exposure to MPs and NPs, their gastrointestinal bioavailability and toxicokinetics, and their potential systemic health effects, with particular emphasis on organ-specific responses, underlying biological mechanisms, and the strength and limitations of the available evidence. Methods: A comprehensive narrative review of the scientific literature published between 2000 and 2026 was conducted using PubMed/MEDLINE, Scopus, Web of Science, and Google Scholar. Original research articles and review papers addressing dietary exposure, occurrence in food and drinking water, migration from food-contact materials, gastrointestinal absorption, translocation, biodistribution, bioaccumulation, elimination, molecular mechanisms, and potential organ-specific or systemic health effects were included. Publications without full-text availability, conference proceedings, editorials, commentaries, duplicate publications, and studies without relevance to human exposure or health were excluded. Results: Food, drinking water, beverages, and food-contact materials represent important sources of human exposure to MPs and NPs. Following ingestion, most larger particles are eliminated through the gastrointestinal tract, whereas smaller MPs and particularly NPs may cross biological barriers and potentially reach the systemic circulation and distant tissues. Experimental studies consistently identify interconnected biological responses involving oxidative stress, inflammation, mitochondrial dysfunction, barrier impairment, immune dysregulation, genotoxicity, apoptosis, and endocrine disruption. These mechanisms have been associated with alterations in the gastrointestinal, respiratory, cardiovascular, nervous, urinary, reproductive, endocrine, and skeletal systems and with biological processes relevant to carcinogenesis. However, most mechanistic evidence derives from in vitro and animal models, whereas human evidence remains limited and predominantly observational. Consequently, the extent to which these experimental findings translate into clinically significant effects in humans remains uncertain. Conclusions: Current evidence supports the biological plausibility of systemic effects associated with MNP exposure but is insufficient to establish causal relationships between chronic dietary exposure and specific human diseases. The detection of MNPs in human tissues and reported associations with pathological conditions should therefore be interpreted cautiously. Standardized analytical methods, improved characterization of realistic human exposure, and well-designed longitudinal epidemiological studies integrating quantitative exposure assessment with validated clinical outcomes are required to clarify dose–response relationships, long-term health effects, and the clinical significance of MNP exposure. Full article

Plastic contamination (plastamination) has become a pervasive environmental threat with growing implications for human health. Among plastic-derived contaminants, micro- and nano-plastics (MNPs) are of particular concern due to their persistence, widespread distribution, and capacity to interact with biological systems. Humans are exposed to MNPs through ingestion, inhalation, dermal contact, and maternal transfer, and these particles can cross biological barriers, including the blood–brain barrier, reaching the central nervous system. MNPs disrupt cellular homeostasis by inducing oxidative stress, mitochondrial dysfunction, and inflammation. In the brain, these processes drive glial activation and chronic neuroinflammation, which are closely associated with neuronal damage and neurological disorders, including Parkinson’s disease (PD). MNPs can also affect systemic pathways such as the gut–brain axis (GBA) and neuroendocrine regulation, suggesting broader physiological consequences. This narrative review synthesizes current evidence on the neurotoxic and pro-inflammatory potential of MNPs. Since MNPs may promote the aggregation of proteins implicated in neurodegeneration, such as alpha-synuclein, their possible role in PD is discussed. Despite several knowledge gaps, MNPs may be emerging environmental risk factors for brain health and neurodegenerative diseases such as PD. Nevertheless, there is a need for further studies in the field, standardized methodologies and longitudinal studies to implement effective mitigation strategies. Full article

Background/Objectives: The stability and biological safety of newly developed formulations must be established to support their therapeutic efficacy and clinical translation in pulmonary drug delivery. Therefore, this follow-up study comprehensively evaluated the short- and long-term stability and the in vitro cytotoxicity of optimized, co-spray-dried theophylline (THN) dry powders for inhalation against A549 lung epithelial cells. Methods: Two established formulations were selected: THN-RAF (raffinose–leucine–glycine based) and THN-TRE (trehalose–leucine based). Stability was assessed under accelerated conditions (40 °C/75% RH, 3 months) and long-term desiccator storage (25 °C, 1 year) using laser diffraction, SEM, XRPD, FTIR, DSC, TGA, and Andersen Cascade Impaction. As THN-TRE had been previously confirmed to be cytocompatible, only THN-RAF and its components were evaluated against A549 human alveolar epithelial cells using the MTT assay. Results: Under accelerated conditions, both formulations exhibited pronounced recrystallization (Xc up to 89.9%), agglomeration (D [0.9] up to 217.08 µm for THN-TRE), and deterioration in aerodynamic performance (FPF as low as 11.55%, MMAD up to 6.68 µm). By contrast, long-term desiccator storage induced substantial recrystallization (Xc up to 80.7%) while preserving thermal, chemical, and aerodynamic performance (FPF ≈ 40%; MMAD 4.99–5.21 µm). THN-RAF was more resistant to stress-induced agglomeration than THN-TRE. Cytotoxicity assessment confirmed cytocompatibility of THN-RAF, with cell viability exceeding 70.99% at all tested concentrations (up to 500 µg/mL). Conclusions: These findings reveal a marked discrepancy between the outcomes of ICH accelerated testing and long-term desiccator storage. They underscore the importance of considering moisture-protective packaging configurations when designing stability protocols for amorphous inhalable formulations. Full article

Atmospheric microplastics are increasingly recognized as mobile particulate contaminants that can be emitted, resuspended, transported, and deposited across indoor, terrestrial, marine, high-altitude, and remote environments. However, reported abundances and particle characteristics remain difficult to compare because studies differ in sampling design, reporting units, particle-size limits, contamination control, and polymer identification. This review combines concise bibliometric mapping with a critical narrative synthesis. A Web of Science Core Collection search for 2000–2024 retrieved 356 English-language articles and reviews, of which 280 met the eligibility criteria. Publication output increased rapidly after 2020. Co-citation and keyword analyses identified three major themes: occurrence, transport, and deposition; sampling and analytical characterization; and exposure and potential ecological and health implications. The synthesis shows that active air sampling and passive deposition collection measure different atmospheric processes, while inconsistent blank correction, recovery assessment, and polymer confirmation limit inter-study comparability. Field observations and modelling support long-range transport and the importance of particle morphology, but quantitative source attribution remains uncertain. Current evidence supports inhalation exposure and biological plausibility, yet is insufficient to establish population-level risks or causal links with specific diseases. Future research should prioritize harmonized monitoring, stronger QA/QC, improved detection of small particles and nanoplastics, and integrated transport–exposure assessment. Full article

Airborne microplastics and nanoplastics (MNPs) are increasingly reported in indoor, outdoor, and occupational air, but their aerobiological significance remains incompletely defined. This narrative review proposes the aeroplastic exposome as a cautious, testable framework for evaluating airborne MNPs as interfaces among aerosol transport, biological and chemical loading, aeroallergen co-exposure, inhalation, respiratory deposition, clearance, and airway immune response. Evidence from environmental monitoring, indoor and occupational exposure studies, and human respiratory-sample and lung-tissue detection studies supports the occurrence of airborne MNPs, the plausibility of inhalation exposure, reported detection in human respiratory samples, and experimental hazard under selected conditions. However, evidence that airborne plastic particles routinely carry bioaerosols or aeroallergens remains insufficient or model-dependent. The aeroplastic exposome is therefore not proposed as a disease entity, validated exposure metric, or established explanation for asthma, chronic obstructive pulmonary disease, fibrosis, infection, or cancer. Instead, it is a framework for organizing testable questions about polymer identity, aerodynamic fraction, morphology, aging state, biological loading, co-exposure context, deposition, clearance, epithelial–immune responses, and host susceptibility. Priority research needs to include standardized airborne sampling, same-particle polymer–bioaerosol–allergen characterization, exposure-relevant aerosol systems, factorial co-exposure experiments, and prospective human studies with repeated personal exposure assessment. Full article

Background: Non-invasive therapies for heart failure represent one of the current major focuses in clinical research. Plant-derived extracellular vesicles (PEVs) have recently emerged as a promising therapeutic modality. Objectives: In this study, we investigated the therapeutic potential of PEVs in heart failure with preserved ejection fraction (HFpEF), focusing on extracellular vesicles derived from Lycium barbarum (Gq-EVs). Methods: We first obtained Gq-EVs with high biological activity and high concentration from Lycium barbarum juice and characterized them by using transmission electron microscopy, nanoparticle tracking analysis, and metabolite composition analysis. Results: Our in vivo findings indicate that nebulized inhalation of Gq-EVs for 7, 14, and 21 days improved abnormal cardiac diastolic function, reduced excessive myocardial hypertrophy, and attenuated inflammatory cell infiltration and collagen deposition in HFpEF mice. Further in vivo and in vitro experiments showed that Gq-EVs can reach injured cardiac tissue, improve mitochondrial function, and are associated with reduced cardiomyocyte apoptosis and amelioration of myocardial hypertrophy, potentially involving TP53-related apoptotic signaling. Conclusions: Overall, nebulized delivery of Gq-EVs may be a relatively non-invasive, well-tolerated, and cost-effective therapeutic strategy for HFpEF, highlighting the potential of PEV-based nanotherapies and offering a sustainable approach for the medical utilization of Lycium barbarum resources. Full article

Background/Objectives: Amb a 1 is the major allergenic component of Ambrosia artemisiifolia pollen and a clinically relevant marker of genuine ragweed sensitization. Heart failure is increasingly recognized as a systemic syndrome shaped by immune activation, endothelial dysfunction, fibrosis, neurohormonal imbalance, pulmonary comorbidity, and environmental exposures. This narrative review aims to synthesize the translational evidence linking Amb a 1-specific IgE, IgE-mediated inflammation, allergic airway disease, and cardiovascular remodeling in heart failure. Methods: A targeted narrative review was performed, integrating evidence on component-resolved ragweed diagnosis, IgE-FcεRI signaling, mast cell and eosinophil biology, pollen exposure, cardiovascular inflammation, and heart failure pathophysiology. Results: No dedicated clinical studies have validated Amb a 1-specific IgE as a diagnostic, prognostic, or therapeutic biomarker in heart failure. However, adjacent evidence supports biologically plausible links between allergen-specific IgE responses and cardiovascular dysfunction, including mast cell activation, cytokine release, endothelial perturbation, oxidative stress, microvascular dysfunction, pulmonary-cardiac interaction, and myocardial fibrosis. Amb a 1-specific IgE may therefore identify a seasonally vulnerable heart failure phenotype, particularly in patients with allergic rhinitis, asthma, eosinophilic inflammation, or recurrent symptom worsening during ragweed season. A systemic/indirect pathway operating through allergic airway disease is distinguished from a postulated direct cardiac pathway; the latter remains strictly speculative, as no direct evidence demonstrates that inhaled Amb a 1 reaches or activates cardiac mast cells in vivo. Conclusions: Amb a 1-specific IgE should not currently be used to infer cardiac causality or modify heart failure therapy. Prospective, phenotype-rich, exposure-informed studies are needed to determine whether ragweed sensitization has clinically meaningful implications for heart failure endotyping, seasonal risk assessment, and cardio-allergology care. These findings may inform patient-centered heart failure management by improving the interpretation of seasonal dyspnea, allergic comorbidity, and symptom fluctuations in ragweed-endemic regions. Full article

Antimicrobial resistance (AMR) in respiratory infections represents a major global health challenge, compounded by biological barriers that limit the effectiveness of conventional antibiotics, including mucus hypersecretion, biofilm formation, and intracellular pathogen persistence. Nanotechnology has emerged as a promising platform for addressing these limitations through advanced drug-delivery strategies. This narrative review provides an integrated overview of nanocarrier systems—including lipid-based (e.g., liposomes, solid lipid nanoparticles), polymeric (e.g., PLGA, chitosan), and inorganic nanoparticles (e.g., silver, gold, zinc oxide)—with emphasis on their pharmaceutical design parameters for pulmonary delivery. Key mechanisms by which nanotechnology enhances antimicrobial efficacy include targeted and controlled drug delivery, improved penetration of mucus and biofilms via surface engineering, synergistic combination therapies, and intrinsic antimicrobial activity through mechanisms such as reactive oxygen species generation. Preclinical studies targeting major respiratory pathogens, including Pseudomonas aeruginosa, Mycobacterium tuberculosis, Streptococcus pneumoniae, and methicillin-resistant Staphylococcus aureus, demonstrate enhanced biofilm disruption, intracellular drug delivery, and reductions in bacterial burden. However, important translational challenges remain, including long-term safety, manufacturing scalability, regulatory complexity, and the potential for microbial adaptation. Future directions focus on stimuli-responsive systems, inhalable formulations, and biomimetic platforms to improve targeting and therapeutic precision. Collectively, nanotechnology represents a delivery-oriented strategy with the potential to enhance existing antimicrobial therapies and support the development of more effective interventions against resistant respiratory infections. Full article

The exponential rise in global plastic production has resulted in the widespread environmental dissemination of micro- and nanoplastics (MNPs) across air, water, and biological systems. Inhalation of airborne MNPs represents a biologically plausible pathway of pulmonary exposure, particularly within indoor and occupational environments. Experimental evidence indicates that inhaled MNPs deposit within distal lung compartments, where their small aerodynamic diameter and surface reactivity may favor cellular uptake, oxidative stress induction, inflammatory activation, and prolonged biopersistence. Experimental studies further indicate that MNP exposure may induce DNA damage, chromosomal instability, and the dysregulation of signaling pathways involved in genomic integrity, thereby providing additional mechanistic support for their potential role in carcinogenesis. Chronic redox imbalance, macrophage dysfunction, inflammasome activation, epithelial–mesenchymal transition, and dysregulated cell adhesion collectively resemble mechanisms implicated in inflammation-associated carcinogenesis. Emerging in vitro and in vivo data further suggest that nanoplastics may function as tumor promoters or co-carcinogenic modifiers, particularly under chronic low-dose exposure or in combination with other airborne toxicants. However, human epidemiological evidence remains limited, and causality has not been established. This review synthesizes current mechanistic evidence regarding inhaled MNPs as potential modifiers of lung carcinogenesis, compares them with established inhaled carcinogens, and outlines critical research priorities necessary to clarify exposure–response relationships and clinical relevance. Current evidence supports biological plausibility rather than confirmed carcinogenic classification. Full article

The therapeutic goals related to chronic airway diseases are evolving from short-term symptom control toward sustained suppression of disease activity and prevention of future risk. In severe asthma, this shift has been captured by the concept of clinical remission, generally defined by absence of exacerbations, no need for oral corticosteroids, symptom control, and stable or improved lung function. In chronic obstructive pulmonary disease (COPD), the analogous concept has more often been described as disease stability. Although remission in asthma and stability in COPD have developed within different biological and clinical frameworks, they may reflect disease-specific expressions of the same therapeutic ambition. Recent studies support COPD stability as a measurable and clinically meaningful state, associated with reduced exacerbation risk and mortality. Evidence from optimized inhaled triple therapy, particularly with fluticasone furoate/umeclidinium/vilanterol, indicates that multidimensional stability can be achieved and maintained in a proportion of patients, while real-world studies reinforce its applicability beyond randomized trials. The emergence of biologic therapies for selected patients with eosinophilic or type 2 COPD further strengthens the rationale for considering stability as an ambitious treatment target. In this narrative review, informed by a structured literature search, we discuss the conceptual relationship between asthma remission and COPD stability, and summarize the evidence supporting disease stability as an attainable and prognostically relevant outcome. In addition, we propose a pragmatic multidimensional definition based on symptom stability, absence of moderate or severe exacerbations, no systemic corticosteroid use, and maintained lung function over 12 months. COPD stability should not be viewed as a weaker goal than asthma remission, but rather as the most appropriate COPD-specific expression of sustained low disease activity. Full article

Pulmonary drug delivery has become a vital route for both local and systemic treatments because of the unique structure and function of the respiratory system. Unlike oral and injectable dosage forms, inhalation offers a non-invasive, direct route to deliver medicines to the lungs, bypassing gastric degradation and first-pass hepatic metabolism. Common forms such as aerosols, solutions, suspensions, and dry powders are frequently used to treat respiratory diseases like asthma and chronic obstructive pulmonary disease (COPD). However, their effectiveness is often limited by physiological and biopharmaceutical barriers, such as mucociliary clearance, enzymatic degradation, and nonspecific deposition, which reduce drug retention and bioavailability. These issues are especially critical for poorly soluble or sensitive molecules, leading to lower drug concentrations at the target site and necessitating frequent dosing. To address these challenges, advanced nanoparticle-based delivery systems are being developed to improve drug stability, targeting, and controlled release within the lungs. At the same time, computational methods, including deposition modeling, physiologically based pharmacokinetic (PBPK) simulations, and AI-driven optimization, are increasingly used in formulation development to predict in vivo performance and boost translational success. This review covers the physiological and biological barriers to pulmonary drug delivery, explores major inhalation routes and dosage forms, and discusses new therapeutic strategies and nanoparticle platforms. It also highlights the growing role of in silico modeling and AI in accelerating the design and optimization of pulmonary treatments, while addressing current challenges, limitations, and regulatory issues in translating pulmonary nanomedicine into clinical practice. Full article

Chikungunya virus (CHIKV), traditionally recognized as a mosquito-borne alphavirus that causes febrile illness and debilitating arthralgia, has increasingly been associated with atypical organ involvement, including respiratory manifestations. These observations raise important questions regarding whether respiratory symptoms reflect severe systemic disease or signal previously underappreciated respiratory exposure routes. This review aimed to synthesize current evidence on respiratory complications of CHIKV infection and to evaluate the plausibility of respiratory or aerosol-associated transmission. A systematic literature search of PubMed, EMBASE, and MEDLINE (Ovid) identified five eligible studies spanning clinical virology, outbreak surveillance, epidemiology, and experimental aerosol models. Across human studies conducted in India, Réunion Island, Puerto Rico, and Brazil, respiratory presentations—including pneumonia, dyspnea, and respiratory failure—were uncommon but consistently associated with increased hospitalization and mortality risk. Respiratory symptoms generally arose in the context of respiratory viral coinfections, systemic inflammation, or cardiopulmonary decompensation rather than primary viral tropism for the respiratory tract. Only one non-human primate study directly evaluated aerosol exposure, demonstrating that cynomolgus macaques could be infected via inhaled CHIKV, confirming biological plausibility but showing no evidence of enhanced respiratory pathology. Importantly, no epidemiologic data support human-to-human airborne or droplet transmission. Collectively, available evidence indicates that respiratory involvement serves as a marker of disease severity rather than a transmission route. Nonetheless, rare aerosol-acquisition events in laboratory settings underscore the need for continued vigilance, strengthened surveillance, and re-evaluation of respiratory risks as climate change and viral evolution expand CHIKV’s global footprint. Full article

Severe treatment-resistant asthma (STRA) in children is often sustained by type 2 inflammation and eosinophil-dependent airway disease that persists despite optimized inhaled therapy and the mitigation of modifiable factors. This review summarizes the clinical and translational evidence on monoclonal antibodies targeting the interleukin-5 (IL-5) axis (anti-IL-5 and anti-IL-5Rα) available in pediatric severe asthma. PubMed/MEDLINE was searched up to January 2026 for English-language studies in patients aged 0–18 years addressing mepolizumab and benralizumab, including randomized trials, high-quality observational studies, meta-analyses, and international guidance. Mepolizumab has the most robust pediatric data, showing consistent reductions in exacerbations and blood eosinophils, and improvements in symptom control and quality of life, with safety broadly comparable to adults. The pediatric evidence for benralizumab is more limited but shows rapid eosinophil depletion, improved outcomes in selected children, and acceptable safety; further trials are ongoing. Overall, IL-5–directed biologics represent a key add-on option for carefully selected children with severe eosinophilic asthma, while pediatric-specific predictors of response, comparative effectiveness, and standardized long-term monitoring and stopping criteria remain priorities. Full article