Micro/nanoplastics (MNPs) are a commonly detected environmental contaminant in indoor and outdoor environments. Airborne MNPs are of various shapes and sizes, some of which are small enough to reach the deep lung if inhaled. Current research into the toxicity of airborne MNPs in the lung has only involved a small number of polymers and shapes due to their limited availability. The most commonly available are polystyrene spheres and to date, these have been used in the majority of studies, though their relevance to environmental MNPs is limited. To address this gap, we aimed to develop a method to fabricate MNPs of three environmentally relevant polymers, producing both micro- and nano-sized particles as well as fibres. Enhancing the consistency and accessibility of test materials will enable researchers to better investigate how size, shape, and polymer type influence lung toxicity, while also reducing variability introduced during fabrication.

Inhaled nanomaterials can translocate from the lungs into systemic circulation and reach the liver, which is the main secondary organ for nanomaterial uptake, potentially causing adverse effects. Understanding how inhaled nanomaterials localize within liver tissue is important for understanding their clearance mechanisms and potential toxicity. Previous in vivo studies have primarily focused on spherical particles, highlighting the need for studies on fiber-shaped nanomaterials.

The escalating accumulation of micro- and nanoplastics (MNPs) in the environment has raised significant concerns regarding their neurotoxic potential in vertebrates. This critical review synthesizes evidence from 234 original research articles across aquatic and terrestrial models, as well as in vitro systems, to evaluate the impacts of MNPs on the brain.

Inhaled black carbon (BC) has been previously shown to reach and accumulate in the kidneys. As kidneys filter toxicants, they may be susceptible to adverse effects caused by BC accumulation. We studied gene expressions and pathways related to BC particle load in kidney biopsy tissue.

Our previous work showed that exposure to multi-walled carbon nanotubes (MWCNTs) exacerbates allergic lung disease in mice induced by house dust mite extract (HDME). Furthermore, mice genetically deficient in the proteinase-activated receptor 2 (PAR2) exhibited reduced airway fibrosis after co-exposure to MWCNTs and HDME. The objective of this study was to determine whether inhibition of PAR2 signaling, using the monoclonal antibody SAM-11, attenuates MWCNT exacerbation of HDME-induced allergic lung disease.

Tin mine dust (MD), a by-product of tin mining and rock drilling, is a significant contributor to miners' pneumoconiosis. This aerosolized dust is a complex mixture of mineral components, including potentially toxic heavy metals such as arsenic, which may contribute to the development of pneumoconiosis and lung cancer. This study investigates the inhalation toxicity of tin MD samples on pulmonary cells using an Air-Liquid Interface (ALI) exposure model.

A growing body of epidemiological evidence links maternal exposure to air pollution with an increased risk of adverse pregnancy outcomes, such as preterm birth and low birth weight. Cerium dioxide nanoparticles (CeO NPs or nanoceria) are emerging pollutants, used as additives in diesel fuels and cigarettes for their catalytic properties, and released into the environment. Due to their high surface-to-volume ratio and reactivity, CeO NPs develop a surface coating during combustion, which may incorporate other released fuel-borne chemicals, such as benzo[a]pyrene (BaP), a known carcinogen, mutagen and reprotoxicant, raising concerns about their combined impacts on human health. To better reflect environmental reality, we produced BaP-coated CeO NPs and exposed primary human trophoblasts and chorionic villi. Our findings show that BaP-coated CeO NPs activate the aryl hydrocarbon receptor (AhR) pathway, enhancing trophoblast differentiation and syncytium formation, with effects distinct from those of BaP or CeO₂ NPs alone, or their unbound mixture. Additionally, exposure to CeO NPs alone altered homeostasis of mitochondria, affecting their phenotype and function. While individual exposures or BaP-coated CeO NPs had no detectable impact, parallel co-exposure resulted in a slight but significant reduction in basal respiration. Finally, uncoated CeO NPs altered placental steroidogenesis, increasing estrone level while decreasing dehydroepiandrosterone level, with sex-specific effects. These findings suggest that CeO NPs can influence the biological effects of BaP in the human placenta, including modulating trophoblast differentiation, as well as disrupting mitochondria homeostasis and steroid production, with potential implications for pregnancy outcomes in polluted environments.

Ambient air pollution is a major risk factor for CVDs, and a plausible mechanism is speculated to be alteration of autonomic nervous system (ANS) function. Yet, the short-term effects of air pollution on heart rate variability (HRV), a measure of ANS balance are inconsistent.

Nanoplastics (NPs) are emerging contaminants posing significant risks to human health due to their enhanced cellular penetration. NPs have been shown to damage human testes and epididymides, impairing male fertility. However, the specific testicular damage and underlying mechanisms induced by NPs at different ages have not been thoroughly investigated.

Air pollution, specifically fine particulate matter (PM), in China is responsible for millions of excess deaths each decade. Examinations of Chinese municipalities have revealed correlations between ambient PM levels and the prevalence and severity of respiratory viral infections. Seasonal sources of ambient PM vary, with coal combustion for indoor heating significantly contributing during colder months. Due to this seasonality, we hypothesized that PM collected in Xinxiang, China would differentially alter the response to subsequent influenza A/California/04/2009 (H1N1) viral infection in a primary human nasal epithelial cell (HNEC) culture model in a seasonality-specific manner. After the PM samples were chemically analyzed, HNECs collected from males (N = 4) and females (N = 3) grown at air-liquid interface were exposed to 22 µg/cm of seasonal PM followed by inoculation with influenza A H1N1 at MOI = 0.001. At 2 and 24 h post infection (p.i.) we assessed transcriptional changes and basolateral release of immune and antiviral mediators.

Wildland fires in the United States have increased in frequency and scale over the past 30 years exposing millions of people to hazardous air pollutants. Among others, aging individuals are particularly vulnerable to the effects of wildfire smoke. In this study, we assessed the neurobiological impacts of wood smoke (WS) on aged mice and the potential of anti-aging therapeutics to mitigate these impacts.

Subway systems reduce traffic congestion, air pollution, and carbon dioxide emissions in cities but the impacts of subway air pollution on the health of subway users remain obscure. We conducted a randomized controlled trial involving 83 healthy adults, with 80 included in the final analysis, randomly grouped to spend 2 h daily for 5 consecutive days either in an office or on a subway platform. The fine (PM) and thoracic (PM) particles concentrations, temperature, and humidity were monitored. Measurements of health parameters were assessed, including lung function and levels of fractional exhaled nitric oxide (FeNO), inflammatory and oxidative stress biomarkers, and metabolites in serum.

The field of fibre toxicology highlights a significant connection between the physicochemical properties of fibres-such as diameter, length, and durability-and their toxicity when inhaled. Among these properties, durability, particularly in terms of biopersistence and retention time in the lungs, is crucial in determining chronic toxicity. This understanding of fibre biopersistence is especially relevant to the regulation and safety assessment of Man-Made Vitreous Fibres (MMVF), also referred to in North American literature as Synthetic Vitreous Fibres (SVF). Despite its importance, current practices rely heavily on in vivo testing methods for evaluating biopersistence, which conflicts with the movement towards reducing animal testing and utilising new approach methodologies (NAMs) for hazard and risk assessment. In vitro assessments of biodurability have long been employed by the research community and industry alike to investigate the persistence of fibres in the lung, offering an alternative to reduce animal testing to evaluate this critical mediator of fibre toxicity. Here, we explore recent developments in acellular in vitro biodurability approaches for assessing fibre durability in the lung, addressing the variations and key challenges associated with using these methods to determine the safety of bio-soluble MMVF.

Exposure to air pollution has been increasingly recognized as a risk factor for neurodevelopmental disorders, and gut microbiome may play a critical role. However, current evidence still remains scarce. In the present study, mice were exposed to real-time ambient air pollution from conception through young adulthood, with neurobehavioral performance and gut microbiome being assessed across different developmental stages. Neurodevelopmental changes including emotional and cognitive impairments were observed in behavioral tests, accompanied by pathological and inflammation changes in brain, which were more pronounced in adolescence than in young adulthood. Alterations in the compositions and functions of gut microbiome were also revealed by fecal metagenomic sequencing. Mediation analysis showed that gut microbiome alterations significantly contributed to the observed neurodevelopmental changes induced by air pollution. Furthermore, after antibiotic (ABX) intervention, the observed neurobehavioral, pathological and inflammatory differences between the exposed and control groups diminished. These findings indicate that the gut microbiome mediates the neurodevelopmental damage caused by exposure to air pollution during developmental stages, adding novel insights on the underlying mechanisms linking air pollution and neurodevelopmental disorders.

Burn pits, a method for disposal of military waste outside the United States, produce toxic substances, to which 3.5 million military personnel have been and continue to be exposed. Mild asthma (persistent or intermittent symptoms of asthma but no change in pulmonary function tests) is found among military personnel. We investigated whether burn pit combustion products (CPs) are more detrimental to the airways of asthmatic than non-asthmatic mice.

The rise of microplastic (MPs) pollution presents a pressing environmental issue, raising concerns about its potential health impacts on human populations. Given the critical role of the liver in detoxification and metabolism, understanding the effects of MPs on the human hepatoma cell line HepG2 cells is essential for comprehensively assessing the dangers associated with MPs pollution to human health. Until now, the assessment of the harmful impact of polyethylene (PE) and polyethylene terephthalate (PET) on HepG2 has been incomplete and lacks certain essential data points. In this particular setting, we examined parameters such as cell viability, oxidative stress, mtDNA integrity, mitochondrial membrane potential, and autophagy in HepG2 cells exposed for 72 h to PET and PE at a concentration of 10 µg/mL. Our data revealed that exposure of HepG2 to MPs causes an increase in cell viability accompanied by a heightened ROS and altered mitochondrial function, as revealed by decreased mtDNA integrity and membrane potential. In addition, results demonstrated that exposure to PET and PE activated autophagic events, as suggested by the increased levels of the specific markers LC3 and p62. This last point was further confirmed using bafilomycin, a specific blocker that hinders the merging of autophagosomes and lysosomes, thereby blocking autophagic degradation processes. Given the increasing evidence of food chain MPs contamination and its possible harmful effects, our data should be carefully considered.

Multiple effects of ultrafine particles (UFP) on human subjects are known but there is less knowledge of how relative exposure levels between ultrafine and fine particles as typically encountered in large cities affect lung function and cardiovascular parameters.

The Safe and Sustainable by Design (SSbD) concept facilitates the design of safer and more sustainable chemicals and materials and is a crucial approach towards reaching the goals set out in the European Green Deal. It is critical that suitable guidance is provided on how to use new approach methodologies (NAMs) to fill hazard data gaps for nanomaterials (NMs) to facilitate SSbD decisions. Here, we showcase a nano-specific in vitro SSbD case study. The five colloidal silica nanoforms (SiO-NFs) under investigation in this study are surface modified with varying amounts of glycerolpropyl-organosilane groups. In this study, we use a simple yet comprehensive in vitro test battery along with thorough particle characterization to investigate the effect of surface silanization on in vitro toxicity to inform SSbD decisions.

While studies demonstrating the adverse effects of air pollution on human health are accumulating, studies on secondary organic aerosol (SOA) are scarce. However, SOA accounts for a significant portion of airborne particulate matter. In particular, pinene biogenic SOA contributes predominantly to SOA loading in the outdoor atmosphere of natural and urban areas and are also emitted indoors because of the presence of terpenes in numerous consumer products. Our aim was to study the immune consequences of acute exposure to β-pinene ozonolysis gaseous and SOA products in mice. This reaction was generated in an atmospheric simulation chamber, and the mice were exposed to the particulate and gaseous products, to the gaseous products only, or to synthetic air 2 h per day for 3 days in real time in a whole-body inhalation chamber. Exposures were performed in adulthood or in utero. Since some adverse effects only occur in individuals weakened by existing immune activation, such as low-grade inflammation, the immune response was measured in the steady state or in a state of moderate systemic inflammation induced by lipopolysaccharide administration.