Billions of disposable face masks are consumed daily due to the COVID-19 pandemic. The role of these masks as a source of nanoplastics (NPs) and microplastics (MPs) in the environment has not been studied in previous studies. We quantified and characterized face mask released particles and evaluated their potential for accumulation in humans and marine organisms. More than one billion of NPs and MPs were released from each surgical or N95 face mask. These irregularly-shaped particles sized from c. 5 nm to c. 600 μm. But most of them were nano scale sized <1 μm. The middle layers of the masks had released more particles than the outer and inner layers. That MPs were detected in the nasal mucus of mask wearers suggests they can be inhaled while wearing a mask. Mask released particles also adsorbed onto diatom surfaces and were ingested by marine organisms of different trophic levels. This data is useful for assessing the health and environmental risks of face masks.

Ambient particulate matter (PM) epidemiologically exacerbates respiratory and immune health, including allergic rhinitis (AR) and bronchial asthma (BA). Although fine and coarse particles can affect respiratory tract, the differences in their effects on the upper and lower respiratory tract and immune system, their underlying mechanism, and the components responsible for the adverse health effects have not been yet completely elucidated. In this study, ambient fine and coarse particles were collected at three different locations in Japan by cyclone technique. Both particles collected at all locations decreased the viability of nasal epithelial cells and antigen presenting cells (APCs), increased the production of IL-6, IL-8, and IL-1β from bronchial epithelial cells and APCs, and induced expression of dendritic and epithelial cell (DEC) 205 on APCs. Differences in inflammatory responses, but not in cytotoxicity, were shown between both particles, and among three locations. Some components such as Ti, Co, Zn, Pb, As, OC (organic carbon) and EC (elemental carbon) showed significant correlations to inflammatory responses or cytotoxicity. These results suggest that ambient fine and coarse particles differently affect nasal and bronchial epithelial cells and immune response, which may depend on particles size diameter, chemical composition and source related particles types.

Air pollution consists of a multi-faceted mix of gases and ambient particulate matter (PM) with diverse organic and non-organic chemical components that contribute to increasing morbidity and mortality worldwide. In particular, epidemiological and clinical studies indicate that respiratory health is adversely affected by exposure to air pollution by both causing and worsening (exacerbating) diseases such as chronic obstructive pulmonary disease (COPD), asthma, interstitial pulmonary fibrosis and lung cancer. The molecular mechanisms of air pollution-induced pulmonary toxicity have been evaluated with regards to different types of PM of various sizes and concentrations with single and multiple exposures over different time periods. These data provide a plausible interrelationship between cellular toxicity and the activation of multiple biological processes including proinflammatory responses, oxidative stress, mitochondrial oxidative damage, autophagy, apoptosis, cell genotoxicity, cellular senescence and epithelial-mesenchymal transition. However, these molecular changes have been studied predominantly in cell lines rather than in primary bronchial or nasal cells from healthy subjects or those isolated from patients with airways disease. In addition, they have been conducted under different cell culture conditions and generally in submerged culture rather than the more relevant air-liquid interface culture and with a variety of air pollutant exposure protocols. Cell types may respond differentially to pollution delivered as an aerosol rather than being bathed in media containing agglomerations of particles. As a result, the actual pathophysiological pathways activated by different PMs in primary cells from the airways of healthy and asthmatic subjects remains unclear. This review summarises the literature on the different methodologies utilised in studying the impact of submicron-sized pollutants on cells derived from the respiratory tract with an emphasis on data obtained from primary human cell. We highlight the critical underlying molecular mechanisms that may be important in driving disease processes in response to air pollution in vivo.

Studies of polycyclic aromatic hydrocarbons (PAHs) and its metabolites in PM10, soils, rat livers and cattle urine in Kumasi, Ghana, revealed high concentrations and cancer potency. In addition, WHO and IARC have reported an increase in cancer incidence and respiratory diseases in Ghana. Human urine were therefore collected from urban and control sites to: assess the health effects associated with PAHs exposure using malondialdehyde (MDA) and 8-hydroxy-2-deoxyguanosine (8-OHdG); identify any association between OH-PAHs, MDA, 8-OHdG with age and sex; and determine the relationship between PAHs exposure and occurrence of respiratory diseases. From the results, urinary concentrations of the sum of OH-PAHs (∑OHPAHs) were significantly higher from urban sites compared to the control site. Geometric mean concentrations adjusted by specific gravity, GMSG, indicated 2-OHNaphthalene (2-OHNap) (6.01 ± 4.21 ng/mL) as the most abundant OH-PAH, and exposure could be through the use of naphthalene-containing-mothballs in drinking water purification, insect repellent, freshener in clothes and/or “treatment of various ailments”. The study revealed that exposure to naphthalene significantly increases the occurrence of persistent cough (OR = 2.68, CI: 1.43–5.05), persistent headache (OR = 1.82, CI: 1.02–3.26), tachycardia (OR = 3.36, CI: 1.39–8.10) and dyspnea (OR = 3.07, CI: 1.27–7.43) in Kumasi residents. Highest level of urinary 2-OHNap (224 ng/mL) was detected in a female, who reported symptoms of persistent cough, headache, tachycardia, nasal congestion and inflammation, all of which are symptoms of naphthalene exposure according to USEPA. The ∑OHPAHs, 2-OHNap, 2-3-OHFluorenes, and -OHPhenanthrenes showed a significantly positive correlation with MDA and 4-OHPhenanthrene with 8-OHdG, indicating possible lipid peroxidation/cell damage or degenerative disease in some participants. MDA and 8-OHdG were highest in age group 21–60. The present study showed a significant sex difference with higher levels of urinary OH-PAHs in females than males.

Triphenyl phosphate (TPHP) is a frequently used flame retardant and indoor semi-volatile pollutant exposing humans with endocrinal disrupting effects. However, its respiratory tract toxicity remains unclear. Herein, we mainly focused on exploring the cytotoxicity of TPHP to the cells from five different parts of the human respiratory tract (from top to bottom): human nasal epithelial (HNEpC) cells, human bronchial epithelial (16HBE) cells, normal nasopharyngeal epithelial (NP69) cells, human lung epithelial cells (Beas-2B) cells, and human lung fibrocells (HFL1 cells) cells. The cell viability, micronucleus induction, endoplasmic reticulum stress gene, intracellular Ca²⁺ concentration, mitochondrial membrane potential (MMP) were investigated in short-term as well as extended exposure of TPHP. HFL1 and HNEpC cells were found to be irreversible damage, while other three type cells achieved homeostasis through self-rescue. Moreover, expression of downstream genes of Nrf2 signaling pathway were upregulated for 1.3–7.0 times and glutathione detoxification enzyme activity changed for 2–10 (U/mg protein) in HNEpC cells. Furthermore, the vascular endothelial growth factor (VEGF), a disease-related factor, increased 1.0–3.5-fold in HNEpC cells. RNA-sequencing results suggested that protein linkage recombination, molecular function regulation and metabolic processes signal pathway were all affected by TPHP exposure in HNEpC. This is a first report to compare respiratory cytotoxicity in whole human respiratory tract under OPFR exposure and found HNEpC cells were the most sensitive target of TPHP. Molecular biological mechanisms uncovered that TPHP exposure in HNEpC can induce the activation of MAPK signal pathway and demonstrate potential respiratory growth differentiation and stress disorder in human nasal cells upon TPHP exposure.

PM₂.₅ (particulate matter ≤2.5 μm in aerodynamic diameter) is a major urban air pollutant worldwide. Its effects on the respiratory system of the susceptible population have been less characterized. This study aimed to estimate the association of short-term PM₂.₅ exposure with respiratory outcomes of the retired adults, and to examine whether these associations were stronger among the subjects with GSTT-null genotype. 32 healthy subjects (55–77 years) were recruited for five follow-up examinations. Ambient concentrations of PM₂.₅ were monitored consecutively for 7 days prior to physical examination. Pulmonary outcomes including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV₁), peak expiratory flow (PEF), and fractional exhaled nitric oxide (FeNO), and nasal fluid concentrations of 8-epi-prostaglandin F2 alpha (8-epi-PGF2α), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and IL-1β were measured. A linear mixed-effect model was introduced to evaluate the associations of PM₂.₅ concentrations with respiratory outcomes. Additionally, GSTT1 genotype-based stratification was performed to characterize modification on PM₂.₅-related respiratory outcomes. We found that a 10 μg/m³ increase in PM₂.₅ was associated with decreases of 0.52 L (95% confidence interval [CI]: -1.04, -0.002), 0.64 L (95% CI: -1.13, -0.16), 0.1 (95% CI: -0.23, 0.04) and 2.87 L/s (95% CI: -5.09, -0.64) in FVC, FEV₁, FEV₁/FVC ratio and PEF at lag 2, respectively. Meanwhile, marked increases of 80.82% (95% CI: 5.13%, 156.50%) in IL-8, 77.14% (95% CI: 1.88%, 152.40%) in IL-1β and 67.87% (95% CI: 14.85%, 120.88%) in 8-epi-PGF2α were observed as PM₂.₅ concentration increased by 10 μg/m³ at lag 2. Notably, PM₂.₅-associated decreases in FVC and PEF and increase in FeNO were stronger among the subjects with GSTT1-null genotype. In summary, short-term exposure to PM₂.₅ is associated with nasal inflammation, oxidative stress and lung function reduction in the retired subjects. Lung function reduction and inflammation are stronger among the subjects with GSTT1-null genotype.

Due to their small dimensions, airborne particles are able to penetrate through inhalation into many human organs, from the lungs to the cardiovascular system and the brain, which can threaten our health. This work establishes a novel approach of collecting quantitative data regarding the fraction, the composition and the size distribution of combustion-emitted particulate matter through the magnetic characterization and analysis of samples received by common air pollution monitoring. To this end, SQUID magnetometry measurements were carried out for samples from urban and suburban areas in Thessaloniki, the second largest city of Greece, taking into consideration the seasonal and weekly variation of airborne particles levels as determined by occurring traffic and meteorological conditions. The level of estimated magnetically-responding atmospheric particulate matter was at least 0.5 % wt. of the collected samples, mostly being present in the form of ultrafine particles with nuclei sizes of approximately 14 nm and their aggregates. The estimated quantities of magnetic particulate matter show maximum values during autumn months (0.8 % wt.) when increased commuting takes place, appearing higher in the city center by up to 50% than those in suburban areas. In combination with high-resolution transmission electron imaging and elemental analysis, it was found that Fe₃O₄ and similar ferrites, some of them attached to heavy metals (Co, Cr), are the dominant magnetic contributors arising from anthropogenic high-temperature processes, e.g. due to traffic emissions. Importantly, nasal cytologic samples collected from residents of both central and suburban areas showed same pattern in what concerns magnetic behavior, thus verifying the critical role of nanosized magnetic particles in the assessment of air pollution threats. Despite the inherent statistical limitations of our study, such findings also indicate the potential transmission of infectious pathogens by means of pollution-derived nanoparticles into the respiratory system of the human body.

The green turtle (Chelonia mydas) is listed as a globally endangered species and is vulnerable to anthropogenic threats, including environmental pollution. This study investigated the antimicrobial resistance of Gram-negative bacteria isolated from wild green turtles admitted to a sea turtle rehabilitation center in Taiwan. For this investigation, cloacal and nasal swab samples were collected from 28 green turtles between 2018 and 2020, from which a total of 47 Gram-negative bacterial isolates were identified. Among these, Vibrio spp. were the most dominant isolate (31.91%), and 89.36% of the 47 isolates showed resistance to at least one of 18 antimicrobial agents tested. Isolates resistant to one (6.38%), two (8.51%), and multiple (74.47%) antimicrobials were observed. The antimicrobial agents to which isolates showed the greatest resistance were penicillin (74.47%), followed by spiramycin, amoxicillin, and cephalexin. The antimicrobial-resistance profiles identified in this study provide useful information for the clinical treatment of sea turtles in rehabilitation facilities. The results of our study also imply that wild green turtles may be exposed to polluting effluents containing antimicrobials when the turtles traverse migratory corridors or forage in feeding habitats. To benefit sea turtle conservation, future research should focus on (1) how to prevent pollution from antimicrobials in major green turtle activity areas and (2) identifying sources of antimicrobial-resistant bacterial strains in coastal waters of Taiwan.

Tight junctions (TJs) in the epithelium play a critical role in the formation of a paracellular epithelial barrier against the extracellular environment. Diesel exhaust particles (DEPs) disrupt the epithelial barrier. The aim of this study was to investigate how DEPs disrupt the epithelial barrier and whether Toll-like receptor 4 (TLR4) is involved in DEP-induced epithelial barrier dysfunction in primary human nasal epithelial (PHNE) cells.PHNE cells were cultured at an air–liquid interface (ALI) to create a fully differentiated in vivo-like model of the epithelium and then exposed to DEPs (particulate matter <4 μm) or lipopolysaccharide (LPS) alone (mono-exposure) and DEPs plus LPS (co-exposure) at the apical side of the PHNE. TJ formation and integrity were monitored by measuring transepithelial electric resistance (TEER) and fluorescently labeled dextran permeability. The expression of TJ proteins was assessed by confocal microscopy and a biochemical assay.PHNE cell viability was reduced in a time- and dose-dependent manner following DEP exposure. TEER was significantly decreased at ALI day 20 but not at day 12 following DEP exposure. The dextran permeability of the PHNE was significantly increased at both ALI day 12 and day 20 following DEP exposure. The increased dextran permeability recovered to that of the control following co-exposure to DEPs plus LPS. In the presence of DEPs, the membrane expression of myosin light chain kinase (MLCK) was dramatically increased, and the expression of occludin, ZO1, claudin-1, and E-cadherin was significantly decreased. Co-exposure to DEPs plus LPS significantly reduced membrane MLCK, claudin-1, and E-cadherin but increased occludin and ZO1 expression at ALI day 12.The activation of TLR4 by LPS inhibits MLCK trafficking to the plasma membrane, and this increased during DEP exposure, resulting in increased occludin expression at the plasma membrane that partially recovered TJ barrier dysfunction following DEP exposure.

Gasification and pyrolysis technologies have been widely employed to produce fuels and chemicals from solid wastes. Rare studies have been conducted to compare the particulate emissions from gasification and pyrolysis, and relevant inhalation exposure assessment is still lacking. In this work, we characterized the particles emitted from the gasification and pyrolysis experiments under different temperatures (500, 600, and 700 °C). The collection efficiencies of existing cyclones were compared based on particle respiratory deposition. Sensitivity analysis was conducted to identify the most effective design parameters. The particles emitted from both gasification and pyrolysis process are mainly in the size range 0.25–1.0 μm and 1.0–2.5 μm. Particle respiratory deposition modelling showed that most particles penetrate deeply into the last stage of the respiratory system. At the nasal breathing mode, particles with sizes ranging from 0.25 to 1.0 μm account for around 91%, 74%, 76%, 90%, 84%, and 79% of the total number of particles that deposit onto the last stage in the cases of 500 °C gasification, 600 °C gasification, 700 °C gasification, 500 °C pyrolysis, 600 °C pyrolysis, and 700 °C pyrolysis, respectively. At the oral breathing mode, particles with sizes ranging from 0.25 to 1.0 μm account for around 92%, 77%, 79%, 91%, 86%, and 81% of the total number of particles that deposit onto the last stage in the six cases, respectively. Sensitivity analysis showed that the particle removal efficiency was found to be most sensitive to the cyclone vortex finder diameter (D₀). This work could potentially serve as the basis for proposing health protective measures against the particulate pollution from gasification and pyrolysis technologies.