Fine particulate matter (PM₂.₅) has been associated with risk of oral and respiratory diseases. However, the biological mechanisms of adverse oral and respiratory health response to PM₂.₅ fluctuation have not been well characterized. This study aims to explore the relationships of PM₂.₅ with airway inflammation, salivary biomarkers and buccal mucosa microbiota. We performed a panel study among 40 college students involving 4 follow-ups from August to October 2021 in Hefei, Anhui Province, China. Health outcomes included fractional exhaled nitric oxide (FeNO), salivary biomarkers [C-reactive protein (CRP), cortisol, lysozyme and alpha-amylase] and buccal mucosa microbial diversity. Linear mixed-effect models were applied to explore the cumulative impacts of PM₂.₅ on health indicators. PM₂.₅ was positively correlated with FeNO, CRP, cortisol and alpha-amylase, while negatively with lysozyme. Per 10-μg/m³ increase in PM₂.₅ was linked to maximum increments in FeNO of 10.71% (95%CI: 2.01%, 19.41%) at lag 0–24 h, in CRP of 7.10% (95%CI: 5.39%, 8.81%) at lag 0–24 h, in cortisol of 1.25% (95%CI: 0.44%, 2.07%) at lag 0–48 h, and in alpha-amylase of 2.12% (95%CI: 0.53%, 3.71%) at lag 0–24 h, while associated with maximum decrement in lysozyme of 0.53% (95%CI: 0.12%, 0.95%) at lag 0–72 h. Increased PM₂.₅ was linked to reduction in the richness and evenness of buccal microbe and o_Bacillales and o_Bacteroidales were identified as differential microbes after PM₂.₅ inhalation. Bio-information analysis indicated that immunity system pathway was the most important enriched abundant process altered by PM₂.₅ exposure. In summary, short-term PM₂.₅ exposure may impair oral and respiratory health by inducing inflammatory and stress responses, weakening immune function and altering buccal mucosa microbial diversity.

Construction workers on highway rehabilitation projects can be exposed to a combination of traffic- and construction-related emissions. To assess the personal exposure a worker experiences, a portable battery-operated Air Quality Device (AQD) was utilised to measure emissions during normal construction operations of a major road rehabilitation project. Emissions measured were nitrogen dioxide (NO₂), Total Volatile Organic Compounds (TVOCs) and Particulate Matter (PM₁₀, PM₂.₅, and PM₁). The objective of the paper is to document the hazardous emissions that construction workers may be exposed to and allow for a basis of informed decision making to mitigate the risks of a road construction project. Most critically, this article is designed to raise awareness of the potential impact to a worker's wellbeing as well as highlight the need for further research. Through statistical analysis, asphalt paving was identified as the most hazardous activity in terms of exposure relative to other activities. This activity was further assessed using discrete-time Markov chain Monte Carlo simulations with results indicating a high probability that workers may be exposed to greater hazardous emission concentrations than measured. Limiting the distance to the source of emissions, large-scale use of warm-mix asphalt and reducing the idling times of construction vehicles were identified as practical mitigation measures to reduce exposure and aid in achieving zero-harm objectives. Finally, it is found that males are more susceptible to long-term implications of hazardous emission inhalation and should be more aware if the scenarios they might work in expose them to this.

Inhalation exposure to fine particulate matter (PM₂.₅) represents a global concern due to the adverse effects in human health. In the last years, scientific community has been adopted the assessment of the PM₂.₅-bound pollutant fraction that could be released (bioaccessible fraction) in simulated lung fluids (SLFs) to achieve a better understanding of PM risk assessment and toxicological studies. Thus, bioaccessibility of 49 organic pollutants, including 18 polycyclic aromatic hydrocarbons (PAHs), 12 phthalate esters (PAEs), 11 organophosphorus flame retardants (OPFRs), 6 synthetic musk compounds (SMCs) and 2 bisphenols in PM₂.₅ samples was evaluated. The proposed method consists of a physiologically based extraction test (PBET) by using artificial lysosomal fluid (ALF) to obtain bioaccessible fractions, followed by a vortex-assisted liquid-liquid microextraction (VALLME) and a final analysis by programmed temperature vaporization-gas chromatography-tandem mass spectrometry (PTV-GC-MS/MS). The highest inhalation bioaccessibility ratio was found for bisphenol A (BPA) with an average of 83%, followed by OPFRs, PAEs and PAHs (with average bioaccessibilities of 68%, 41% and 34%, respectively). Correlations between PM₂.₅ composition (major ions, trace metals, equivalent black carbon (eBC) and UV-absorbing particulate matter (UVPM)) and bioaccessibility ratios were also assessed. Principal Component Analysis (PCA) suggested that PAHs, PAES and OPFRs bioaccessibility ratios could be positively correlated with PM₂.₅ carbonaceous content. Furthermore, both inverse and positive correlations on PAHs, PAEs and OPFRs bioaccessibilites could be accounted for some major ions and metal (oid)s associated to PM₂.₅, whereas no correlations comprising considered PM₂.₅ major ions and metal (oid)s contents and BPA bioaccessibility was observed. In addition, health risk assessment of target PM₂.₅-associated PAHs via inhalation was assessed in the study area considering both total and bioaccessible concentrations, being averaged human health risks within the safe carcinogenic and non-carcinogenic levels.

Several recent studies have looked into the differences in air qualities inside popular commute modes. The impact of daily commuting patterns and work-related trips on inhalation doses, however, are not investigated. The purpose of this study is to quantify the variation in air pollutants within popular commute modes in Mumbai, India, and to estimate the variation in exposure as a result of occupational or work-related trips across different sub-groups. Real-time pollutants, both gaseous and particulate matters (PM), were measured on a pre-defined route during rush and non-rush hours on buses, cars, auto-rickshaws, sub-urban trains, and motorbikes through several trips (N = 98). Household surveys were conducted to estimate the exposures of different occupational subgroups (cab-driver, auto-rickshaw drivers, delivery persons) and people commuting to their offices daily. Participants (N = 800) from various socioeconomic backgrounds in the city were asked about their job categories, work-activity patterns, and work-related commute trips. Mass concentrations of particles in different size ranges (PM₁, PM₂.₅, and PM₁₀) were substantially higher (p < 0.05) inside auto-rickshaws (44.6 μg/m³, 84.7 μg/m³, and 138.3 μg/m³) compared to other modes. Inside cars, gaseous pollutants such as carbon monoxide (CO) and total volatile organic compounds (TVOC) were significantly higher (p < 0.05). Although both gaseous and particulate concentrations were lower (p < 0.05) inside buses, bus-commuters were found to be highly exposed to the pollutants due to the extended trip time (∼1.2 times longer than other modes) and driving conditions. Office commuters inhale a large fraction of their daily doses (25–30%) during their work-related travel. Occupational sub-groups, on the other hand, inhale ∼90% of the pollutants during their work. In a day, an auto-rickshaw driver inhales 10–15% more (p < 0.05) pollutants than cab driver or delivery personnel. Therefore, this study highlights the inequalities in occupational exposure as a combined effect of in-cabin air qualities and commute patterns due to occupational obligations.

Atmospheric bioaerosols contain live and dead biological components that can enter the human respiratory tract (HRT) and affect human health. Here, the total microorganisms in a coastal megacity, Qingdao, were characterized on the basis of long-term observations from October 2013 to January 2021. Particular attention was given to the size dependence of inhalable bioaerosols in concentration and respiratory deposition in different populations on foggy and hazy days. Bioaerosol samples stained with 4,6-diamidino-2-phenylindole (DAPI) were selected to measure the total airborne microbe (TAM) concentrations with an epifluorescence microscope, while a multiple-path particle dosimetry model was employed to calculate respiratory deposition. The mean TAM concentrations in the particle size range of 0.65–1.1 μm (TAM₀.₆₅–₁.₁) were 1.23, 2.02, 1.60 and 2.33 times those on sunny reference days relative to the corresponding values on days with slight, mild, moderate and severe levels of haze, respectively. The mean concentration of TAMs in the particle size range of 0.65–2.1 μm (TAM₀.₆₅–₂.₁) on severely hazy days was (2.02 ± 3.28) × 10⁵ cells/m³, with a reduction of 4.16% relative to that on the reference days. The mean TAM₀.₆₅–₂.₁ concentration changed from (1.50 ± 1.37) × 10⁵ cells/m³ to (1.76 ± 1.36) × 10⁵ cells/m³, with TAM₀.₆₅–₁.₁ increasing from (7.91 ± 7.97) × 10⁴ cells/m³ to (1.76 ± 1.33) × 10⁵ cells/m³ on days with light fog days and medium fog, respectively. The modeling results showed that the majority of TAM₀.₆₅–₂.₁ deposition occurred in the extrathoracic (ET) region, followed by the alveolar (AL) region. When different populations were examined separately, the deposition doses (DDs) in adult females and in children ranked at the minimum value (6.19 × 10³ cells/h) and maximum value (1.08 × 10⁴ cells/h), respectively. However, the inhalation risks on polluted days, such as hazy, foggy and mixed hazy–foggy (HF) days, were still below the threshold for adverse impacts on human health.

This international scale study measured the prevalence of indoor microplastics (MPs) in deposited dust in 108 homes from 29 countries over a 1-month period. Dust borne MPs shape, colour, and length were determined using microscopy and the composition measured using μFTIR. Human health exposure and risk was assessed along with residential factors associated with MPs via a participant questionnaire. Samples were categorised according to each country's gross national income (GNI). Synthetic polymers dominated in low income (LI) (39%) and high income (HI) (46%) while natural fibres were the most prevalent in medium income (MI) (43%) countries. Composition and statistical analysis showed that the main sources of MPs and dust were predominantly from indoor sources. Across all GNI countries, greater vacuuming frequency was associated with lower MPs loading. High income country samples returned higher proportions of polyamides and polyester fibres, whereas in LI countries polyurethane was the most prominent MPs fibre. Exposure modelling showed infants (0–2 years) were exposed to the highest MPs dose through inhalation (4.5 × 10⁻⁵ ± 3 × 10⁻⁵) and ingestion (3.24 × 10⁻² ± 3.14 × 10⁻²) mg/kg-Bw/day. Health risk analysis of constituent monomers of polymers indicates cancer incidence was estimated at 4.1–8.7 per million persons across age groups. This study's analysis showed socio-economic factors and age were dominant variables in determining dose and associated health outcomes of MPs in household dust.

Legionella species are the etiological agent of Legionnaires' disease, a pathology easily contracted from water circuits and by the inhalation of aerosol droplets. This bacterium mainly proliferates in water: Legionella pneumophila is the most commonly isolated specie in water environments and consequently in water system, although further Legionella species have frequently been isolated, including Legionella dumoffii. The simultaneous presence of the two species in the water system can therefore lead to the simultaneous infection of several people, giving rise to harmful outbreaks. Ultraviolet inactivation of waterborne microorganisms offers a rapid and effective treatment technique and recently is getting more attention mostly to eliminate unsafe level of contamination. To tackle the issue, the inactivation of the two species of Legionella spp., namely L. pneumophila and L. dumoffii, by means of UV-A light emitting diodes (UV-A LED) system is explored. We used a commercially available UV-A LED at 365 nm wavelength, and the UV-A dose is given incrementally to the Legionellae with a concentration of 10⁶ CFU/mL in 0.9% NaCl (aq) solution. In this study, with a UV-A-dose of 1700 mJ/cm², the log-reduction of 3-log (99.9% inactivation) for L. pneumophila and 2.1-log (99.1% inactivation) for L. dumoffii of the contaminated water are achieved. The Electrical Energy per Order (EEO) is evaluated and showed this system is more economic and efficient in comparison with UV-C and UV-B LEDs. Following the support of this preliminary study with additional tests, aiming to validate the technology, we expect this device may be installed in water plants such as cooling systems or any water purification station in either industrial or home scales to reduce the risk of this infectious disease, preventing consumers' health.

Single-chemical thresholds cannot comprehensively evaluate the risk of chemical mixture exposure in indoor air. Moreover, a large number of researches have focused on short-term and high-concentration co-exposure scenarios related to different species, based on diverse endpoints, which hampers the application and improvement of existing risk evaluation models of chemical mixture exposures. More importantly, current risk evaluation models are not user-friendly for construction practitioners who do not have sufficient toxicological knowledge. Therefore, in this study, an inhalation experiment system and a hazard index (HI) were developed to investigate the risks associated with low-concentration and long-term inhalation exposure scenarios of formaldehyde and benzene, individually and combined, based on Drosophila melanogaster mortality. The results showed that the system exhibited good reproducibility in providing stable exposure concentrations during D. melanogaster life cycle. Furthermore, in a range of experimental concentrations, the interaction between formaldehyde and benzene was additive or synergistic, which was concentration- and ratio-dependent. This study is of great significance in harmonising and providing toxicity data under long-term and low-concentration exposure scenarios, which is beneficial for establishing a new user-friendly risk evaluation model for indoor chemical mixture exposures. It should be noted that the proposed HI value could indicate the hazard degrees of long-term inhalation exposures of formaldehyde and benzene, individually and combined, to D. melanogaster. However, the applicability of this index requires further experiments to evaluate the exposure risks of other volatile organic compounds (VOCs) to D. melanogaster.

In recent years, the cardiovascular toxicity of urban fine particulate matter (PM₂.₅) has sparked significant alarm. Mitochondria produce 90% of ATP and make up 30% of the volume of cardiomyocytes. Thus knowledge of myocardial mitochondrial dysfunction due to PM₂.₅ exposure is essential for further cardiotoxic effects. Here, the mechanism of PM₂.₅-induced cardiac hypertrophy through calcium overload and mitochondrial dysfunction was investigated in vivo and in vitro. Male and female BALB/c mice were given 1.28, 5.5, and 11 mg PM₂.₅/kg bodyweight weekly through oropharyngeal inhalation for four weeks and were assigned to low, medium, and high dose groups, respectively. PM₂.₅-induced myocardial edema and cardiac hypertrophy were detected in the high-dose group. Mitochondria were scattered and ruptured with abnormal ultrastructural morphology. In vitro experiments on human cardiomyocyte AC16 showed that exposure to PM₂.₅ for 24 h caused opened mitochondrial permeability transition pore --leading to excessive calcium production, decreased mitochondrial membrane potential, weakened mitochondrial respiratory metabolism capacity, and decreased ATP production. Nevertheless, the administration of calcium chelator ameliorated the mitochondrial damage in the PM₂.₅-treated group. Our in vivo and in vitro results confirmed that calcium overload under PM₂.₅ exposure triggered mTOR/AKT/GSK-3β activation, leading to mitochondrial bioenergetics dysfunction and cardiac hypertrophy.

Silicosis is a disease mainly caused by pulmonary interstitial fibrosis caused by long-term inhalation of dust with excessively high content of free SiO₂. Transdifferentiation of lung fibroblasts into myofibroblasts is an important cellular basis for silicosis, but the key transcription factors (TFs) involved in this process are still unclear. In order to explore the biological regulation of transcription factor PPARγ/LXRα in silica-induced pulmonary fibrosis, this study explored the molecular mechanism of PPARγ/LXRα involved in regulating transcription factors related to SiO₂-induced lung injury at the cellular level and in animal models. ChIP-qPCR detected that PPARγ directly regulated the transcriptional activity of the LXRα gene promoter, while the PPARγ agonist RSG increased the expression of LXRα. In addition, we demonstrated in the cell model that upregulation of LXRα can inhibit silica-mediated fibroblast transdifferentiation, accompanied by an increase in the expression of SREBF1, PLTP and ABCA1. The results of LXRα silencing experiment matched those of overexpression experiment. These studies explored the role of LXRα in plasticity and phenotypic transformation between lung fibroblasts and myofibroblasts. Therefore, inhibiting or reversing the transdifferentiation of lung fibroblasts to myofibroblasts by intervening PPARγ/LXRα may provide a new therapeutic target for the treatment of silicosis.