Inhalation of respirable silica particles can cause serious lung diseases (e.g., silicosis and lung cancer), and the toxicity of respirable silica is highly dependent on its crystal form. Common combustion processes such as coal and biomass burning can provide high temperature environments that may alter the crystal forms of silica and thus affect its toxic effects. Although crystalline silica (i.e., quartz, tridymite, and cristobalite) were widely found at different temperatures during the burning processes, the sources and crystal transformation pathways of silica in the burning processes are still not well understood. Here, we investigate the crystal transformation of silica in the coal and biomass combustion processes and clarify the detailed transformation pathways of silica for the first time. Specifically, in coal burning process, amorphous silica can transform into quartz and cristobalite starting at 1100 °C, and quartz transforms into cristobalite starting at 1200 °C; in biomass burning process, amorphous silica can transform into cristobalite starting at 800 °C, and cristobalite transforms into tridymite starting at 1000 °C. These transformation temperatures are significantly lower than those predicted by the classic theory due to possibly the catalysis of coexisting metal elements (e.g., aluminum, iron, and potassium). Our results not only enable a deeper understanding on the combustion-induced crystal transformation of silica, but also contribute to the mitigation of population exposure to respirable silica.

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 is the most frequent route and the lung is the primary damaged organ for human exposure to benzene, toluene, ethylbenzene, xylene, and styrene (BTEXS). However, there is limited information on the risk and dose-effect of the BTEXS mixture on pulmonary function, particularly the overall effect. We conducted a cross-sectional study in a petrochemical plant in southern China. Spirometry and cumulative exposure dose (CED) of BTEXS were used to measure lung function and exposure levels for 635 workers in 2020, respectively. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV₁) were tested and interpreted as percentages to predicted values [FVC or FEV₁% predicted], and FEV₁ to FVC ratio [FEV₁/FVC (%)]. We found the reduction in FVC% predicted and the risk of lung ventilation dysfunction (LVD) and its two subtypes (mixed and restrictive ventilation dysfunction, MVD, and MVD) were significantly associated with BTEXS individuals. In addition, pulmonary function damage associated with BTEXS was modified by the smoking status and age. Generalized weighted quantile sum (gWQS) regressions were used to estimate the overall dose-effect on lung function damage induced by the BTEXS mixture. Our results show wqs, an index of weighted quartiles for BTEXS, was potentially associated with the reduction in FVC and FEV₁% predicted with the coefficients [95% confidence intervals (CI)] between −1.136 (−2.202, −0.070) and −1.230 (−2.265, −0.195). Odds ratios (ORs) and 95% CIs for the wqs index of LVD, MVD, and RVD were 1.362 (1.129, 1.594), 1.323 (1.084, 1.562), and 1.394 (1.096, 1.692), respectively. Furthermore, xylene, benzene, and toluene in the BTEXS mixture potentially contribute to the development of lung function impairment. Our novel findings demonstrated the dose-response relationships between pulmonary function impairment and the BTEXS mixture and disclosed the potential key pollutants in the BTEXS mixture.

The adverse health effects associated with the inhalation and ingestion of naturally occurring radon gas produced during the uranium decay chain mean that there is a need to identify high-risk areas. This study detected radon-prone areas using a geographic information system (GIS)-based probabilistic and machine learning methods, including the frequency ratio (FR) model and a convolutional neural network (CNN). Ten influencing factors, namely elevation, slope, the topographic wetness index (TWI), valley depth, fault density, lithology, and the average soil copper (Cu), calcium oxide (Cao), ferric oxide (Fe₂O₃), and lead (Pb) concentrations, were analyzed. In total, 27 rock samples with high activity concentration index values were divided randomly into training and validation datasets (70:30 ratio) to train the models. Areas were categorized as very high, high, moderate, low, and very low radon areas. According to the models, approximately 40% of the study area was classified as very high or high risk. Finally, the radon potential maps were validated using the area under the receiver operating characteristic curve (AUC) analysis. This showed that the CNN algorithm was superior to the FR method; for the former, AUC values of 0.844 and 0.840 were obtained using the training and validation datasets, respectively. However, both algorithms had high predictive power. Slope, lithology, and TWI were the best predictors of radon-affected areas. These results provide new information regarding the spatial distribution of radon, and could inform the development of new residential areas. Radon screening is important to reduce public exposure to high levels of naturally occurring radiation.

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.

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.

Airborne microplastics (MPs) have recently drawn the attention of the scientific community due to their possible human inhalation risk. Indoor environments are of relevance as people spend about 90% of their time indoors. This study evaluated MPs concentrations in three indoor environments: houses, public transport and working places, which are representative of urban life. Sampling involved the collection of airborne particulate matter on nylon 20 μm pore size filters. Samples were first visually inspected, and particles were characterized (colour, length or area). Polymer identification was performed through μFTIR analysis. Working conditions were controlled to guarantee quality assurance and avoid background contamination. Limits of detection, recovery tests and repeatability were performed with home-made polyethylene (PE), polypropylene (PP), and polystyrene (PS) standards. The highest average MP concentrations were found in buses (17.3 ± 2.4 MPs/m³) followed by 5.8 ± 1.9 MPs/m³ in subways, 4.8 ± 1.6 MPs/m³ in houses, and 4.2 ± 1.6 MPs/m³ in the workplaces. Polyamide, PA (51%), polyester PES (48%) and PP (1%) were the polymers identified and most common in personal care products and synthetic textiles. Most of these polymers were below 100 μm in size for both fibres (64 ± 8%) and fragments (78 ± 11%). The frequency of MP particles in our study decreased with increasing size, which points to their potential as an inhalation hazard.

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.

Limited attention has been given to the presence of MPs in the atmospheric environment, particularly in indoor environments where people spend about 90% of their time. This study quantitatively assesses the prevalence, source and type of MPs in Australian homes with the goal of evaluating human health exposure potential. Thirty-two airborne indoor deposited dust samples were collected in glass Petri dishes from Sydney (Australia) homes, over a one-month period in 2019. Participants completed a questionnaire on their household characteristics. Samples were analysed using a stereomicroscope, a fluorescent microscope and micro-Fourier transform infrared (FTIR) spectroscopy for their colour, size, shape and composition. Inhalation and ingestion rates were modelled using US EPA exposure factors. Microplastic fibre deposition rates ranged from 22 to 6169 fibres/m²/day. Deposited dust comprised 99% fibres. The highest proportion of fibres (19%) were 200–400 μm in length. The majority were natural (42%); 18% were transformed natural-based fibres; and 39% were petrochemical based. A significant difference was observed between the deposition rate and the main floor covering (p-value <0.05). Polyethylene, polyester, polyamide, polyacrylic, and polystyrene fibres were found in higher abundance in homes with carpet as the main floor covering. Where carpet was absent, polyvinyl fibres were the most dominant petrochemical fibre type, indicating the role of flooring materials (e.g. wood varnishes) in determining MP composition. Vacuum cleaner use was significantly related to MP deposition rates (p-value <0.05). MP ingestion rates peaked at 6.1 mg/kg-Bw/year for ages 1–6, falling to a minimum of 0.5 mg/kg-Bw/year in >20 years age group. Mean inhaled MP weight and count was determined to be 0.2±0.07 mg/kg-Bw/year and 12891±4472 fibres/year. Greatest inhalation intake rates were for the <0.5-yr age group, at 0.31 mg/kg-Bw/year. The study data reveal that MPs are prevalent in Australian homes and that the greatest risk of exposure resides with young children. Notwithstanding the limited number of global studies and the different methods used to measure MPs, this study indicates Australian deposition and inhalation rates are at the lower end of the exposure spectrum.

Cigarette smoke (CS) affects immune functions, leading to severe outcomes in smokers. Robust evidence addresses the immunotoxic effects of combustible tobacco products. As heat-not-burn tobacco products (HNBT) vaporize lower levels of combustible products, we here compared the effects of cigarette smoke (CS) and HNBT vapor on Jurkat T cells. Cells were exposed to air, conventional cigarettes or heatsticks of HNBT for 30 min and were stimulated or not with phorbol myristate acetate (PMA). Cell viability, proliferation, reactive oxygen species (ROS) production, 8-OHdG, MAP-kinases and nuclear factor κB (NFκB) activation and metallothionein expression (MTs) were assessed by flow cytometry; nitric oxide (NO) and cytokine levels were measured by Griess reaction and ELISA, respectively. Levels of metals in the exposure chambers were quantified by inductively coupled plasma mass spectrometry. MT expressions were quantified by immunohistochemistry in the lungs and liver of C57Bl/6 mice exposed to CS, HNBT or air (1 h, twice a day for five days: via inhalation). While both CS and HBNT exposures increased cell death, CS led to a higher number of necrotic cells, increased the production of ROS, NO, inflammatory cytokines and MTs when compared to HNBT-exposed cells, and led to a higher expression of MTs in mice. CS released higher amounts of metals. CS and HNBT exposures decreased PMA-induced interleukin-2 (IL-2) secretion and impaired Jurkat proliferation, effects also seen in cells exposed to nicotine. Although HNBT vapor does not activate T cells as CS does, exposure to both HNBT and CS suppressed proliferation and IL-2 release, a pivotal cytokine involved with T cell proliferation and tolerance, and this effect may be related to nicotine content in both products.