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.

Size-fractionated particulate matters (SPMs) in a range of 9.0 to 0.43 μm, classified based on aerodynamic diameter (dₐₑ) as fine PMs (0.43 μm ≤ dₐₑ < 2.1 μm) and coarse PMs (2.1 μm ≤ dₐₑ < 9.0 μm) were collected by cascade impactors (7 fractions) during smoke haze (SH) and non-smoke haze (NSH) seasons in urban and rural areas of Chiang Mai, Thailand. Their polycyclic aromatic hydrocarbons (PAHs) compositions were determined for respiratory health risk assessment. During SH episode, concentrations of SPMs and PAHs in the rural area were approximately two times higher than in the urban area and about 62–68% of the SPMs were fine particles. Conversely, during NSH season the concentrations in the urban area were higher due to traffic emission. The finest particle sizes (0.65–0.43 μm) contained the highest PAHs concentrations among the other PM sizes. Benzo[b]fluoranthene was a main PAH component found during SH season suggesting biomass burning is a major pollutant source. High molecular weight (5–6 rings) PAHs with high carcinogenicity were likely to concentrate in fine particles. Distribution patterns of SPMs and PAHs during SH season were bimodal with the highest peak at a fine size range (0.65–0.43 μm) and a small peak at a coarse size range (5.8–4.7 μm). Respiratory health risk was estimated based on toxicity equivalent concentrations of PAHs bound-SPMs and inhalation cancer risk (ICR). Relatively high ICR values (1.14 × 10⁻⁴ (rural) and 6.80 × 10⁻⁵ (urban)) were found during SH season in both areas, in which fine particles played an important role. It revealed that high concentration of fine particles in ambient air is related to high respiratory health risk due to high content of carcinogenic substances.

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.

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.

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.

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.

Polycyclic aromatic hydrocarbons (PAHs) and certain ingredients in personal care products, such as parabens, bisphenols, triclosan and phthalate metabolites, have become ubiquitous in the world. Concerns of human exposure to these pollutants have increased during recent years because of various adverse health effects of these chemicals. Multiple compounds including parabens, bisphenols, triclosan, phthalate metabolites (mPAEs) and hydroxyl PAHs (OH-PAHs) in urine samples from Guangzhou were determined simultaneously to identify the human exposure pathways without external exposure data combined with data analysis, and the toxicants posed the highest risk to human health were screened in the present study. The detection frequencies for the chemicals exceeded 90%. Among the contaminants, mPAEs showed the highest concentrations, followed by OH-PAHs, with triclosan present at the lowest concentrations. Mono-n-butyl phthalate, methylparaben, bisphenol A, and hydroxynaphthalene represented the most abundant mPAE, parabens, bisphenol, and OH-PAH compounds, respectively. The present PAHs are mainly exposed to human through inhalation, while the chemicals added to personal care products are mainly exposed to human through oral intake and dermal contact. The urine samples from suburban subjects showed significantly higher OH-PAH levels than the urine samples from urban subjects, and females had lower OH-PAH levels than males. Urinary concentrations of the analyzed contaminants were significantly correlated with age, body mass index, residence time, as well as the frequencies of alcohol consumption and swimming. Risk assessments based on Monte Carlo simulation indicated that approximately 30% of the subjects suffered non-carcinogenic risks from mPAEs and OH-PAHs, with mPAEs accounting for 89% of the total risk.

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.

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.

Polycyclic aromatic hydrocarbons (PAHs) are pollutants produced during incomplete combustion of organic matter and several industrial processes. Humans can be exposed to PAHs through ingestion of food, inhalation of tobacco smoke or polluted air, and dermal contact, causing immunologic, developmental, and reproductive problems.In the present research, eleven metabolites of PAHs were analyzed in the urine of 110 lactating women living in Spain (2015). PAH metabolites were extracted from the urine samples by liquid-liquid extraction and their determination was performed by liquid chromatography coupled to tandem mass spectrometry. In addition, information on lifestyle and dietary habits of the participants was collected using a questionnaire.All the PAH metabolites were detected in more than 70% of the samples, except for 3-hydroxybenzo(a)pyrene which was detected in less than 1% of the samples. The highest urinary levels were found for naphthalene metabolites, with geometric means of 0.8 (1-hydroxynaphthalene) and 7.1 ng ml⁻¹ (2-hydroxynaphthalene). The statistical analysis showed that smoking status, as well as the ingestion of certain food groups (vegetables, cereals, oils and fats, smoked fish and coffee), were the main influencing factors of exposure to PAHs.The estimated daily intake (EDI) was calculated for naphthalene, fluorene, phenanthrene, and pyrene, ranging from 6 to 1522 ng kg⁻¹·day⁻¹. The non-cancer risk associated to PAH exposure was estimated, showing hazard quotients (HQs) and hazard indexes (HIs) below 1. Therefore, it did not reveal a significant health risk for Spanish women due to PAH exposure.