Lung cancer remains the leading cause of cancer mortality worldwide, with tobacco smoke and radon exposure being the primary risk factors. The interaction between these two factors has been described as sub-multiplicative, but a better understanding is needed of how they jointly contribute to lung carcinogenesis. In this context, a comprehensive analysis of current knowledge regarding the effects of radon and tobacco smoke on lung cancer was conducted using a computational approach. Information on this co-exposure was extracted and clustered from databases, particularly the literature, using the text mining tool AOP-helpFinder and other artificial intelligence (AI) resources. The collected information was then organized into Aggregate Exposure Pathway (AEP) and Adverse Outcome Pathways (AOP) models. AEPs and AOPs represent analytical concepts useful for assessing the potential risks associated with exposure to various stressors. AOPs provide a structured framework to organize knowledge of essential Key Events (KEs) from a Molecular Initiating Event (MIE) to an Adverse Outcome (AO) at an organism or population level, while AEPs model exposures from the initial source of the stressor to the internal exposure site within the target organism, situated upstream of the AOP. Combining these frameworks offered an integrated method for knowledge consolidation of radon and tobacco smoke, detailing the association from the environment to a mechanistic level, and highlighting specific differences between the two stressors in DNA damage, mutational profiles, and histological types. This approach also identified gaps in understanding joint exposure, particularly the lack of mechanistic studies on the precise role of certain KEs such as inflammation, as well as the need for studies that more closely replicate real-world exposure conditions. In conclusion, this study demonstrates the potential of AI and machine learning tools in developing alternative toxicological models. It highlights the complex interaction between radon and tobacco smoke and encourages collaboration among scientific communities to conduct future studies aiming to fully understand the mechanisms associated with this co-exposure.

Uncontrolled waste burning and accidental waste fires are an important source of emissions into the air. However, there are currently only few field studies providing data on these emissions. In this study, we investigated the emission rates, pollutant dispersion and particle composition for a large waste fire in Stockholm county, Sweden. Our results show that the waste fire, while burning, may have contributed as much as 5 times the mean PM₁₀ emissions from road traffic of the municipality it was located in (ca 95 000 inhabitants), which highlights the potential impact of temporary events such as waste fires on air quality. Gaussian dispersion calculations were used to model the spatial distribution of measured PM₁₀ data, demonstrating its use for assessment of exposure and deposition. Particles impacted by the waste fire were enriched in several potentially toxic metals and metalloids including arsenic, copper, cadmium and, in particular, lead when compared to particles collected after the fire. In addition, they may also pose an increased cancer risk on a per-mass basis compared to the post-fire period due to the larger mass fraction of relevant PAHs.

In this study, we investigated the impact of iron-rich nanoparticles derived from different locations in the subway on the innate immune system in blood. Nanoparticles were generated from Third Rail, Rail, and Wheel materials and characterized using several techniques. The response in a human whole-blood model was analyzed using ELISA and capillary immunoelectrophoresis. All nanoparticles were iron oxides, but Third Rail nanoparticles also contained Silicon and were highly thrombo-inflammatory, activating Factor XI-induced coagulation and pro-inflammatory kallikrein/kinin pathways. Wheel and Rail nanoparticles were less reactive, mainly activating the kallikrein/kinin pathway, leading to milder inflammatory reactions. The strong thrombo-inflammatory properties of Third Rail nanoparticles are attributed to their high Silicon content. None of the nanoparticles significantly activated the complement system. In conclusion, we found that the elemental composition of nanoparticles is crucial in determining whether activation leads to kallikrein/kinin system activation and bradykinin release or Factor XI activation and thrombosis.

Airborne quasi-ultrafine particle samples were collected from different outdoor sites in Barcelona (NE Spain, 35 samples) and the Valencia subway (about 400 km south of Barcelona, 3 samples). Locations and schedules were designed to cover cold and warm seasons and to represent the impact of different types of transport (cars, trains, ships, and planes). Extracts from PTFE filters (methanol:dichloromethane 1:2) were used to test toxic effects in human cell lines (Induction of reactive oxygen species, inflammatory response) and in zebrafish embryos (expression of xenobiotic response-related genes, cyp1a1, gsa1 and hao1). We observed distinct toxic effects related to different forms of oxidative stress and to inflammatory response, the two types of negative outcomes more closely related to the known epidemiological impacts of air pollution. The highest toxicity values were detected in sites receiving car and/or ship emissions, with maximums during the cold season. Chemical analysis followed by correlation and source apportionment analyses identified PAHs, combustion engines, and biomass burning emissions as the main drivers of the observed toxic effects. Therefore, traffic restrictions, car emission limits, and reduction of combustion processes are necessary to eliminate or at least to limit airborne toxicity in urban environments.

Traffic-related air pollution is a major public health concern, contributing to respiratory and cardiovascular diseases worldwide. The aim of this study was to investigate the feasibility of using a mobile Air-Liquid Interface (ALI) system to assess the cytotoxicity and inflammatory potential of freshly generated PM_2.5 (particle matter with aerodynamic diameter <2.5 μm) in a road tunnel in Stockholm. We hypothesized that cellular effects would be detectable at lower doses compared to submerged exposures. The mean particle dose in ALI was 1.4 ± 0.8 μg/cm², whereas a wide range of doses was used for submerged exposures. ALI and submerged results showed that PM_2.5 from the road tunnel did not affect the viability of A549 cells, whereas a significant and dose-dependent decrease in viability of dTHP-1 (in submerged exposure) was observed. Furthermore, in A549 in ALI a slight increase in inflammatory response (IL-8, IL-6, and IL-1β) was observed. In submerged exposure, the inflammatory response was clearer, particularly in the dTHP-1 cells. In conclusion, this study presents the first successfully conducted in situ ALI exposure in a road tunnel. The results demonstrate that dTHP-1 cells exhibit clear cytotoxic and inflammatory responses, while A549 show only weak effects. These findings suggest that co-cultures of A549 and dTHP-1 may be valuable in future ALI studies.

Nanoparticles (ultrafine particles) are prevalent in various environments and raise concerns due to their potential health effects. In this study, we aimed to enhance the understanding of the toxicity associated with nanoparticles generated within subway systems. Specifically, we investigated nanoparticles produced using spark discharge from electrodes made of the same material as the third rail (which provides electric power), rail, and wheel components in the Stockholm subway system. Characterization revealed that the generated nanoparticles typically had a primary size of 6–10 nm and exhibited high agglomeration. They consisted mainly of iron, along with varying amounts of manganese and silicon. Despite having low oxidative potential, they showed some cytotoxicity and clearly induced DNA strand breaks in both dTHP-1 cells (monocyte-derived macrophages) and A549 cells (lung epithelial cells). In addition, gene expression analysis showed an upregulation of the cytokine IL-8 in dTHP-1 cells. No increased release of IL-1β, IL-8, IL-6, and TNF-a was noted. Consistent differences in toxicity between the nanoparticles from different materials were not observed. In conclusion, the results show that subway-related nanoparticles can cause DNA damage in cultured lung cells, but the inflammatory potential in terms of cytokine release was limited.

Road traffic is an important source of urban air pollutants. Due to increasingly strict controls of exhaust emissions from road traffic, their contribution to the total emissions has strongly decreased over time in high-income countries. In contrast, non-exhaust emissions from road vehicles are not yet legislated and now make up the major proportion of road traffic emissions in many countries. Brake wear, which occurs due to friction between brake linings and their rotating counterpart, is one of the main non-exhaust sources contributing to particle emissions. Since the focus of brake wear emission has largely been on particulate pollutants, little is currently known about gaseous emissions such as volatile organic compounds from braking and their fate in the atmosphere. This study investigates the oxidative ageing of gaseous brake wear emissions generated with a pin-on-disc tribometer, using an oxidation flow reactor. The results demonstrate, for the first time, that the photooxidation of gaseous brake wear emissions can lead to formation of secondary particulate matter, which could amplify the environmental impact of brake wear emissions.

Purpose: Epidemiological studies show that radon and cigarette smoke interact in inducing lung cancer, but the contribution of nicotine in response to alpha radiation emitted by radon is not well understood. Materials and methods: Bronchial epithelial BEAS-2B cells were either pre-treated with 2 µM nicotine during 16 h, exposed to radiation, or the combination. DNA damage, cellular and chromosomal alterations, oxidative stress as well as inflammatory responses were assessed to investigate the role of nicotine in modulating responses. Results: Less γH2AX foci were detected at 1 h after alpha radiation exposure (1–2 Gy) in the combination group versus alpha radiation alone, whereas nicotine alone had no effect. Comet assay showed less DNA breaks already just after combined exposure, supported by reduced p-ATM, p-DNA-PK, p-p53 and RAD51 at 1 h, compared to alpha radiation alone. Yet the frequency of translocations was higher in the combination group at 27 h after irradiation. Although nicotine did not alter G2 arrest at 24 h, it assisted in cell cycle progression at 48 h post radiation. A slightly faster recovery was indicated in the combination group based on cell viability kinetics and viable cell counts, and significantly using colony formation assay. Pan-histone acetyl transferase inhibition using PU139 blocked the reduction in p-p53 and γH2AX activation, suggesting a role for nicotine-induced histone acetylation in enabling rapid DNA repair. Nicotine had a modest effect on reactive oxygen species induction, but tended to increase alpha particle-induced pro-inflammatory IL-6 and IL-1β (4 Gy). Interestingly, nicotine did not alter gamma radiation-induced γH2AX foci. Conclusions: This study provides evidence that nicotine modulates alpha-radiation response by causing a faster but more error-prone repair, as well as rapid recovery, which may allow expansion of cells with genomic instabilities. These results hold implications for estimating radiation risk among nicotine users.

Air pollution is one of the most severe environmental health hazards, and airborne nanoparticles (diameter <100 nm) are considered particularly hazardous to human health. They are produced by various sources such as internal combustion engines, wood and biomass burning, and fuel and natural gas combustion, and their origin, among other parameters, determines their intrinsic toxicity for reasons that are not yet fully understood. Many constituents of the nanoparticles are considered toxic or at least hazardous, including polycyclic aromatic hydrocarbons (PAHs) and heavy metal compounds, in addition to gaseous pollutants present in the aerosol fraction, such as NOx, SO2, and ozone. All these compounds can cause oxidative stress, mitochondrial damage, inflammation in the lungs and other tissues, and cellular organelles. Epidemiological investigations concluded that airborne pollution may affect the respiratory, cardiovascular, and nervous systems. Moreover, particulate matter has been linked to an increased risk of lung cancer, a carcinogenic effect not related to DNA damage, but to the cellular inflammatory response to the pollutants, in which the release of cytokines promotes the proliferation of pre-existing mutated cancer cells. The mechanisms behind toxicity can be investigated experimentally using cell cultures or animal models. Methods for gathering particulate matter have been explored, but standardized protocols are needed to ensure that the samples accurately represent chemical mixtures in the environment. Toxic constituents of nanoparticles can be studied in animal and cellular models, but designing realistic exposure settings is challenging. The air–liquid interface (ALI) system directly exposes cells, mimicking particle inhalation into the lungs. Continuous research and monitoring of nanoparticles and other airborne pollutants is essential for understanding their effects and developing active strategies to mitigate their risks to human and environmental health.

Fires in waste facilities are a common occurrence. Since many waste facilities are located adjacent to densely populated areas, these fires could potentially expose large populations to the emitted pollutants. However, at the moment there are only few field studies investigating the impact of waste fire emissions on air quality since the unpredictable nature of these events makes them challenging to capture. This study investigated the impact of a large and persistent un-prescribed fire in a waste storage facility in Stockholm county, Sweden, on the local air quality of two residential areas in close proximity to the fire. In-situ measurements of particulate matter, black carbon and nitrogen oxide concentrations were conducted both during open burning and after the fire was fully covered. In addition, filter samples were collected for offline analysis of organic composition, metal content and toxicity. Strongly increased concentrations of PM10, PM2.5 and black carbon were found during the open burning period, especially when the wind was coming from the direction of the fire. In addition, elevated concentrations of particulate heavy metals and polycyclic aromatic hydrocarbons were observed in the air during the open burning period. These results show that waste fires can have a strong impact on the air quality of nearby residential areas.