Purpose: While cigarette smoke (CS) is known to modify the risk of radon-induced lung cancer, the mechanisms remain poorly understood. Experimental studies on their combined effects are limited by the lack of suitable in vitro exposure platforms. This study provides proof-of-concept validation of a novel ALI exposure system for controlled, simultaneous exposure to radon and CS.

Materials and methods: The system comprises a ²²⁶Ra source, radon monitor, smoking machine, particle counter, siphon mixing unit, and an ALI system. The CS unit maintained the target concentration at 5 mg/m³ and induced dose-response toxicity in BEAS-2B cells following 0.5, 1 and 2 h exposures. For a 2-h radon exposure, the estimated average dose to the cells was 1 mGy (range 0.3–7.5 mGy), with a localized dose of 171 mGy per hit nucleus.

Results: Separate exposure to radon (2 h, 228 ± 54 kBq/m³) and CS (1 h, 5 mg/m³) resulted in 75 ± 9% and 83 ± 16% cell viability, respectively, while combined exposure led to a significantly lower cell viability (55 ± 8%). A trend toward an increase in pro-inflammatory IL-8 secretion was noted for all exposures; however, it did not reach statistical significance.

Conclusion: The developed ALI-based exposure system enables precise dosimetry and biological assessment, establishing a validated proof-of-concept platform for future research on environmental co-exposures.

As vehicle technologies evolve toward electrification and advanced aftertreatment, understanding the biological implications of their exhaust emissions remains essential. This study presents a harmonized comparative toxicological assessment of five Euro 6 vehicles representing gasoline, hybrid, plug-in hybrid, compressed natural gas (CNG), and diesel technologies. Vehicles were tested under realistic driving conditions on a chassis dynamometer. Diluted exhaust was delivered directly to human lung epithelial cells (A549) using a controlled air–liquid interface (ALI) exposure system. Solid and total particle number emissions were measured, and deposited particle mass was estimated from size-resolved distributions and deposition efficiency. Vehicles equipped with particulate filtration showed lower solid particle emissions overall, while differences between gasoline particulate filter-equipped vehicles indicated that hybridization can further influence emission levels. Diesel operation during active diesel particulate filter (DPF) regeneration produced more than two orders of magnitude higher particle number emissions compared to normal operation. When expressed as deposited mass, vehicle ranking differed from number-based emissions, highlighting that emission metrics do not directly translate into delivered biological dose. Exposure to whole exhaust consistently induced stronger cytotoxic and inflammatory responses than to gaseous phase alone. Membrane integrity disruption and IL-1β release showed clear particle-associated amplification, with the strongest effects observed during diesel DPF regeneration. These findings demonstrate persistent technology-dependent differences in particle emissions and acute biological responses among modern low-emission vehicles.

Subway stations are enclosed environments that can have elevated concentrations of PM2.5 (particulate matter with an aerodynamic diameter of <2.5 μm). These particles are primarily generated by mechanical wear from trains and are therefore rich in transition metals and suspected to affect health upon inhalation. To simulate real-world inhalation scenarios, this study aimed to assess the toxicity of airborne subway PM2.5 using a mobile air–liquid interface (ALI) exposure system directly on the platform, using monoculture (A549) and coculture (A549 + dTHP-1) cell models, alongside laboratory submerged exposures. In ALI exposures, a dose of 0.12 ± 0.07 μg/cm2 could not induce any change in cell viability or inflammatory markers after 24 h of incubation. In submerged experiments, a higher dose was applied than in ALI, inducing a decrease in cell viability in both A549 and dTHP-1 cells. A549 cells exhibited increased IL-6 and TNF-α release at the highest dose (100 μg/mL). In dTHP-1 cells, IL-8 release was significantly elevated even at the lowest dose (10 μg/mL), and all four cytokines (IL-8, IL-6, IL-1β, and TNF-α) were significantly increased at 100 μg/mL. These findings highlight the critical role of exposure conditions in toxicological studies and support the use of both in situ and laboratory-based approaches. Moreover, longer in situ exposures may be necessary to achieve doses comparable to those in a laboratory setup for comparison.

Poor air quality is a significant risk to human health and the environment, with a direct correlation to respiratory diseases and premature death. Ultra fine particles (UFPs) in the atmosphere are particularly hazardous. This study evaluates the toxicological response of epithelial cells (A549) and macrophages (dTHP-1) to particulate matter (PM) emissions from car brake wear, under both submerged and Air-Liquid Interface (ALI) conditions. Toxicity was assessed using cell viability (Resazurin assay) and cytokine assays. Emissions were collected using a dynamometric bench simulating driving and braking conditions. Under ALI, freshly emitted particles were directly deposited onto cells, while in submerged conditions, particles were collected on filters and then deposited onto cells. M1a and M1b materials were tested, both materials are falling into category of ECE R90 Low Metallic pads. M1a showed slight toxicity under ALI and significant immune response in submerged conditions, while M1b showed no toxicity in either condition.

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.

This study investigated the impact of Diesel Particulate Filter (DPF) regeneration on the composition and toxicity of exhaust emissions from a Euro 6d diesel passenger vehicle. Multiple real-world–simulated driving cycles were performed under two DPF conditions: normal operation and active regeneration. Exhaust emissions were characterized in real time for gaseous and particulate pollutants, while the nanoparticle fraction of the particulate mass was chemically analyzed for its organic and inorganic components. The toxicological effects of DPF regeneration were evaluated using an in vitro Air–Liquid Interface (ALI) exposure system with human lung cells. The results indicate that DPF regeneration accounted for more than 95 % of total particle number emissions, while significant amounts of carbon monoxide and methane were emitted as well. Exposures in the absence of particles led to similar reductions in cell viability and inflammatory responses, regardless of the DPF condition. In contrast, when particles were present, the cellular response became significantly stronger, indicating that the increased toxicity is primarily driven by the particulate fraction. Chemical analyses of nanoparticle mass revealed higher concentrations of water-soluble elements and oxygenated polycyclic aromatic hydrocarbons during regeneration. Overall, DPF regeneration transiently but substantially alters emission characteristics and significantly increases their toxicological potential.

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.

The emission of volatile organic compounds (VOCs) from brake wear is a relatively underexplored aspect of nonexhaust traffic emissions. We employed a proton-transfer-reaction time-of-flight mass spectrometer to investigate the real-time emissions of VOCs from two commercially prevalent brake materials: low-metallic copper-free (LMCF) and nonasbestos organic (NAO). Experiments were conducted using a pin-on-a-disc tribometer integrated with a fast-mobility particle sizer spectrometer. The results reveal that NAO brake pads emit higher concentrations of VOCs than LMCF pads. Over 200 different sum formulas were identified for both materials, and siloxanes were observed as characteristic of NAO emissions. The ultrafine particle formation was systematically preceded by an increase in gaseous emissions. This observation supports the thesis that ultrafine particle formation emitted by brake wear occurs through VOCs nucleation, addressing a significant gap in the literature.

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.