The adverse effects of air pollutants on the respiratory and cardiovascular systems are unquestionable. However, in recent years, indications of effects beyond these organ systems have become more evident. Traffic-related air pollution has been linked with neurological diseases, exacerbated cognitive dysfunction, and Alzheimer’s disease. However, the exact air pollutant compositions and exposure scenarios leading to these adverse health effects are not known. Although several components of air pollution may be at play, recent experimental studies point to a key role of ultrafine particles (UFPs). While the importance of UFPs has been recognized, almost nothing is known about the smallest fraction of UFPs, and only >23 nm emissions are regulated in the EU. Moreover, the role of the semivolatile fraction of the emissions has been neglected. The Transport-Derived Ultrafines and the Brain Effects (TUBE) project will increase knowledge on harmful ultrafine air pollutants, as well as semivolatile compounds related to adverse health effects. By including all the major current combustion and emission control technologies, the TUBE project aims to provide new information on the adverse health effects of current traffic, as well as information for decision makers to develop more effective emission legislation. Most importantly, the TUBE project will include adverse health effects beyond the respiratory system; TUBE will assess how air pollution affects the brain and how air pollution particles might be removed from the brain. The purpose of this report is to describe the TUBE project, its background, and its goals.

Background: Only a few studies have reported on chlorinated paraffin (CP) levels, especially long-chain chlorinated paraffins (LCCPs), in submicron particulate matter (PM₁) in the outdoor air around primary and secondary schools. Methods: This study examined concentrations of short-chain CPs (SCCPs), medium-chain CPs (MCCPs), and LCCPs in PM₁ samples from 96 schools across six cities in China’s Pearl River Delta region during the winter (October to December 2018). Results: The median total CP concentration was 34 ng/m³, with median values for SCCP, MCCP, and LCCP of 17.3, 15, and 0.7 ng/m³, respectively. The primary congeners were C₁₃Cl_6–8 for SCCPs, C₁₄Cl_6–9 for MCCPs, and C₁₈Cl_7–10 for LCCPs. The SCCPs and MCCPs largely originated from fugitive dust, whereas the LCCPs were mainly sourced from organic chemical industries. Air masses from the South China Sea contributed most to SCCP and MCCP levels, while those from the east coast accounted for the highest LCCP levels. The concentrations of CP in PM₁ were significantly positively correlated with PM₁ levels. Conclusions: The exposure risk assessments by age indicated a very low current health risk from PM₁-related CP inhalation, although prolonged pollution could raise these risks as CP concentrations in ambient PM may continue to increase.

Short-chain chlorinated paraffins (SCCPs) are widespread in atmospheric particulate matter (PM), but their toxicological contribution when adsorbed onto PM remains unclear. Using a respiratory A549/THP-1 co-culture cell model, we evaluated the effects of low-dose SCCPs (based on levels in real environment) combined with carbon particles (60 nm). Carbon particles significantly impaired cellular metabolic activity and induced oxidative stress, whereas SCCPs alone at low doses had minimal cytotoxic or oxidative effects. Co-exposure to SCCPs and carbon particles did not consistently exacerbate toxicity compared to carbon particles alone, and in some cases, even attenuated specific effects. Inflammatory cytokine expression revealed a general dose-dependent suppression, particularly in co-exposure groups, with IL-8 and TNF-α levels significantly reduced. Cell cycle alterations were minor across all groups, though subtle shifts in DNA replication phases were observed. Toxic potency evaluation showed that carbon particles combined with high-dose SCCPs (Maoming-equivalent) had slightly greater overall toxicity (0.228) than carbon particles alone (0.220) or low-dose SCCPs (Guangzhou-equivalent, 0.211), indicating a potential threshold effect for SCCP contribution at low environmental levels. This study highlights the complex and non-linear interactions between SCCPs and PM in terms of cellular toxicity and emphasizes the importance of considering environmentally relevant co-exposure scenarios in health risk assessments.

Semivolatile organic compounds (SVOCs) in exhaust gas, though not directly regulated by emission standards, play a crucial role in assessing both conventional and alternative fuels. Our aim is to compare the differences in and toxicological effects of SVOC exhaust emissions from conventional and alternative fuels under sub-freezing conditions. High levels of NO_x, CO₂ and PAHs in SVOCs were observed in DI-E2 (EN590 winter-grade diesel), with E10 (gasoline with 10% ethanol) exhibiting higher CO₂ and PAH levels compared to E85 (high-blend ethanol with an 83/17% ethanol–gasoline ratio). SVOCs from DI-E6 (EN590 diesel) demonstrated significant cytotoxicity, while E10 resulted in higher inflammatory mediators and genotoxicity. Our findings show that SVOC composition and toxicity in exhaust gas differ based on the fuel type. Despite new emissions regulations reducing diesel vehicle emissions, SVOC toxicity remains unchanged. Toxicity from SVOCs in compressed natural gas and ethanol/gasoline vehicles is notable, with gasoline exhaust showing high inflammatory and genotoxic potential.

Although previous toxicological studies on F-53B (a substitute for perfluorooctanesulfonic acid) have primarily employed relatively high exposure doses, none have simulated environmentally relevant concentrations of F-53B found in atmospheric particulate matter (PM) to assess its contribution to particle-induced toxicity. In this study, we addressed this gap by using real-world F-53B concentrations adsorbed onto PM2.5 as a basis for setting exposure levels. Pure carbon particles were used as a surrogate for atmospheric particles, and their toxicological effects-alone and in combination with trace-level F-53B-were comprehensively evaluated using an A549/THP-1 coculture model. Despite its extremely low concentration, F-53B significantly amplified the toxicity of carbon particles, as demonstrated by decreased mitochondrial activity, elevated oxidative stress, and disruptions in cell cycle regulation. Carbon particles alone suppressed the expression of most inflammatory and tissue-repair cytokines, while F-53B alone modestly increased several pro-inflammatory mediators. The combined exposure dampened some of the immune responses triggered by F-53B alone, indicating a complex interplay between these pollutants. Integrated potency analyses further confirmed that coexposure resulted in greater overall toxicity than exposure to carbon particles alone. These findings highlight the need to account for trace-level emerging pollutants such as F-53B when assessing the health risks associated with atmospheric PM.