Exposure to particulate matter (PM) has been associated with a wide range of adverse health effects, but it is still unclear how particles from various transport modes differ in terms of toxicity and associations with different human health outcomes. This literature review aims to summarize toxicological and epidemiological studies of the effect of ultrafine particles (UFPs), also called nanoparticles (NPs, <100 nm), from different transport modes with a focus on vehicle exhaust (particularly comparing diesel and biodiesel) and non-exhaust as well as particles from shipping (harbor), aviation (airport) and rail (mainly subway/underground). The review includes both particles collected in laboratory tests and the field (intense traffic environments or collected close to harbor, airport, and in subway). In addition, epidemiological studies on UFPs are reviewed with special attention to studies aimed at distinguishing the effects of different transport modes. Results from toxicological studies indicate that both fossil and biodiesel NPs show toxic effects. Several in vivo studies show that inhalation of NPs collected in traffic environments not only impacts the lung, but also triggers cardiovascular effects as well as negative impacts on the brain, although few studies compared NPs from different sources. Few studies were found on aviation (airport) NPs, but the available results suggest similar toxic effects as traffic-related particles. There is still little data related to the toxic effects linked to several sources (shipping, road and tire wear, subway NPs), but in vitro results highlighted the role of metals in the toxicity of subway and brake wear particles. Finally, the epidemiological studies emphasized the current limited knowledge of the health impacts of source-specific UFPs related to different transport modes. This review discusses the necessity of future research for a better understanding of the relative potencies of NPs from different transport modes and their use in health risk assessment.

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.

The transition metal copper (Cu) is an essential trace element for humans and serves as a cofactor for numerous enzymes. Therefore, intracellular Cu homeostasis must be tightly regulated. Meanwhile, Cu is increasingly used in industrial and biomedical applications, particularly in nanoparticle (NP) form. However, studies have demonstrated that Cu(II) oxide (CuO) NPs are highly toxic. Therefore, understanding the underlying toxic effects of such compounds is of the utmost importance. In this context, transcriptomic profiling is regarded as a valuable tool. Nevertheless, comparative studies addressing organ-relevant models, such as the liver and lungs, are scarce. Furthermore, no transcriptomic studies have been conducted on human bronchial lung epithelial cells exposed to CuO NPs and Cu²⁺. In this study, we compared the cellular effects of human bronchial lung epithelial cells exposed to both CuO NPs and Cu²⁺ to the effects in human liver cells exposed to Cu²⁺ by applying RNA sequencing. Although cytotoxicity was comparable, we showed that Cu uptake was highly dependent on both the cell type and the form of Cu. The most pronounced concentration-dependent transcriptional changes were observed with CuO NP exposure in BEAS-2B cells. The only differentially expressed genes (DEGs) found by all exposures and treatments were metallothioneins (MTs). The most sensitive targets of Cu-induced toxicity were related to nuclear factor erythroid 2-related factor 2 (NRF2), nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), and mitogen-activated protein kinase (MAPK) signaling. Furthermore, the effects observed at the transcriptome level were studied at the functional level, such as cell cycle regulation and cytokine release. Thus, we demonstrated that the two cell types differ in susceptibility, and that complementing transcriptome profiling with functional studies provides important mechanistic insights.

Although exposure to heavy metals such as cadmium and inorganic arsenic has declined in recent decades, they remain prevalent environmental contaminants in food, drinking water, and tobacco smoke. This study aimed to identify and compare molecular endpoints of arsenite and cadmium toxicity at the gene and protein expression levels, with a focus on metal homeostasis, the oxidative stress response and redox-regulated processes. Human bronchial epithelial cells (BEAS-2B) were used as an in vitro model. First, the appropriate exposure conditions were defined by assessing cytotoxicity and intracellular metal accumulation. The cells were then incubated with 1–10 µM NaAsO₂ or 1–5 µM CdCl₂ for 24 h, after which gene and protein expression were analyzed. When compared to arsenite, cadmium was a markedly stronger inducer of metallothionein (MT) expression, indicating distinct effects on metal homeostasis. Both metals induced a concentration-dependent upregulation of oxidative stress-related genes. Cadmium led to a stronger activation of NF-κB signaling, while arsenite decreased selenoprotein-associated gene expression and affected genes involved ferroptosis regulation. Differences in gene and protein expression patterns were also observed, suggesting that transcriptional responses do not necessarily translate into corresponding changes at the protein level after 24 h. These findings highlight shared and compound-specific mechanisms, as well as the importance of multi-level analyses.