Halloysite nanotubes (HNTs) have been increasingly used in many industrial and biomedical fields. Therefore, the assessment of risk and consequences of exposure to HNTs is very important to better protect human safety. This study aims to investigate the short- (24 or 72 h) and long-term (7 days) cytotoxic effects of HNTs at doses 10–200 µg/mL on human alveolar carcinoma epithelial cells (A549) and human bronchial epithelial cells (BEAS-2B). The effect of HNTs on cell viability, apoptosis, cell proliferation, oxidative/antioxidative status and cell morphology was evaluated. Our results showed that cytotoxicity of HNTs is dependent on dose, cell model and time of exposure. During the time of exposition toxic effects were intensified. To the best of our knowledge, this is the first study to use holo-tomographic microscopy (HTM) to visualise changes in cell morphology due to exposure from HNTs. We observed cells contraction, changes in the size and shape, cell surface folding and cytoplasmic vacuolization, peripheral arrangement of cell nuclei and even increase number of nucleus, which undoubtedly confirmed cytotoxic effect of HNTs at low doses (5 µg/mL and 25 µg/mL). Our results demonstrated that HTM technique provides a new insight into the assessment of HNTs toxicity. Further studies with different cell models are recommended to assess the toxic effect of HNTs on whole human body.

Metabolic and toxicodynamic interactions of some organic solvents in rats repeatedly treated with medium dose levels were examined. It was shown that both n-hexane and ethylbenzene significantly inhibited tetrachloroethylene metabolism during a 2-week period. n-Hexane and tetrachloroethylene enhanced metabolism of ethylbenzene whereas ethylbenzene suppressed n-hexane metabolism only at the end of the experiment. Biochemical changes, especially the drop in the level of non-protein sulfhydryl groups in tissues of rats treated with organic solvent mixtures, were significantly less pronounced than those observed after these chemicals were administered separately. These results demonstrate that metabolic interactions between hydrocarbons and chloroalkene may lead to a modification of the biological response to these compounds.

This study aimed to investigate the cytotoxicity and pro-inflammatory responses induced by tungsten disulphide (WS2) and molybdenum disulphide (MoS2) nanoparticles (NPs) in human bronchial cells (BEAS-2B). For cytotoxicity assessment, the cells were exposed to different concentrations (2.5–200 µg/mL) of WS2-NPs or MoS2-NPs for 24 and 48 h and then the MTT assay was performed. Afterwards, long-term toxicity was assessed by the colony forming efficiency assay (CFEA) during a 10 days’ exposure of the cells. For pro-inflammatory responses, the expression of interleukin-6 (IL-6) and interleukin-1β (IL-1β) mRNA was estimated by the real-time PCR method. Both nanomaterials showed similar cytotoxic effects on BEAS-2B cells assessed by the MTT assay, i.e. reduction in cell viability to approx. 60–70% at concentrations of 2.5 and 5 μg/mL after 24 and 48 h. The percentage viability remained relatively constant at this level across all concentrations above 5 μg/mL. In long-term exposure, both nanomaterials inhibited colony formation in a wide range of concentrations up to 100 µg/mL. MoS2-NPs were slightly more cytotoxic than WS2-NPs. Additionally, MoS2-NPs caused an increase in mRNA levels of cytokines, IL-1β, and IL-6 at concentration of 50 µg/mL, while WS2-NPs did not cause any changes in the level of mRNA for both cytokines. We also visualised the changes in the cells as a result of WS2-NPs or MoS2-NPs exposure (2.5 and 25 µg/mL) via holotomographic microscopy. This work demonstrates the hazardous potential of both nanomaterials and indicate that WS2 and MoS2 nanoparticles should be included in the occupational risk assessment.

Exposure to various ethylene glycol monoalkyl ethers (EGAEs) is known to result in hemolytic effect caused by their metabolites, appropriate alkoxyacetic acids, generated via both alcohol dehydrogenase and aldehyde dehydrogenase. It has been shown in many studies that administration of single doses of EGAEs to rats lead to dose- and time-dependent hemolytic anemia. The repeated exposure to isopropoxyethanol (IPE), and butoxyethanol (BE), contrary to methoxyethanol (ME) and ethoxyethanol (EE), resulted in significantly less pronounced hematological changes. While the majority of hematological effects were dramatic at the beginning of the exposure, later these changes clearly regressed despite continued weekly exposure to these ethers. The gradual recovery from the hemolytic anemia may be associated with tolerance development to the hemolytic effect of IPE and BE. ME demonstrated high hematotoxicity, which increased progressively and reached a maximum at the end of 4 week exposure, whereas EE revealed moderate hematological effects. It might be suspected that ME and EE may modified of IPE hemolytic activity in rats simultaneously treated with these compounds. In the rats co-exposed to IPE and ME subcutaneously at a relatively low doses of 0.75 mM + 0.75 mM for 4 weeks, a significantly less pronounced hematological changes at the beginning of the exposure in comparison with animals treated with IPE (0.75 mM) alone were observed. At the later period, i.e., at the end of 4 weeks exposure, the hematological alterations in the same animals were markedly pronounced and progressively elevated with exposure time, except for mean corpuscular volume (MCV) values, which were significantly lower in comparison with IPE group. ME at the higher dose of 1.25 mM/kg and EE at both doses of 0.75 and 1.25 mM/kg did not modify the hematotoxicity of IPE (at doses of 0.75 mM and 1.25 mM) at the beginning of the exposure, whereas increased its harmful effects at the end of the treatment. The amelioration in the majority of the hematological parameters at the beginning of the exposure may be caused by inhibitory effect of ME on IPE metabolism. On the contrary, an accumulation of the methoxyacetic acid and ethoxyacetic acid, toxic metabolites of ME and EE, respectively, and no tolerance development to the hemolytic effect of these two chemicals may be responsible for elevated hematological alterations at the end of the exposure.

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