Healthcare waste (HCW) is generated in different healthcare facilities (HCFs), such as hospitals, laboratories, veterinary clinics, research centres and nursing homes. It has been assessed that the majority of medical waste does not pose a risk to humans. It is estimated that 15% of the total amount of produced HCW is hazardous and can be infectious, toxic or radioactive. Hazardous waste is a special type of waste which, if not properly treated, can pose a risk to human health and to the environment. HCW contains potentially harmful microorganisms that can be spread among healthcare personnel, hospital patients and the general public, causing serious illnesses. Healthcare personnel are the specialists especially exposed to this risk. The most common medical procedure, which pose the highest risk, is injection (i.e, intramuscular, subcutaneous, intravenous, taking blood samples). The World Health Organization (WHO) estimates that around 16 billion injections are administered worldwide each year. However, if safety precautions are not followed, and needles and syringes are not properly disposed of, the risk of sharps injuries increases among medical staff, waste handlers and waste collectors. What is more, sharps injuries increase the risk of human immunodeficiency virus (HIV), hepatitis B and C viruses (HBV/HCV), tuberculosis (TB), diphtheria, malaria, syphilis, brucellosis and other transmissions. Disposing of medical waste in a landfill without segregation and processing will result in the entry of harmful microorganisms, chemicals or pharmaceuticals into soil and groundwater, causing their contamination. Open burning or incinerator malfunctioning will result in the emission of toxic substances, such as dioxins and furans, into the air. In order to reduce the negative impact of medical waste, waste management principles should be formulated. To minimize health risks, it is also important to build awareness among health professionals and the general public through various communication and educational methods. The aim of this paper is to present a general overwiev of medical waste, its categories, the principles of its management and the risks to human health and the environment resulting from inappropriate waste management.

Pathogens and their toxins can cause various diseases of different severity. Some of them may be fatal, and therefore early diagnosis and suitable treatment is essential. There are numerous available methods used for their rapid screening. Conventional laboratory-based techniques such as culturing, enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction (PCR) are dominant. However, culturing still remains the “gold standard” for their identification. These methods have many advantages, including high sensitivity and selectivity, but also numerous limitations, such as long experiment-time, costly instrumentation, and the need for well-qualified personnel to operate the equipment. All these existing limitations are the reasons for the continuous search for a new solutions in the field of bacteria identification. For years, research has been focusing on the use of immunosensors in various types of toxin- and pathogen-detection. Compared to the conventional methods, immunosensors do not require well-trained personnel. What is more, immunosensors are quick, highly selective and sensitive, and possess the potential to significantly improve the pathogen and toxin diagnostic-processes. There is a very important potential use for them in various transport systems, where the risk of contamination by bioagents is very high. In this paper, the advances in the field of immunosensor usage in pathogenic microorganism- and toxin-detection, are described.

T-2 toxin is produced by different Fusarium species, and it can infect crops such as wheat, barley, and corn. It is known that the T-2 toxin induces various forms of toxicity such as hepatotoxicity, nephrotoxicity, immunotoxicity, and neurotoxicity. In addition, T-2 toxin possesses a strong dermal irritation effect and can be absorbed even through intact skin. As a dermal irritant agent, it is estimated to be 400 times more toxic than sulfur mustard. Toxic effects can include redness, blistering, and necrosis, but the molecular mechanism of these effects still remains unknown. This in vitro study focused on the direct toxicity of T-2 toxin on human skin—fibroblast Hs68 cell line. As a result, the level of toxicity of T-2 toxin and its cytotoxic mechanism of action was determined. In cytotoxicity assays, the dose and time-dependent cytotoxic effect of T-2 on a cell line was observed. Bioluminometry results showed that relative levels of ATP in treated cells were decreased. Further analysis of the toxin’s impact on the induction of apoptosis and necrosis processes showed the significant predominance of PI-stained cells, lack of caspase 3/7 activity, and increased concentration of released Human Cytokeratin 18 in treated cells, which indicates the necrosis process. In conclusion, the results of an in vitro human skin fibroblast model revealed for the first time that the T-2 toxin induces necrosis as a toxicity effect. These results provide new insight into the toxic T-2 mechanism on the skin.

T-2 toxin is produced by different Fusarium species and belongs to the group of type A trichothecene mycotoxins. T-2 toxin contaminates various grains, such as wheat, barley, maize, or rice, thus posing a risk to human and animal health. The toxin has toxicological effects on human and animal digestive, immune, nervous and reproductive systems. In addition, the most significant toxic effect can be observed on the skin. This in vitro study focused on T-2 toxicity on human skin fibroblast Hs68 cell line mitochondria. In the first step of this study, T-2 toxin’s effect on the cell mitochondrial membrane potential (MMP) was determined. The cells were exposed to T-2 toxin, which resulted in dose- and time-dependent changes and a decrease in MMP. The obtained results revealed that the changes of intracellular reactive oxygen species (ROS) in the Hs68 cells were not affected by T-2 toxin. A further mitochondrial genome analysis showed that T-2 toxin in a dose- and time-dependent manner decreased the number of mitochondrial DNA (mtDNA) copies in cells. In addition, T-2 toxin genotoxicity causing mtDNA damage was evaluated. It was found that incubation of Hs68 cells in the presence of T-2 toxin, in a dose- and time-dependent manner, increased the level of mtDNA damage in both tested mtDNA regions: NADH dehydrogenase subunit 1 (ND1) and NADH dehydrogenase subunit 5 (ND5). In conclusion, the results of the in vitro study revealed that T-2 toxin shows adverse effects on Hs68 cell mitochondria. T-2 toxin induces mitochondrial dysfunction and mtDNA damage, which may cause the disruption of adenosine triphosphate (ATP) synthesis and, in consequence, cell death.