Wear and tear from tyres significantly contributes to the flow of (micro-)plastics into the environment. This paper compiles the fragmented knowledge on tyre wear and tear characteristics, amounts of particles emitted, pathways in the environment, and the possible effects on humans. The estimated per capita emission ranges from 0.23 to 4.7 kg/year, with a global average of 0.81 kg/year. The emissions from car tyres (100%) are substantially higher than those of other sources of microplastics, e.g., airplane tyres (2%), artificial turf (12–50%), brake wear (8%) and road markings (5%). Emissions and pathways depend on local factors like road type or sewage systems. The relative contribution of tyre wear and tear to the total global amount of plastics ending up in our oceans is estimated to be 5–10%. In air, 3–7% of the particulate matter (PM2.5) is estimated to consist of tyre wear and tear, indicating that it may contribute to the global health burden of air pollution which has been projected by the World Health Organization (WHO) at 3 million deaths in 2012. The wear and tear also enters our food chain, but further research is needed to assess human health risks. It is concluded here that tyre wear and tear is a stealthy source of microplastics in our environment, which can only be addressed effectively if awareness increases, knowledge gaps on quantities and effects are being closed, and creative technical solutions are being sought. This requires a global effort from all stakeholders; consumers, regulators, industry and researchers alike.
Recent research highlighted the impact of ROS as upstream regulators of tissue regeneration. We investigated their role and targeted processes during the regeneration of different body structures using the planarian Schmidtea mediterranea, an organism capable of regenerating its entire body, including its brain. The amputation of head and tail compartments induces a ROS burst at the wound site independently of the orientation. Inhibition of ROS production by diphenyleneiodonium (DPI) or apocynin (APO) causes regeneration defaults at both the anterior and posterior wound sites, resulting in reduced regeneration sites (blastemas) and improper tissue homeostasis. ROS signaling is necessary for early differentiation and inhibition of the ROS burst results in defects on the regeneration of the nervous system and on the patterning process. Stem cell proliferation was not affected, as indicated by histone H3-P immunostaining, fluorescence-activated cell sorting (FACS), in situ hybridization of smedwi-1, and transcript levels of proliferation-related genes. We showed for the first time that ROS modulate both anterior and posterior regeneration in a context where regeneration is not limited to certain body structures. Our results indicate that ROS are key players in neuroregeneration through interference with the differentiation and patterning processes.
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