Polycyclic aromatic hydrocarbons in consumer goods made from recycled rubber material: A review.

Vast amounts of rubber waste are produced every year, where end-of-life tires (ELT) mount up the largest share with several million tonnes in the EU each year. This points up the necessity for reusing end-of-life rubber material. The recycled material shows nearly the same advantages like the origin materials. In consequence, the recycled material is predestined for the use in sport facilities, which explains that around half of the recycled ELTs are used to produce artificial turf, sports flooring and injury-prevention pavements on playgrounds. Since tires contain potentially toxic components, there is worry concerning the release of such chemical substances stemming from these products. As tires contain highly aromatic oils and carbon black, the presence of polycyclic aromatic hydrocarbons (PAH) and their carcinogenic properties are discussed controversially. This review issues a comprehensive overview of PAH release and a conclusive assessment on human health risk. Analytical studies dealing with the PAH content of consumer goods made from recycled rubber material and associated risk assessments are reviewed. In conclusion PAHs can be detected in consumer goods made from recycled rubber and are released into the environment. They reach humans via leaching (soil, ground water, rivers), oral intake, dermal exposure and inhalation. Thereby, dermal contact or inhalation is the primary route of exposure, whereas oral intake and environmental pollution are regarded as secondary risks. The amount of PAHs that could potentially harm humans is in the magnitude of urban pollution. Risk assessment studies reviewed in this article show no serious risk potential.

[Intestinal pseudoobstructions and gastric necrosis in mitochondrial myopathy]. / Intestinale Pseudoobstruktionen und Magenwandnekrose bei mitochondrialer Myopathie.

HISTORY AND CLINICAL FINDINGS: A 24-year-old female patient suffered for 4 months from recurrent abdominal pain, vomiting and diarrhea. Signs of an acute abdomen were the initial reason for admitting the patient to our hospital. The slim, pale patient had a complete bloated abdomen. Neurological status was normal. INVESTIGATIONS, TREATMENT AND COURSE: Radiographic examination showed a paralytic ileus with a megacolon. The recurrent abdominal symptoms were due to a covered perforation of the stomach. This was shrunken, scarred and had to be resected. Further intestinal pseudoobstructions were accompanied by substantial exsudations in the lungs, intestines and abdomen. At this time mutism like behavior patterns and an ophthalmoplegia appeared. Leukoencephalopathy in brain MRI scans and increased liquor-lactate suggested mitochondrial myopathy. DIAGNOSIS: The diagnosis of a mitochondrial myopathy was confirmed by increased liquor-lactate level, muscle biopsy with ragged-red fibers as well as abnormal mitochondrias and molecular-genetic investigations (mtDNA point mutation A3243G). Associations to MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) and MNGIE (mitochondrial neuro-gastrointestinal encephalomyopathy) syndrome are discussed. CONCLUSIONS: Unclear recurrent gastrointestinal symptoms even in the absence of neurological changes may reflect a mitochondrial disease. This applies especially to young patients with recurrent anorexia, vomiting and pseudoobstruction. In case of additional symptoms like ophthalmopathy, deafness, diabetes mellitus or signs of a MELAS syndrome the search for a mitochondrial system disorder is mandatory.