The Ontario High School at the center of controversy for having a male teaching young students while donning a large prosthetic bust has issued a full defense of the teacher in a newly-leaked email sent to parents.
On September 16, Reduxx confirmed the identity and employment status of the subject of viral images and videos which depicted a male instructor teaching students while wearing an unnaturally large prosthetic bust, complete with prominently protruding nipples.
While the images and videos had circulated for a few days prior, there was widespread confusion and disbelief as to whether or not the images were real, or, as some speculated, part of an elaborate hoax or comedy sketch.
The lowest lethal dose for a child is 143 mg/kg. Human deaths from rotenone poisoning are rare because its irritating action causes vomiting. Deliberate ingestion of rotenone can be fatal.
The compound decomposes when exposed to sunlight and usually has an activity of six days in the environment. It oxidizes to rotenolone, which is about an order of magnitude less toxic than rotenone. In water, the rate of decomposition depends upon several factors, including temperature, pH, water hardness and sunlight. The half-life in natural waters ranges from half a day at 24 °C to 3.5 days at 0 °C.
In 2000, injecting rotenone into rats was reported to cause the development of symptoms similar to those of Parkinson’s disease (PD). Rotenone was continuously applied over a period of five weeks, mixed with DMSO and PEG to enhance tissue penetration, and injected into the jugular vein. The study does not directly suggest rotenone exposure is responsible for PD in humans, but is consistent with the belief that chronic exposure to environmental toxins increases the likelihood of the disease.
In addition, studies with primary cultures of rat neurons and microglia have shown low doses of rotenone (below 10 nM) induce oxidative damage and death of dopaminergicneurons, and it is these neurons in the substantia nigra that die in Parkinson’s disease. Another study has also described toxic action of rotenone at low concentrations (5 nM) in dopaminergic neurons from acute rat brain slices. This toxicity was exacerbated by an additional cell stressor – elevated intracellular calcium concentration – adding support to the ‘multiple hit hypothesis’ of dopaminergic neuron death.
The neurotoxinMPTP had been known earlier to cause PD-like symptoms (in humans and other primates, though not in rats) by interfering with complex I in the electron transport chain and killing dopaminergic neurons in the substantia nigra. Further studies involving MPTP have failed to show development of Lewy bodies, a key component to PD pathology. However at least one study recently has found evidence of protein aggregation of the same chemical makeup as that which makes up Lewy bodies with similar pathology to Parkinson’s disease in aged Rhesus monkeys from MPTP. Therefore, the mechanism behind MPTP as it relates to Parkinson’s disease is not fully understood. Because of these developments, rotenone was investigated as a possible Parkinson-causing agent. Both MPTP and rotenone are lipophilic and can cross the blood–brain barrier.
In 2010, a study was published detailing the progression of Parkinson’s-like symptoms in mice following chronic intragastric ingestion of low doses of rotenone. The concentrations in the central nervous system were below detectable limits, yet still induced PD pathology.