In article ,
Roy wrote:

On Monday, July 15, 2013 7:41:51 AM UTC-6, songbird wrote:
as our space is usually limited and i can't

cook it anyways we've never actually grown

cabbages before this year. the difference

this year is someone we know who makes

saurkraut and Ma wanting to do something

nice for them. we put in 12 plants.


some deletion
Derris dust will control those cabbage moths...why don't you use it?


==

Toxicity

Rotenone is classified by the World Health Organization as moderately
hazardous.[14] It is mildly toxic to humans and other mammals, but
extremely toxic to insects and aquatic life, including fish. This higher
toxicity in fish and insects is because the lipophilic rotenone is
easily taken up through the gills or trachea, but not as easily through
the skin or the gastrointestinal tract. Rotenone is toxic to
erythrocytes in vitro. [15]

The lowest lethal dose for a child is 143 mg/kg. Human deaths from
rotenone poisoning are rare because its irritating action causes
vomiting.[16] Deliberate ingestion of rotenone can be fatal.[17]

The compound decomposes when exposed to sunlight and usually has a
lifetime of six days in the environment.[18] In water, rotenone may last
six months.[citation needed]
Parkinson's disease

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.[19] 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.[20]

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 dopaminergic neurons,[21] 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.[22] 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 neurotoxin MPTP 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. However, further studies involving MPTP
have failed to show development of Lewy bodies, a key component to PD
pathology. Therefore, the mechanism behind MPTP as it relates to
Parkinson's disease is not fully understood.[23] 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.[24]

In 2011, a US National Institutes of Health study showed a link between
rotenone use and Parkinson's disease in farm workers.[25]
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