Insect Resistance to Pesticides and Human Consequences
Subject: FYI. More on your "registered" POISONS. Steve
Date: Sat, 19 Jan 2002 17:17:39 -0500
From: Stephen Tvedten <steve@getipm.com>
Organization: Get Set Inc. (www.getipm.com)
To: Paul Helliker <phelliker@cdpr.ca.gov>
Director, State of
California, Department of Pesticide Regulation
cc: Christine Whitman whitman.christine@epa.gov
I am a retired insecticide toxicologist who spent many years figuring out how insects get resistant to insecticides. The knowledge gained with insects seems to be applicable to what is happening to humans with autoimmune diseases such as MCS and sick building syndrome (SBS).
In resistant insects levels of juvenile hormone have been up-regulated compared to that of susceptible insects. This up-regulation allows for increased synthesis of the enzymes that degrade pesticides, resulting in resistance to them.
In humans, retinoic acid (RA) is the hormone analogous to insect juvenile hormone. RA plays a critical role in the up-regulation of levels of immune system proteins that defend us against viruses and environmental chemicals. When RA levels are low, we get sick. For reasons not yet understood, once the sickness occurs recovery is often very difficult.
For humans, exposure to formaldehyde and retinaldehyde, common agents in building materials, produces illness. The reason is that these aldehydes are oxidized by the same enzyme that oxidizes retinaldehyde to (RA). I suggest that lack of RA is the primary cause of most human autoimmune diseases including MCS and SBS
A more general means of protection is to avoid exposure to chemical pesticides, particularly insecticides such as organophosphates such as diazinon and chlorpyrifos, pyrethroids such as permethrin and cypermethrin, and carbamates such as carbaryl (Sevin) which poison esterases. This is important because retinoic acid is derived from retinyl ester precursors which have to be activated by reacting with esterases.
The best way to deal with these problems is prevention, banning the use of aldehydes in building materials and avoiding exposure to pesticides and other environmental chemicals which poison esterases. The second approach may be treatment with carotenoids and other plant-based chemicals that get converted to RA. This may compensate for the lack of RA resulting from chemical exposure.
From questioning many individuals with MCS, SBS, and similar health problems, it seems that having night blindness and/or photosensitivity is characteristic of individuals most at risk for MCS and SBS. The numbers involved, 15-20 % of the population parallel the proportion that seem to have lower than average levels of vitamin A.
The ways to measure this involve determining levels of the enzyme(s) known as retinyl esterases that activate retinol from fat-stored precursors. Measurements of levels of retinol (vitamin A) and RA may also be pertinent. All of these parameters can be dealt with once the medical community understands the critical role of RA in up-regulation of the synthesis of immune system proteins.
In summary, it seems that human autoimmune diseases as a general rule are associated with lower than average levels of vitamin A and RA. These low levels may be genetic. They may also result from poisoning of the process that produces RA.
Those that combine the genetic deficiency with exposures to environmental chemicals are those most at risk. The solutions: determine levels of RA in individuals and also, ban or otherwise avoid exposures to chemicals which may trigger these conditions.
F.W. Plapp, Jr., Professor Emeritus of Insecticide Toxicology, Texas A&M University
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