Instead of blanketing the planet with pesticides to combat mosquitoes, why aren’t we using x-rays or gamma ray technology that since the 1950s has been used effectively to control and eliminate problem insects.
The sterile insect technique, or SIT, has been used for decades to control insects such as the Mediterranean fruit fly. Basically, insects are exposed to radiation, which makes them sterile, and then they’re released into the wild to mate. However, since they’re sterile, no viable offspring are produced.
This is what they claim the GMO mosquito is intended to do as well, but for some of us anything GMO raises suspicion. If the SIT sterilizing technique works why not continue to use it? By doing so we would significantly reduce human exposure to harmful reproductive toxins and neurotoxins.
From Silent Spring, chapter 16, published 1962, Rachel Carson
“About a quarter century ago Dr. Knipling startled his colleagues by proposing a unique method of insect control. If it were possible to sterilize and release large numbers of insects, he theorized, the sterilized males would, under certain conditions, compete with the normal wild males so successfully that, after repeated releases, only infertile eggs would be produced and the population would die out.
The proposal was met with bureaucratic inertia and with skepticism from scientists, but the idea persisted in Dr. Knipling’s mind. One major problem remained to be solved before it could be put to the test–a practical method of insect sterilization had to be found. Academically, the fact that insects could be sterilized by exposure to X-ray had been known since 1916, when an entomologist by the name of G.A. Runner reported such sterilization of cigarette beetles. Hermann Muller’s pioneering work on the production of mutations by Z-ray opened up vast new areas of thought in the late 1920’s, and by the middle of the century various workers had reported the sterilization by X-rays or gamma rays of at least a dozen species of insects…
Beginning in August 1954, screw-worms reared and sterilized in an Agirculture Department laboratory in Florida were flown to Curacao and released from airplanes at the rate of about 400 per square mile per week. Almost at once the number of egg masses deposited on experimental goats began to decrease, as did their fertility. Only seven weeks after the releases were started all eggs were fertile. Soon it was impossible to find a single egg mass, sterile or otherwise. The screw-worm had indeed been eradicated on Curacao.
The resounding success of the Curacao experiment whetted the appetites of Florida livestock raisers for a similar feat that would relieve them of the scourge of screw-worms. Although the difficulties here were relatively enormous– an area 300 times as large as the small Caribbean island–in 1957 the United States Department of Agriculture and the State of Florida joined in providing funds for an eradication effort. The project involved the weekly production of about 50 million screw-worms at a specially constructed “fly factory,” the use of 20 light airplanes to fly pre-arranged flight patterns, five to six hours daily, each plane carrying a thousand paper cartons, each carton containing 200 to 400 irradiated flies.
The cold winter of 1957-58, when freezing temperatures gripped northern Florida, gave an unexpected opportunity to start the program while the screw-worm populations were reduced and confined to a small area. By the time the program was considered complete at the end of 17 months, 3.5 billion artificially reared, sterilized flied had been released over Florida and sections of Georgia and Alabama. The last-known animal wound infestation that could be attributed to screw-worms occurred in February 1959. In the next few weeks several adults were taken in traps. Thereafter no trace of the screw-worm could be discovered. Its extinction in the Southeast had been accomplished–a triumphant demonstration of the worth of scientific creativity, aided by thorough basic research, persistence, and determination.”
Which Pesticides are Used to Control Mosquitoes?
Four pesticides are commonly used for mosquito control. The trade names of these pesticides are:
- • Scourge
- • Anvil
- • Permethrin
- • Malathion
Scourge, Anvil, and Permethrin are pyrethroid (synthetic) insecticides. Malathion is an organophosphate insecticide.
What Should You Know About These Pesticides?
- SCOURGE (active ingredient: Resmethrin) is a synthetic pyrethroid insecticide. Pyrethroids affect the nervous system. They have been linked with liver and thyroid problems and they can also interfere with the immune and endocrine systems. Scourge contains the synergist (a chemical that increases the effectiveness of the active ingredient), pipernyl butoxide, which is classified by the EPA as a possible human carcinogen
- ANVIL (active ingredient: Sumithrin) is a synthetic pyrethroid insecticide, which may affect the central nervous system. Anvil contains 10% pipernyl butoxide. Sumithrin was shown to demonstrate significant estrogenicity in a 1999 study.¹ at the Mt. Sinai School of Medicine. This means it may promote tumor growth in cancers of the reproductive organs including breast cancer and prostate cancer. 1. Estrogenic and Antiprogestagenic Activities of Pyrethroid Insecticides. Biochemical and Biophysical Research Communications, October 1998, vol.251, no.3, p.855-859.
- PERMETHRIN is a synthetic pyrethroid insecticide and neurotoxin. It is more acutely toxic to children than to adults. The US Environmental Protection Agency (EPA) has classified it as a human carcinogen and it has been shown to cause immune system damage as well as birth defects. Note: Pyrethroids are highly toxic to fish, crustaceans, and bees. For that reason, EPA has established restrictions that prohibit their direct application to open water within 100 feet of lakes, steams, rivers, or bays.
- MALATHION is an organophosphate insecticide that can cause acute and long-term neurological health problems. Malathion is being reviewed by the EPA for its potential as a low level carcinogen. It is toxic to fish and highly toxic to aquatic invertebrates and amphibians. Organophosphate pesticides (malathion, glyphosate, neonicitinoids…) are cholinesterase inhibitors.
WHICH PESTICIDES CAN INHIBIT CHOLINESTERASE? (from Extoxnet, a project provided through Cornell University, Michigan State and UC Davis)
Any pesticide that can bind, or inhibit, cholinesterase, making it unable to breakdown acetylcholine, is called a “cholinesterase inhibitor,” or “anticholinesterase agent.” The two main classes of cholinesterase inhibiting pesticides are the organophosphates (OPs) and the carbamates (CMs). Some newer chemicals, such as the chlorinated derivatives of nicotine can also affect the cholinesterase enzyme.
Organophosphate insecticides include some of the most toxic pesticides. They can enter the human body through skin absorption, inhalation and ingestion. They can affect cholinesterase activity in both red blood cells and in blood plasma, and can act directly, or in combination with other enzymes, on cholinesterase in the body. The following list includes some of the most commonly used OPs:
- acephate (Orthene)
- azinphos-methyl (Guthion)
- carbofuran (Furadan, F formulation)
- carbophenothion (Trithion)
- chlorfenvinphos (Birlane)
- chlorpyrifos (Dursban, Lorsban)
- coumaphos (Co-Ral)
- crotoxyphos (Ciodrin, Ciovap)
- crufomate (Ruelene)
- demeton (Systox)
- diazinon (Spectracide)
- dichlorvos (DDVP, Vapona)
- dicrotophos (Bidrin)
- dimethoate (Cygon, De-Fend)
- dioxathion (Delnav)
- disulfoton (Di-Syston)
- ethoprop (Mocap)
- fenamiphos (Nemacur)
- fenitrothion (Sumithion)
- fensulfothion (Dasanit)
- fenthion (Baytex, Tiguvon)
- fonofos (Dyfonate)
- isofenfos (Oftanol, Amaze)
- malathion (Cythion)
- methamidophos (Monitor)
- methidathion (Supracide)
- methyl parathion
- mevinphos (Phosdrin)
- naled (Dibrom)
- oxydemeton-methyl(Meta systox-R)
- parathion (Niran, Phoskil)
- phorate (Thimet)
- phosalone (Zolonc)
- phosmet (Irnidan, Prolate)
- phosphamidon (Dimecron)
- temephos (Abate)
- terbufos (Counter)
- tetrachlorvinphos (Rabon, Ravap)
- trichlorfon (Dylox, Neguvon)
Carbamates, like organophosphates, vary widely in toxicity and work by inhibiting plasma cholinesterase. Some examples of carbamates are listed below:
- aldicarb (Temik)
- bendiocarb (Ficam)
- carbaryl (Sevin)
- formetanate (Carzol)
- methiocarb (Mesurol)
- methomyl (Lannate, Nudrin)
- oxamyl (Vydate)
- pinmicarb (Pirimor)
- propoxur (Baygon)
WHAT HAPPENS AS A RESULT OF OVEREXPOSURE TO CHOLINESTERASE INHIBITING PESTICIDES?
Overexposure to organophosphate and carbamate insecticides can result in cholinesterase inhibition. These pesticides combine with acetylcholinesterase at nerve endings in the brain and nervous system, and with other types of cholinesterase found in the blood. This allows acetylcholine to build up, while protective levels of the cholinesterase enzyme decrease. The more cholinesterase levels decrease, the more likely symptoms of poisoning from cholinesterase inhibiting pesticides are to show.
Sterilization Insect Technique machine, image courtesy of the FAO