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Pesticide Chemicals
and
Their Effect On Our Health and Our Environment

by

Kate Smith-Morse

lmiprothrin. Cypermethrin. Atrazine. Chlorpyrifos. You probably won't recognize these words, though almost all of them may have a great impact on your everyday life. They are chemicals found in pesticides. Some of them have been restricted by the Environmental Protection Agency (EPA), but many that can be harmful are still in common use. For instance, Sulfuric Acid, which is a substance so powerful it can strip the paint off a car in two seconds flat, was commonly used in pesticide production up until September, 1999.

The purpose of my paper is to draw a conclusion as to whether chemicals used in pesticides, be they used for household pest control or crop pest control, are harmful to our health and our environment. I believe that if we and the earth are exposed to some of these chemicals for too long, then they can have harmful effects upon ourselves and our world.

I will be speaking mainly about 3 chemicals. Two of them, Cypermethrin and lmiprothrin, can be found in everyday pesticides, like Raid. The other, DDT, was used in crop pesticides until it was banned after the publishing of Silent Spring by Rachel Carson. In fact, this book revolutionized the pesticide industry, and is one of the main reasons we have pesticide chemical reforms this day. Hopefully, by the end of this paper, you will know a little more about pesticide reform, as well as pesticide chemicals in general.

I'd like to start out by talking about a fairly new chemical to the United States. It's in the chemical family of Synthetic Pyrethroids. Synthetic Pyrethroids are a synthetic form of a chemical extracted from the Chrysanthemum flower, known as Pyrethrum. The pesticidal chemical I am speaking of is known as lmiprothrin.

lmiprothrin was first registered in the US by the EPA in March of 1998. It was used commonly before us in other countries such as Japan. Because of Imiprothrin's newness to the States, we don't know very much about it. However, the following is some general information about it, and the limited knowledge we have, so far, on its effects.

Imiprothrin, in its physical form, is a liquid. The liquid is a golden-yellow, the color of amber. It has a slight sweetly-sour scent to it, which isn't surprising, for it's pH level is 5.22 - 5.95, meaning it would be an acid.

lmiprothrin has a chemical formula of C17H22N204, and a generic name of [2,5-dioxo-3-(2-propynyl)-1 -imidazolidinyl] methyl (1 RS)- cis- trans-chrysanthemate. Its trade name is Pralle. lmiprothrin is an Insecticide, specifically targeted at Roaches, Waterbugs, Ants, Silverfish, Crickets, and Spiders. Basically, your common household-pest remover. The type and method of application is crack, crevice, and spot application.

lmiprothrin is broken down easily by sunlight, and partially soluble in water. One of the main problems with it is the fact that it binds to soil very easily. Also, its half life is moderately persistent, being about 30 days; it also has a Pesticide Movement Rating of Moderately High. All these factors added together make it potentially health and environmentally harmful. Allow me to explain.

Half life is how long it takes for half of a chemical to, basically, wear off. So, every month or so, half of what's left of the chemical wears off. However, if you continue adding onto this, the chemical is not going to wear out at the normal rate. Also, Pesticide Movement is how fast it can move through the soil. So, this means that firstly, lmiprothrin doesn't wear out very quickly. Secondly, it moves through soil rather effectively. Thirdly, it can attach itself to that soil. Fortunately, because it is such a new chemical, it is only used in about 5 products out of many. This means that it is not yet very dangerous, but the more research that is done on it, and the more commonly it is used, may show dangerous effects.

Besides this, Imiprothrin has been shown to have effects directly on human health. It irritates the skin and eyes, even when they are not in direct contact with the chemical. The EPA did a study on the effects of the chemical on rats as well as rabbits. In rats, their body weight decreased significantly, but the liver and other organs' weight increased. In Rabbits, premature labor, abortion or mortality were observed. An Acute Toxicity Test was preformed, but the results were extremely varied. Detailed results of all these tests, including a mutation test which was preformed on Salmonella, can be found in Appendix A- Test Results.

The next chemical I'll talk about is, like the one before it, a Synthetic Pyrethroid. However, it's been around for a while longer than Imiprothrin. It was first synthesized in 1974, and first marketed in 1977 by Shell. The chemical I'm talking about is Cypermethrin. The following is information about it in general, and on its effects.

Cypermethrin is a dark yellow, or brownish solid. It is often supplied as a concentrated yellow or brownish solution. It's melting point is 62 - 75 degrees Celsius, and is insoluble in water. Cypermethrin is generally stable, but incompatible with bases and strong oxidizing agents. This means it's probably an acid, seeing as acids and bases are incompatible, or react together.

Cypermethrin is an Insecticide, as well as an Acaricide. It's generic name is cyano(3~phenoxyphenyl)fl1ethyI 3-(2,2-dichloroethenyl)-2,2-dimethylcycloprOpanecarbOXylate, and it's chemical formula is C22H19C12N03

Cypermethrin targets pests about the same as lmiprothrin, for they are used in many of the same products. It kills insects which eat or come into contact with it, and works quickly by affecting the insect's central nervous system. Cypermethrin also has 4 isomers which have their own ISO common names- alpha-cypermeth ri n, beta-cypermethrin, theta-cypermeth rin, and zeta-cypermethrin.

Cypermethrin's short-term effects include burning or tingling sensations on the skin, and possible irritation to skin and eyes. Long term effects include possible liver changes, and pathological changes were observed in the cortex of the thymus, liver, adrenal glands, lungs, and skin in rabbits repeatedly fed Cypermethrin.

"It interacts with the sodium channels in nerve cells through which sodium enters the cell in order to transmit a nerve signal. These channels can remain open for up to seconds, compared to the normal period of a few milliseconds, after a signal has been transmitted. Cypermethrin also interferes with other receptors in the nervous system. The effect is that of long-lasting trains of repetitive impulses in sense organs." (Directly quoted from a Cypermethrin Fact Sheet.)

Cypermethrin has been classified as a possible human carcinogen. Tests on animals show that it is a weak carcinogen (some female mice developed non-cancerous lung tumors, however), but no evidence so far shows that it has cancerous effects on humans.

Fortunately, however, Cypermethrin can be excreted very quickly. Male and female rats were observed to have excreted 50-65% of the chemical in their urine within 48 hours. They excreted 30% of it in their feces within 3 days. Men who voluntarily ingested Cypermethrin (in low doses, only a little over a milligram per killogram of body weight) in corn oil excreted between 49-78% within 24 hours. These tests indicate Cypermethrin isn't likely to accumulate in the body.

Cypermethrin was also found to be slightly mutagenic. It was found to be genotoxic in mouse spleen and bone marrow, but all other tests have proved negative.

Cypermethrin is mildly toxic, and was classified by the World Health Organization (WHO) and 'moderately hazardous'. Cypermethrin is insoluble in water, and extremely toxic to fish, as well as to water insects and water invertebres. It is practically non-toxic to birds, but highly toxic to bees. Typically, the half life of Cypermethrin is approximately 30 days, although it can range anywhere from two to eight weeks. The average half life on foliage is approximately 5 days. It has an extremely low potential of moving in soil, having a very low potential to contaminate groundwater because it tightly binds to soil particles, though soil microbes are able to rapidly break it down.

Finally, I'd like to talk about a dangerous and deadly toxin. Ironically enough, the chemical's name would be an acronym for that description of the chemical. DDT. What I'll familiarize you with now is what exactly it is, and why it was banned.

DDT stands for dichlro-diphenyl-trichloroethane. In its physical form, DDT is a white, crystalline solid with no odor or taste. It's generic name is (1,1 ,1-trichloro-2,2-bis(p-chlorophenyl)ethane) and its chemical formula is C14H9C15 It is an Insecticide used to control agricultural pests, as well as lice and mosquitos which could carry diseases, such as malaria and typhus (malaria being carried by mosquitos, and typhus being carried by lice). It was used commonly for the purpose during WWII, which is why, at first, everyone believed it to be harmless, for it didn't show any harm to the soldier it was used on.

DDT was the first of the chlorinated insecticides. It was originally prepared in 1873, but not until 1939 did Paul Muller of Geigy Pharmaceutical in Switzerland discover the effectiveness of DDT as an insecticide. He was awarded the Nobel Prize in medicine and physiology in 1948 for this discovery.

DDT increased widely in use after the war, because of its effectiveness against insects. In fact, when it was used against those two (lice and mosquitos) disease-carrying insects, the WHO estimated approximately 25 million lives were saved. DDT seemed, at first, to be the ideal insecticide. It was cheap, and was of relatively low toxicity to mammals. But problems related to the extensive use of DDT began to appear in the late 1940s. Many species of insects began to develop a resistance to the chemical, and it was also found to have a high toxicity towards fish. It was discovered to remain in the environment for a long time, and have very damaging effects on reproduction in bird populations.

The chemical stability of DDT and it's fat solubility compounded the problem. DDT is not metabolized very rapidly by animals; instead, it is deposited and stored in the fatty tissues. The biological half-life of DDT is about eight years; that is, it takes about eight years for an animal to metabolize half of the amount it assimilates. If ingestion continues at a steady rate, DDT builds up within the animal over time.

DDT was finally banned in 1973. The main reason the truth about it came out had everything to do with a woman by the name of Rachel Carson, and her book, Silent Spring. It told of the horrors that DDT produced, and, though everyone from Chemical Companies to the government tried to convince the public that she was completely hysterical (Time magazine added that she had simply used "emotion-fanning words"; by others, she was dismissed as nothing but a "priestess of nature") and that every accusation of hers was without foundation (Robert White Stevens can be quoted with "The crux, the fulcrum over which the argument chiefly rests, is that Miss Carson maintains that the balance of nature is a major force in the survival of man, whereas the modern chemist, the modern biologist and scientist, believes that man is steadily controlling nature."), the public had collectively gasped, sat up, and listened.

Miss Carson had checked and rechecked every one of her sources. Not only that, but when sent to investigate her charges, researchers had found that, if anything, her truths were understated.

For example, when tested on lab animals, it was found that DDT causes tumors in the liver, adrenals, lungs, and lymphatic tissues. DDT is suspected, also, to help "promote" carcinogens in breast cancer; when DDT and a carcinogen were administered together, breast cancer was found to appear faster than when just the carcinogen was applied.

Unfortunately, DDT is still in widespread use, not in the US, but in other, mostly unindustrialized countries. The WHO permits its use only for the treatment of malaria, but the World Wildlife Federation (WWF) wishes to call for a complete and total ban on the chemical and its production. As they state in an online article on the matter "Currently, DDT's only official use, as specified by the World Health Organization (WHO), is for the control of disease vectors in indoor house spraying - although other (illegal) uses are suspected. Because of the availability of safer and effective alternatives for fighting malaria, WWF is calling for a global phaseout and eventual ban on DDT production and use."

Referring back to the beginning of this paper, I find that I must come up with a conclusion to my hypothesis- "If we and the earth, are exposed to some of these chemicals for too long, then they can have harmful effects upon ourselves and our environment." My conclusion is that my hypothesis was correct. Of course, that wasn't a hard conclusion to draw, because many people had already asked themselves that, and their research is what this paper is.

To sum it up briefly, the ideal solution would be to stop using pesticides. To just let nature take its course, because it seems that before, nature did a pretty good job of keeping things under control. Pesticides are always going to have pros and cons, but the cons so heavily outweigh the pros, that it just doesn't really seem worth it to try to tamper with a system that was already running smoothly.

I believe that if given more time, two things would occur. One, we would find out continually the horrors of pesticidal chemicals on us and the environment. Two, we would find that there are so many safer, more effective ways of "tampering" with nature; or just let nature take its natural corse.

Perhaps this world is destined for doom, maybe it's not, but I believe, when all is said, done, and over with, things will turn out right in the end.

Appendix A: Test Results

Subchronic Toxicity:

A 13-week oral rat study showed significantly body weight loss and suppression of feeding rateat doses of 3000, 6000 or 10000 ppm. Hematology and blood chemistry values were also altered at these doses as compared to the lowest dose (100 ppm) and the control group. The weights of the liver and other organs increased in the three higher dose groups. The NOEL was judged to be 100 ppm and the LOEL to be 3000 ppm. A 21 day demial study with rats conducted at 100, 300 or 1000 mg/kg body weight showed an increase in the incidence of dermal acanthosis and hyperkeratosis in the high dose group. The NOEL was 300 mg/kg body weight based on these effects and the LOEL was 1000 mg/kg body weight/day.

A 4- week inhalation study exposed rats to 2.4, 22.0 or 186 mg/m3 of imiprothrin with a median aerodynamic diameter of 0.80 to 0.86 urn. The NOEL was 22.0 mg/m3 based on lower total body weight gain, changes in hematology and clinical chemistry parameters, and changes in liver and the salivary glands. The LOEL was 186 mg/rn3.

Develonmental Toxicity

Rabbits were fed with imiprothrin at 30, 100 or 300 mg/kg body weight/day. The maternal NOEL was 30 mg/kg/body weight/day based upon suppressed body weight gain and food consumption, while the LOEL was 100 mg/kg body weight/day. At 300 mg/kg body weight/day premature labor, abortion and mortality were noted. The developmental NOEL was not determined (i.e. it was less than 100 mg/kg body weight/day), on the basis of decreased fetal body weight and frontal bone hypoplasia. An increased incidence of the 27th pre- sacral vertebra occurred in all treatment groups. The LOEL was not determined.

An additional developmental study was conducted on rabbits at doses of 3, 10 or 30 mg/kg body weight/day to determine the developmental end points which the earlier study had not been able to define. This study showed no treatment related developmental effects. The developmental NOEL, based on both studies, was 30 mg/kg/body weight/day while the LOEL was 100 mg/kg/body weight/day.

Mutagenicity

lmiprothrin was subjected to Ames tests with Salmonella and with E. coli. Both tests showed imiprothrin not to be mutagenic. An in vitro gene mutation assay with Chinese hamster cells showed that this chemical does not have the potential to cause gene mutations. An in vitro chromosome aberration assay showed that imiprothrin did have the potential to cause chromosome aberrations in Chinese hamster lung cells in the presence of S9 metabolic activation. An in vivo mouse bone marrow micronucleus test did not show chromosome damage. Two in vivo/in vitro unscheduled DNA synthesis tests were conducted with primary rat hepatocytes; time course and dose response. Neither UDS test showed an increase in such synthesis. The weight- of- evidence indicates imiprothrin is not genotoxic.

Toxicoloy Characteristics

End- Use Formulations:

A. Pralle (50.5% imiprothrin)

Acute Oral Toxicity (Rats: male and female): The acute oral LD5O was 4500 mg/kg for males and 2400 mg/kg for females.
Toxicology Category III.

Acute Dermal Toxicity (Rats: male and female): The acute dermal LD5O is greater than 2000 mg/kg.
Toxicity Category III.

Acute Inhalation Toxicity (Rats: male and female): The acute inhalation LC5O is greater than 2 mg/L for male and female rats.
Toxicity Category IV.

Primary Eye Irritation (Rabbits): non-irritating.
Toxicity Category IV.

Primary Dermal Irritation (Rabbits): non- irritating.
Toxicity Category IV.

Dermal Sensitization- Not a sensitizer.

B. Multicide Intermediate 2734 (16% imiprothrin, 11.2% d-phenothrin, 5 2.8% MGK 264)

Acute Oral Toxicity (Rats: male and female): Combined LD5O is greater than 5 g/kg.
Toxicology Category IV.

Acute Dermal Toxicity (Rabbits: male and female): Combined LD5O is greater than 2 g/kg.
Toxicity Category III.

Acute Inhalation Toxicity (Rabbits: male and female): Combined LC5O is greater than 2.69 mg/L.
Toxicity Category IV.

Primary Eye Irritation (Rabbits): mild irritant. Toxicity Category III.

Primary Dermal Irritation (Rabbits): non-irritating. Toxicity Category IV.

Dermal Sensitization- Sensitizer.

C. Multicide Pressurized Roach Spray 27341 (0.4% imiprothrin, 0.5% d- phenothrin, 1% MGK 264)

Acute Oral Toxicity (Rats: male and female): Combined LD5O is greater than 5 g/kg.
Toxicology Category IV.

Acute Dermal Toxicity (Rabbits: male and female): Combined LD5O is greater than 2 g/kg.
Toxicity Category III.

Acute Inhalation Toxicity (Rabbits: male and female) Combined LC5O is greater than 3.82 mg/L.
Toxicity Category IV.

Primary Eye Irritation (Rabbits) Mild irritant.
Toxicity Category III.

Primary Dermal Irritation (Rabbits): moderate irritation.
Toxicity Category III.

Dermal Sensitization- Sensitizer.

D. Raid Ant & Roach 17 (0.1 % imiprothrin, 0.1 % cypermethrin)

Acute Oral Toxicity (Rats: male and female): Combined LD5O is greater than 5 g/kg.
Toxicity Category IV.

Acute Dermal Toxicity (Rabbits: male and female): Combined LDSO is greater than 5 g/kg.
Toxicity Category IV.

Acute Inhalation Toxicity (Rabbits: male and female) Combined LC5O is greater than 5.1 mg/L.
Toxicity Category IV.

Primary Eye Irritation (Rabbits) No corneal irritation.
Toxicity Category IV.

Primary Dermal Irritation (Rabbits) moderate irritation.
Toxicity Category III.

Dermal Sensitization- Not a dermal sensitizer.

ENVIROMENTAL FATE CHARACTERISTICS: Technical Grade imiprothrin

Hydrolysis Data- lmiprothrin degrades by pH sensitive hydrolysis with calculated half- lives of less than one day at pH 9 and approximately 59 days at pH 7. Degradation did not occur at pH 5. There was only one degradate which accounted for more than 10% of the radioactivity at pH 7 and 9. this compound was identified as N-carbamoyl- N- propargyglycine (CPC).

ECOLOGI CAL EFFECTS CHARACTERISTICS: Technical Grade imiprothrin

Freshwater Fish
Rainbow trout: LCSO = 0.038 ppm.

Aquatic Invertebrate
Daphia magna: EC5O =0.051 ppm.

Avian Dietary
Bobwhite quail and mallard ducks: LC5O = are both greater than 5620 ppm.

Warmwater Fish
Bluegill: LC5O = 0.07 ppm.

SUMMARY OF DATA GAPS: There are no data gaps for this use.

Appendix B: Bibliography

ATSCR Information Center. "DDT, DDE, and DDD FAQ." ToxFAOs. Online. January 19. 2001.
http://www.atsdr.cdc.gov/tfacts35 .html.

Author Unavailable. "cypermethrin [523 15-07-8]." ChemFinder.com. Online. December 30, 2000.
http://www.chemfinder.com/result.asp?molrel_id523 1 5-07-8.

Author Unavailable. "Cypermethrin". Toxin. Online. December 30, 2000.
http://www.nccnsw.org.au/member/tec/proj ects/tcye/tox/cypermethrin.html.

Author Unavailable. "Cypermethrin Fact Sheet." Pesticide Action Network UK. Online. January 19, 2001.
http ://www.pan-uk.org/actives/cyperrnet.htm.

Author Unavailable. "Safety Data for Cypermethrin." Physical & Theoretical Chemistry Lab. Safety Home Page. Online. January 19, 2001.
http ://physchern .ox.ac. uk/MSDS/C/cypermethrin.html.

Author Unavailable. "WWF's Efforts to Phase Out DDT."World Wildlife Federation. Online. January 19, 2001.
http://www.worldwildlife.org/toxics/progareas/pop/ddt.htm.

Beeder, Owen. Telephone Interview. January 18, 2001.

Carson, Rachel. Silent Spring. Boston: Houghton Mifflin Company. 1994.

DeLuise, Linda. "Imiprothrin."EPA New Pesticide Fact Sheets. Online. January 18, 2001.
http ://www .epa.gov/opprd00 I /factsheets/im iproth.htm.

Harrison, Karl. "DDT a Banned Insecticide."Molecules of the Month. Online. January 19, 2001.
http ://www.chem.ox.ac. uk/mom/ddt/ddt.html.

Jenkins, J.J. and Kerle, L.A. "OSU Extension Pesticide Properties Database."NPTN. Online. January 19, 2001.
http://ace.orst.edu/info/nptn/ppdmove.htm.

National Pesticides Telecommunications Network. Cypermethrin. Oregon: NPTN Oregon State University. 1998.

NPTN Telephone Staff Member. Telephone Interview. January 19, 2001.

Snedeker, Suzanne. "DDT, DDE and the Risk of Breast Cancer."BCERF Home. Online. January 19, 2001.
http ://www.cfe.cornell.edu/beerf/factsheet/Pesticide/fs2.ddt.cfm.

Wood, Alan. "Cypermethrin Data Sheet."Compendium of Pesticide Common Names. Online. January 19, 2001.
http://www.helrss.demon.co.uk/cypermethrin.html.

Wood, Alan. "Alpha-Cypermethrin."Compendium of Pesticide Common Names. Online. January 19, 2001.
http ://www.helrss.demon.co.uk/alpha-cypermethrin.htrnl.

Wood, Alan. "Beta-Cypermethrin."Compendium of Pesticide Common Names. Online. January 19, 2001.
http://www.helrss.demon.co.uk/beta-cypermethrin.html.

Wood, Alan. "Theta-Cypermethrin."Compendium of Pesticide Common Names. Online. January 19, 2001.
http://www.helrss.demon.co. uk/theta-cypermethrin.html.

Wood, Alan. "Zeta- Cypermethrin."Compendium of Pesticide Common Names. Online. January 19, 2001.
http://www.helrss.demon.co.uk/zeta-cypermethrin.html.

Wood, Alan. "Imiprothrin Data Sheet."Compendium of Pesticide Common Names. Online. January 19, 2001.
http://www.helrss.demon.co.uk/imiprothrin.html.

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