Pesticidesare substances meant for attracting, seducing, and then destroying, or mitigating anypest.They are a class ofbiocide. The most common use of pesticides is as plant protection products (also known as crop protection products), which in general protect plants from damaging influences such asweeds,plant diseasesorinsects. This use of pesticides is so common that the termpesticideis often treated as synonymous withplant protection product, although it is in fact a broader term, as pesticides are also used for non-agricultural purposes.. In general, a pesticide is achemicalor biological agent (such as avirus,bacterium , antimicrobial, ordisinfectant) that deters, incapacitates, kills, or otherwise discourages pests. Target pests can include insects, plantpathogens, weeds, mollusks,birds,mammals,fish,nematodes(roundworms), andmicrobesthat destroy property, cause nuisance, or spread disease, or are diseasevectors. Although pesticides have benefits, some also have drawbacks, such as potential toxicity to humans and other desired species. According to theStockholm Convention on Persistent Organic Pollutants, 9 of the 12 most dangerous and persistentorganic chemicalsare organochlorine pesticides.

DefinitionTheFood and Agriculture Organization(FAO) has definedpesticideas:Any substance or mixture of substances intended for preventing, destroying, or controlling any pest, including vectors of human or animal disease, unwanted species of plants or animals, causing harm during or otherwise interfering with the production, processing, storage, transport, or marketing of food, agricultural commodities, wood and wood products or animal feedstuffs, or substances that may be administered to animals for the control of insects, arachnids, or other pests in or on their bodies. The term includes substances intended for use as a plant growth regulator, defoliant, desiccant, or agent for thinning fruit or preventing the premature fall of fruit. Also used as substances applied to crops either before or after harvest to protect the commodity from deterioration during storage and transport.

Pesticides can be classified by targetorganism(e.g.,herbicides,insecticides,fungicides,rodenticides, andpediculicides- see table), chemical structure (e.g., organic, inorganic, synthetic, orbiological (biopesticide), although the distinction can sometimes blur), and physical state (e.g.gaseous (fumigant)).Biopesticidesinclude microbial pesticides and biochemical pesticides.Plant-derived pesticides, or "botanicals", have been developing quickly. These include the pyrethroids,rotenoids,nicotinoids, and a fourth group that includes strychnineandscilliroside.Many pesticides can be grouped into chemical families. Prominent insecticide families includeorganochlorines,organophosphates, and carbamates.Organochlorinehydrocarbons (e.g.,DDT) could be separated into dichlorodiphenylethanes, cyclodiene compounds, and other related compounds. They operate by disrupting the sodium/potassium balance of the nerve fiber, forcing the nerve to transmit continuously. Their toxicities vary greatly, but they have been phased out because of their persistence and potential to bioaccumulate.Organophosphateandcarbamateslargely replaced organochlorines. Both operate through inhibiting the enzymeacetylcholinesterase, allowingacetylcholineto transfer nerve impulses indefinitely and causing a variety of symptoms such as weakness or paralysis. Organophosphates are quite toxic to vertebrates, and have in some cases been replaced by less toxic carbamates. Thiocarbamate and dithiocarbamates are subclasses of carbamates. Prominent families of herbicides include phenoxy and benzoic acid herbicides (e.g.2,4-D), triazines (e.g.,atrazine), ureas (e.g.,diuron), and Chloroacetanilides (e.g.,alachlor). Phenoxy compounds tend to selectively kill broad-leaf weeds rather than grasses. The phenoxy and benzoic acid herbicides function similar to plant growth hormones, and grow cells without normal cell division, crushing the plant's nutrient transport system. Triazines interfere with photosynthesis. Many commonly used pesticides are not included in these families, includingglyphosate.Pesticides can be classified based upon their biological mechanism function or application method. Most pesticides work by poisoningpests.A systemic pesticide moves inside a plant following absorption by the plant. With insecticides and most fungicides, this movement is usually upward (through thexylem) and outward. Increased efficiency may be a result. Systemic insecticides, which poisonpollenandnectarin theflowers, may killbeesand other neededpollinators.In 2009, the development of a new class of fungicides called paldoxins was announced. These work by taking advantage of natural defense chemicals released by plants called phytoalexins, which fungi then detoxify using enzymes. The paldoxins inhibit the fungi's detoxification enzymes. They are believed to be safer and greener. UsesPesticides are used to control organisms that are considered to be harmful. For example, they are used to kill mosquitoesthat can transmit potentially deadly diseases likeWest Nile virus,yellow fever, andmalaria. They can also kill bees,waspsorantsthat can cause allergic reactions. Insecticides can protect animals from illnesses that can be caused by parasitessuch asfleas. Pesticides can prevent sickness in humans that could be caused bymoldyfood or diseased produce. Herbicides can be used to clear roadside weeds, trees and brush. They can also kill invasiveweedsthat may cause environmental damage. Herbicides are commonly applied in ponds and lakes to controlalgaeand plants such as water grasses that can interfere with activities like swimming and fishing and cause the water to look or smell unpleasant. Uncontrolled pests such as termites and mould can damage structures such as houses.Pesticides are used in grocery stores and food storage facilities to managerodentsand insects that infest food such as grain. Each use of a pesticide carries some associated risk. Proper pesticide use decreases these associated risks to a level deemed acceptable by pesticide regulatory agencies such as theUnited States Environmental Protection Agency(EPA) and the Pest Management Regulatory Agency (PMRA) of Canada.Pesticides can save farmers' money by preventing crop losses to insects and other pests; in the U.S., farmers get an estimated fourfold return on money they spend on pesticides.One study found that not using pesticides reduced crop yields by about 10%. DDT, sprayed on the walls of houses, is an organochloride that has been used to fightmalariasince the 1950s. Recent policy statements by theWorld Health Organizationhave given stronger support to this approach.Dr. Arata Kochi, WHO's malaria chief, said, "One of the best tools we have against malaria is indoor residual house spraying. Of the dozen insecticides WHO has approved as safe for house spraying, the most effective is DDT."A later October 2007 study linked breast cancer from exposure to DDT prior topuberty.Other studies have found no link.Symptoms include nervous excitement, tremors, convulsions, or death. Scientists estimate that DDT and other chemicals in the organophosphate class of pesticides have saved 7 million human lives since 1945 by preventing the transmission of diseases such asmalaria,bubonic plague,sleeping sickness, andtyphus.However, DDT use is not always effective, as resistance to DDTwas identified in Africa as early as 1955, and by 1972 nineteen species of mosquito worldwide were resistant to DDT. Health effects

A sign warning about potential pesticide exposure.Pesticides may cause acute and delayed health effects in people who are exposed.Pesticide exposure can cause a variety of adverse health effects, ranging from simple irritation of the skin and eyes to more severe effects such as affecting the nervous system, mimicking hormones causing reproductive problems, and also causing cancer.A 2007systematic reviewfound that "most studies on non-Hodgkin lymphoma and leukemia showed positive associations with pesticide exposure" and thus concluded that cosmetic use of pesticides should be decreased.]Limited evidence also exists for other negative outcomes from pesticide exposure including neurological,birth defects,fetal deathand neurodevelopmental disorder. The American Academy of Pediatrics recommends limiting exposure of children to pesticides and using safer alternatives: The World Health Organization and theUN Environment Programmeestimate that each year, 3 million workers in agriculture in the developing world experience severepoisoning from pesticides, about 18,000 of whom die. Owing to inadequate regulation and safety precautions, 99% of pesticide related deaths occur in developing countries that account for only 25% of pesticide usage. According to one study, as many as 25 million workers in developing countries may suffer mild pesticide poisoning yearly. One study found pesticide self-poisoning the method of choice in one third of suicides worldwide, and recommended, among other things, more restrictions on the types of pesticides that are most harmful to humans.

Environmental effect Pesticide use raises a number of environmental concerns. Over 98% of sprayed insecticides and 95% of herbicides reach a destination other than their target species, including non-target species, air, water and soil.Pesticide driftoccurs when pesticides suspended in the air as particles are carried by wind to other areas, potentially contaminating them. Pesticides are one of the causes ofwater pollution, and some pesticides arepersistent organic pollutantsand contribute tosoil contamination.In addition, pesticide use reducesbiodiversity, contributes topollinator decline,destroys habitat (especially for birds), and threatensendangered species. Pests can develop a resistance to the pesticide (pesticide resistance), necessitating a new pesticide. Alternatively a greater dose of the pesticide can be used to counteract the resistance, although this will cause a worsening of the ambient pollution problem.Since chlorinated hydrocarbon pesticidesdissolve in fatsand are not excreted, organisms tend to retain them almost indefinitely.Biological magnificationis the process whereby these chlorinated hydrocarbons (pesticides) are more concentrated at each level of the food chain. Among marine animals, pesticide concentrations are higher in carnivorous fishes, and even more so in the fish-eating birds and mammals at the top of theecological pyramid. Global distillationis the process whereby pesticides are transported from warmer to colder regions of the Earth, in particular the Poles and mountain tops. Pesticides that evaporate into the atmosphere at relatively high temperature can be carried considerable distances (thousands of kilometers) by the wind to an area of lower temperature, where they condense and are carried back to the ground in rain or snow. BenefitsThere are two levels of benefits for pesticide use, primary and secondary. Primary benefits are direct gains from the use of pesticides and secondary benefits are effects that are more long-term. Primary benefits1. Controlling pests and plant disease vectors Improved crop/livestock yields Improved crop/livestock quality Invasive species controlled2. Controlling human/livestock disease vectors and nuisance organisms Human lives saved and suffering reduced Animal lives saved and suffering reduced Diseases contained geographically3. Controlling organisms that harm other human activities and structures Drivers view unobstructed Tree/brush/leaf hazards prevented Wooden structures protected.AlternativesAlternatives to pesticides are available and include methods of cultivation, use ofbiological pest controls(such as pheromones and microbial pesticides),genetic engineering, and methods of interfering with insect breeding.Application of composted yard waste has also been used as a way of controlling pests.These methods are becoming increasingly popular and often are safer than traditional chemical pesticides. In addition, EPA is registering reduced-risk conventional pesticides in increasing numbers.Cultivation practices includepolyculture(growing multiple types of plants),crop rotation, planting crops in areas where the pests that damage them do not live, timing planting according to when pests will be least problematic, and use oftrap crops that attract pests away from the real crop.In the U.S., farmers have had success controlling insects by spraying with hot water at a cost that is about the same as pesticide spraying.Release of other organisms that fight the pest is another example of an alternative to pesticide use. These organisms can include naturalpredatorsorparasitesof the pests.[20]Biological pesticidesbased onentomopathogenic fungi,bacteriaand virusescause disease in the pest species can also be used.[20]Interfering with insects' reproduction can be accomplished bysterilizing malesof the target species and releasing them, so that theymatewith females but do not produce offspring. This technique was first used on thescrewworm flyin 1958 and has since been used with themedfly, thetsetse fly,and thegypsy moth.However, this can be a costly, time consuming approach that only works on some types of insects. Agroecologyemphasize nutrient recycling, use of locally available andrenewable resources, adaptation to local conditions, utilization of microenvironments, reliance on indigenous knowledge and yield maximization while maintaining soil productivity.Agroecology also emphasizes empowering people and local communities to contribute to development, and encouraging multi-directional communications rather than the conventional top-down method.TypesPesticides are often referred to according to the type of pest they control. Pesticides can also be considered as either biodegradable pesticides, which will be broken down by microbes and other living beings into harmless compounds, or persistent pesticides, which may take months or years before they are broken down: it was the persistence of DDT, for example, which led to its accumulation in the food chain and its killing of birds of prey at the top of the food chain. Another way to think about pesticides is to consider those that are chemical pesticides or are derived from a common source or production method. Some examples of chemically-related pesticides are:Organophosphate pesticidesOrganophosphatesaffect the nervous system by disrupting the enzyme that regulates acetylcholine, a neurotransmitter. Most organophosphates are insecticides. They were developed during the early 19th century, but their effects on insects, which are similar to their effects on humans, were discovered in 1932.Some are very poisonous. However, they usually are not persistent in the environment.Carbamate pesticidesCarbamate pesticides affect the nervous system by disrupting an enzyme that regulates acetylcholine, a neurotransmitter. The enzyme effects are usually reversible. There are several subgroups within the carbamates.Organochlorine insecticidesThey were commonly used in the past, but many have been removed from the market due to their health and environmental effects and their persistence (e.g., DDT and chlordane).Pyrethroid pesticidesThey were developed as a synthetic version of the naturally occurring pesticide pyrethrin, which is found in chrysanthemums. They have been modified to increase their stability in the environment. Some synthetic pyrethroids are toxic to the nervous system.Sulfonylurea herbicidesThe following sulfonylureas have been commercialized for weed control: amidosulfuron, azimsulfuron, bensulfuron-methyl, chlorimuron-ethyl, ethoxysulfuron, flazasulfuron, flupyrsulfuron-methyl-sodium, halosulfuron-methyl, imazosulfuron, nicosulfuron, oxasulfuron, primisulfuron-methyl, pyrazosulfuron-ethyl, rimsulfuron, sulfometuron-methyl Sulfosulfuron, terbacil, bispyribac-sodium, cyclosulfamuron, and pyrithiobac-sodiumNicosulfuron,triflusulfuron methyl,and chlorsulfuron are broad-spectrum herbicides that kill plants by inhibiting the enzymeacetolactate synthaseBiopesticidesBiopesticides are certain types of pesticides derived from such natural materials as animals, plants, bacteria, and certain minerals. For example, canola oil and baking soda have pesticidal applications and are considered biopesticides. Biopesticides fall into three major classes: Microbial pesticides consist of a microorganism e.g., a bacterium, fungus, virus, or protozoan as the active ingredient. Microbial pesticides can control many different kinds of pests, although each separate active ingredient is relatively specific for its target pest. For example, there are fungi that control certain weeds, and other fungi that kill specific insects. The most widely used microbial pesticides are subspecies and strains of Bacillus thuringiensis, or Bt. Each strain of this bacterium produces a different mix of proteins, and specifically kills one or a few related species of insect larvae. While some Bt's control moth larvae found on plants, other Bt's are specific for larvae of flies and mosquitoes. The target insect species are determined by whether the particular Bt produces a protein that can bind to a larval gut receptor, thereby causing the insect larvae to starve. Plant-Incorporated-Protectants (PIPs) are pesticidal substances that plants produce from genetic material that has been added to the plant. For example, scientists can take the gene for the Bt pesticidal protein, and introduce the gene into the plant's own genetic material. Then the plant, instead of the Bt bacterium, manufactures the substance that destroys the pest. The protein and its genetic material, but not the plant itself, are regulated by EPA. Biochemical pesticides are naturally occurring substances that control pests by non-toxic mechanisms. Conventional pesticides, by contrast, are, in general, synthetic materials that directly kill or inactivate the pest. Biochemical pesticides include substances, such as insect sex pheromones, that interfere with mating, as well as various scented plant extracts that attract insect pests to traps. Because it is sometimes difficult to determine whether a substance meets the criteria for classification as a biochemical pesticide, EPA has established a special committee to make such decisions.

Preparation for anapplicationof hazardous herbicide. DDT(dichlorodiphenyltrichloroethane) is a colorless,crystalline, tasteless and almost odorlessorganochlorideknown for itsinsecticidalproperties. DDT has been formulated in almost every conceivable form, includingsolutionsinxyleneorpetroleumdistillates,emulsifiableconcentrates, water-wettable powders, granules,aerosols,smoke candlesand charges for vaporizers and lotions.[3]First synthesized in 1874, DDT's insecticidal action was discovered by the Swiss chemistPaul Hermann Mllerin 1939. Mller was awarded theNobel Prize in Physiology or Medicine"for his discovery of the high efficiency of DDT as a contact poison against several arthropods" in 1948. Along with the passage of theEndangered Species Act, the US ban on DDT is cited by scientists as a major factor in the comeback of thebald eagle(thenational bird of the United States) and theperegrine falconfrom near-extirpationin thecontiguous United States

Properties and chemistryDDT is similar in structure to the insecticidemethoxychlorand theacaricidedicofol. Being highlyhydrophobic, it is nearlyinsolubleinwaterbut has good solubility in mostorganicsolvents,fatsandoils. DDT does not occur naturally, but is produced by the reaction ofchloral(CCl3CHO) withchlorobenzene(C6H5Cl) in the presence ofsulfuric acidas acatalyst. Trade names that DDT has been marketed under include Anofex (Geigy Chemical Corp.), Cezarex, Chlorophenothane, Clofenotane, Dicophane, Dinocide, Gesarol (Syngenta Corp.), Guesapon, Guesarol, Gyron (Ciba-Geigy Corp.), Ixodex, Neocid (Reckitt & Colman Ltd), Neocidol (Ciba-Geigy Corp.) and Zerdane.Isomers and related compounds

o,p'-DDT, a minor component in commercial DDT.Commercial DDT is a mixture of several closelyrelated compounds. The major component (77%) is thep,p'isomerwhich is pictured at the top of this article. Theo,p'isomer (pictured to the right) is also present in significant amounts (15%).Dichlorodiphenyldichloroethylene(DDE) anddichlorodiphenyldichloroethane(DDD) make up the balance. DDE and DDD are also the majormetabolitesand breakdown products in the environment. The term "total DDT" is often used to refer to the sum of all DDT related compounds (p,p'-DDT,o,p'-DDT, DDE, and DDD) in a sample.Mechanism of insecticide actionIn insects it openssodium ion channelsinneurons, causing them to fire spontaneously, which leads to spasms and eventual death. Insects with certainmutationsin their sodium channelgeneare resistant to DDT and other similar insecticides. DDT resistance is also conferred by up-regulation of genes expressingcytochrome P450in some insect species,[19]as greater quantities of some enzymes of this group accelerate metabolism of the toxin into inactive metabolites.

Commercial product concentrate containing 50% DDT, circa 1960s

Commercial product (Powder box, 50 g) containing 10% DDT; Environmental impactDegradation of DDT to form DDE (by elimination of HCl, left) and DDD (by reductive dechlorination, right)DDT is apersistent organic pollutantthat is readily adsorbed tosoilsandsediments, which can act both as sinks and as long-term sources of exposure contributing to terrestrial organisms.Depending on conditions, its soilhalf lifecan range from 22 days to 30 years. Routes of loss and degradation include runoff, volatilization,photolysisandaerobicandanaerobicbiodegradation. Due tohydrophobicproperties, inaquatic ecosystemsDDT and its metabolites are absorbed by aquatic organisms and adsorbed on suspended particles, leaving little DDT dissolved in the water itself. Because of itslipophilicproperties, DDT has a high potential tobioaccumulate, especially inpredatory birds. Effects on human health

A US soldier is demonstrating DDT hand-spraying equipment. DDT was used to control the spread oftyphus-carryinglice.DDT is an endocrine disruptor.It is considered likely to be a human carcinogen although the majority of studies suggest it is not directlygenotoxicThe DDT metaboliteDDEacts as anantiandrogen, but not as anestrogen. p,p'-DDT, DDT's main component, has little or no androgenic or estrogenic activity. The minor component o,p'-DDT has weak estrogenic activity.Developmental toxicityDDT and DDE, like other organochlorines, have been shown to havexenoestrogenicactivity, meaning they are chemically similar enough to estrogens to trigger hormonal responses in animals. Thisendocrine disruptingactivity has been observed inmiceandrattoxicological studies, and availableepidemiologicalevidence indicates that these effects may be occurring in humans as a result of DDT exposure..

CarcinogenicityIn 2002, the Centers for Disease Control reported that "Overall, in spite of some positive associations for some cancers within certain subgroups of people, there is no clear evidence that exposure to DDT/DDE causes cancer in humans."The NTP classifies it as "reasonably anticipated to be a carcinogen," theInternational Agency for Research on Cancerclassifies it as a "possible" human carcinogen, and the EPA classifies DDT, DDE, and DDD as class B2 "probable"carcinogens. These evaluations are based mainly on the results of animal studies. A Lancet review of epidemiological studies concluded that that DDT causes cancersof the liver, andpancreas, that there is mixed evidence that it causes cancers of the testes, and that it probably does not contribute to cancers of the rectum, prostate, endometrium, lung, or stomach. A second review, whose co-authors included persons engaged in DDT-related litigation, reached broadly similar conclusions, but also found possible associations with breast cancer, leukemia, lymphoma, and testicular cancer. Breast cancerThe question of whether DDT or DDE arerisk factors in breast cancerhas not been conclusively answered. Several meta analyses of observational studies have concluded that there is no overall relationship between DDT exposure and breast cancer risk.[68][69]The United States Institute of Medicine reviewed data on the association of breast cancer with DDT exposure in 2012 and concluded that a causative relationship could neither be proven nor disproven.[70]A 2007 case control study using archived blood samples found that breast cancer risk was increased 5-fold among women who were born prior to 1931 and who had high serum DDT levels in 1963. Reasoning that DDT use became widespread in 1945 and peaked around 1950, they concluded that the ages of 14-20 were a critical period in which DDT exposure leads to increased risk. This study, which suggests a connection between DDT exposure and breast cancer that would not be picked up by most studies, has received variable commentary in third party reviews. One review suggested that "previous studies that measured exposure in older women may have missed the critical period."A second review suggested a cautious approach to the interpretation of these results given methodological weaknesses in the study design.The National Toxicology Program notes that while the majority of studies have not found a relationship between DDT exposure and breast cancer that positive associations have been seen in a "few studies among women with higher levels of exposure and among certain subgroups of women"Initial effectiveness of DDT against malariaWhen it was first introduced in World War II, DDT was very effective in reducing malariamorbidityandmortality.The WHO's anti-malaria campaign, which consisted mostly of spraying DDT and rapid treatment and diagnosis to break the transmission cycle, was initially very successful as well. For example, inSri Lanka, the program reduced cases from about one million per year before spraying to just 18 in 1963and 29 in 1964. Thereafter the program was halted to save money and malaria rebounded to 600,000 cases in 1968 and the first quarter of 1969. The country resumed DDT vector control but the mosquitoes had evolved resistance in the interim, presumably because of continued agricultural use. The program switched tomalathion, but despite initial successes, malaria continued its resurgence into the 1980s. Today, DDT remains on the WHO's list of insecticides recommended for IRS. Since the appointment ofArata Kochias head of its anti-malaria division, WHO's policy has shifted from recommending IRS only in areas of seasonal or episodic transmission of malaria, to also advocating it in areas of continuous, intense transmission.The WHO has reaffirmed its commitment to eventually phasing out DDT, aiming "to achieve a 30% cut in the application of DDT world-wide by 2014 and its total phase-out by the early 2020s if not sooner" while simultaneously combating malaria. The WHO plans to implement alternatives to DDT to achieve this goal. South Africa is one country that continues to use DDT under WHO guidelines. In 1996, the country switched to alternative insecticides and malaria incidence increased dramatically. Returning to DDT and introducing new drugs brought malaria back under control.Malaria cases increased inSouth Americaafter countries in that continent stopped using DDT. Research data shows a significantly strong negative relationship between DDT residual house sprayings and malaria rates. In a research from 1993 to 1995, Ecuador increased its use of DDT and resulted in a 61% reduction in malaria rates, while each of the other countries that gradually decreased its DDT use had large increase in malaria rates. Residents' concernsIRS is effective if at least 80% of homes and barns in a residential area are sprayed.Lower coverage rates can jeopardize program effectiveness. Many residents resist DDT spraying, objecting to the lingering smell, stains on walls, and the potential exacerbation of problems with other insect pests.Pyrethroidinsecticides (e.g.deltamethrinandlambda-cyhalothrin) can overcome some of these issues, increasing participation.

Criticism of restrictions on DDT useCritics argue that limitations on DDT use for public heath purposes have caused unnecessary morbidity and mortality from vector borne diseases, with some claims of malaria deaths ranging as high as the hundreds of thousands,and millions. Robert Gwadz of the USNational Institutes of Healthsaid in 2007, "The ban on DDT may have killed 20 million children."In his novelState of Fear, authorMichael Crichtonwrote "Banning DDT killed more people than Hitler." These arguments have been dismissed as "outrageous" by former WHO scientist Socrates Litsios. May Berenbaum,University of Illinoisentomologist, says, "to blame environmentalists who oppose DDT for more deaths than Hitler is worse than irresponsible."Investigative journalist Adam Sarvana and others characterize this notion as a "myth" promoted principally byRoger Bateof the pro-DDT advocacy groupAfrica Fighting Malaria(AFM). Criticisms of a DDT "ban" often specifically reference the 1972 US ban (with the erroneous implication that this constituted a worldwide ban and prohibited use of DDT in vector control). Reference is often made toRachel Carson'sSilent Spring,even though she never pushed for a ban on DDT specifically.John Quigginand Tim Lambert wrote, "the most striking feature of the claim against Carson is the ease with which it can be refuted." It has also been alleged that donor governments and agencies have refused to fund DDT spraying, or made aid contingent upon not using DDT. According to a report in theBritish Medical Journal, use of DDT inMozambique"was stopped several decades ago, because 80% of the country's health budget came from donor funds, and donors refused to allow the use of DDT."Roger Bate asserts, "many countries have been coming under pressure from international health and environment agencies to give up DDT or face losing aid grants: Belize and Bolivia are on record admitting they gave in to pressure on this issue from [USAID]." TheUnited States Agency for International Development(USAID) has been the focus of much criticism. While the agency is currently funding the use of DDT in some African countries,in the past it did not. WhenJohn Stosselaccused USAID of not funding DDT because it wasn't "politically correct," Anne Peterson, the agency's assistant administrator for global health, replied that "I believe that the strategies we are using are as effective as spraying with DDT ... So, politically correct or not, I am very confident that what we are doing is the right strategy."USAID's Kent R. Hill states that the agency has been misrepresented: "USAID strongly supports spraying as a preventative measure for malaria and will support the use of DDT when it is scientifically sound and warranted."The Agency's website states that "USAID has never had a 'policy' as such either 'for' or 'against' DDT for IRS. The real change in the past two years [2006/07] has been a new interest and emphasis on the use of IRS in general with DDT or any other insecticide as an effective malaria prevention strategy in tropical Africa.The website further explains that in many cases alternative malaria control measures were judged to be more cost-effective that DDT spraying, and so were funded instead. Dieldrin

IUPAC name[hide](1aR,2R,2aS,3S,6R,6aR,7S,7aS)-3,4,5,6,9,9-hexachloro-1a,2,2a,3,6,6a,7,7a-octahydro-2,7:3,6-dimethanonaphtho[2,3-b]oxirene

Other names[hide]Dieldrin

Identifiers

CAS number60-57-1

ChemSpider10292746

KEGGC13718

ChEBICHEBI:34696

ChEMBLCHEMBL481118

Jmol-3D imagesImage 1

SMILES[show]

InChI[show]

Properties

Molecular formulaC12H8Cl6O

Molar mass380.91 g mol1

Density1.75 g/cm3

Melting point176 to 177C (349 to 351F; 449 to 450K)

Boiling point385C (725F; 658K)

Hazards

MSDSExternal MSDS

Except where noted otherwise, data are given for materials in theirstandard state(at 25C (77F), 100kPa)

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Infoboxreferences

Dieldrinis anorganochlorideoriginally produced in 1948 by J. Hyman & Co, Denver, as aninsecticide. Dieldrin is closely related toaldrin, which reacts further to form dieldrin. Aldrin is not toxic to insects; it is oxidized in the insect to form dieldrin which is the active compound. Both dieldrin and aldrin are named after theDiels-Alder reactionwhich is used to form aldrin from a mixture of norbornadiene andhexachlorocyclopentadiene.Originally developed in the 1940s as an alternative toDDT, dieldrin proved to be a highly effective insecticide and was very widely used during the 1950s to early 1970s.Endrinis astereoisomerof dieldrin.However, it is an extremelypersistent organic pollutant; it does not easilybreak down. Furthermore it tends tobiomagnifyas it is passed along thefood chain. Long-term exposure has proven toxic to a very wide range of animals including humans, far greater than to the original insect targets. For this reason it is nowbannedin most of the world.It has been linked to health problems such asParkinson's,breast cancer, and immune, reproductive, and nervous system damage. It can also adversely affect testicular descent in thefetusif a pregnant woman is exposed to it.Sodium chlorate

IUPAC name[hide]Sodium chlorate

Other names[hide]Sodium chlorate(V)

Identifiers

CAS number7775-09-9

PubChem516902

ChemSpider22895

UNIIT95DR77GMR

EC number231-887-4

UN number1495, 2428

KEGGC18765

MeSHSodium+chlorate

ChEBICHEBI:65242

RTECS numberFO0525000

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InChI[show]

Properties

Molecular formulaClNaO3

Molar mass106.44 g mol1

AppearanceColorless or white solid,hygroscopic

OdorOdorless

Density2.49 g/cm3(15 C)[1]2.54 g/cm3(20.2 C)[2]

Melting point248261C (478502F; 521534K)

Boiling point300400C (572752F; 573673K)decomposes[1]

Solubilityinwater79 g/100 mL (0 C)89 g/100 mL (10 C)105.7 g/100 mL (25 C)125 g/100 mL (40 C)220.4 g/100 mL (100 C)[3]

Sodium chlorateis aninorganic compoundwith thechemical formulaNaClO3. It is a whitecrystallinepowder that is readily soluble in water. It ishygroscopic. It decomposes above 300C to releaseoxygenand leavesodium chloride. Several hundred million tons are produced annually, mainly for applications inbleachingpaper. .UsesThe main commercial use for sodium chlorate is for makingchlorine dioxide(ClO2). The largest application of ClO2, which accounts for about 95% of the use of chlorate, is in bleaching of pulp. All perchlorate compounds are produced industrially by the oxidation of solutions of sodium chlorate by electrolysis. HerbicidesSodium chlorate is used as a non-selectiveherbicide. It is consideredphytotoxicto all green plant parts. It can also kill through root absorption.Sodium chlorate may be used to control a variety of plants includingmorning glory,canada thistle,johnson grass,bamboo,Ragwort, andSt John's wort. The herbicide is mainly used on non-crop land for spot treatment and for total vegetation control on areas including roadsides, fenceways, and ditches. Sodium chlorate is also used as adefoliantanddesiccantfor: Cotton Safflower Corn Flax Peppers Soybeans Grainsorghum Southern peas Dry beans Rice Sunflowers

If used in combination withatrazine, it increases the persistence of the effect. If used in combination with2,4-D, performance is improved. Sodium chlorate has asoil sterilanteffect. Mixing with other herbicides in aqueous solution is possible to some extent, so long as they are not susceptible to oxidation.

Chemical oxygen generationChemical oxygen generators, such as those in commercial aircraft, provide emergency oxygen to passengers to protect them from drops in cabin pressure. Oxygen is generated by high-temperature decomposition of sodium chlorate. Heat is generated byoxidationof a small amount of iron powder mixed with the sodium chlorate, and the reaction consumes less oxygen than is produced.Barium peroxide(BaO2) is used to absorb the chlorine which is a minor product in the decomposition.An ignitor charge is activated by pulling on the emergency mask. Similarly, theSolidoxwelding system used pellets of sodium chlorate mixed with combustible fibers to generate oxygen.Toxicity in humansDue to its oxidative nature, sodium chlorate can be very toxic if ingested. The oxidative effect onhemoglobinleads tomethaemoglobinformation, which is followed bydenaturationof theglobinprotein and across-linkingoferythrocytemembrane proteins with resultant damage to the membrane enzymes. This leads to increased permeability of the membrane, and severehemolysis. The denaturation of hemoglobin overwhelms the capacity of theG6PDmetabolic pathway. In addition, this enzyme is directly denatured by chlorate reducing its activity.Therapy withascorbic acidandmethylene blueare frequently used in the treatment ofmethemoglobinemia. However, since methylene blue requires the presence ofNADPHthat requires normal functioning of G6PD system, it is less effective than in other conditions characterized by hemoglobin oxidation.FormulationsSodium chlorate comes indust,sprayandgranuleformulations. There is a risk of fire and explosion in dry mixtures with other substances, especiallyorganicmaterials, and otherherbicides,sulfur,phosphorus, powderedmetals, and strongacids. In particular, when mixed withsugar, it has explosive properties. If accidentally mixed with one of these substances it should not be stored in human dwellings. Marketed formulations contain afire retardant, but this has little effect if deliberately ignited. Most commercially available chlorate weedkillers contain approximately 53% sodium chlorate with the balance being a fire depressant such assodium metaborateorammonium phosphates.Herbicides, also commonly known asweedkillers, arepesticidesused to kill unwantedplants.[1]Selective herbicides kill specific targets, while leaving the desiredcroprelatively unharmed. Some of these act by interfering with the growth of theweedand are often synthetic mimics of naturalplant hormones. Herbicides used to clear waste ground, industrial sites, railways and railway embankments are not selective and kill allplantmaterial with which they come into contact. Smaller quantities are used in forestry, pasture systems, and management of areas set aside as wildlifehabitat.Some plants produce natural herbicides, such as the genusJuglans(walnuts), or thetree of heaven; such action of natural herbicides, and other related chemical interactions, is calledallelopathy.Herbicides are widely used inagricultureand landscape turf management. In the US, they account for about 70% of all agricultural pesticide use.[1]First herbicides

2,4-D, the first chemical herbicide, was discovered during theSecond World War.Although research into chemical herbicides began in the early 20th century, the first major breakthrough was the result of research conducted in both the UK and the US during theSecond World Warinto the potential use of agents asbiological weapons.The first modern herbicide,2,4-D, was first discovered and synthesized byW. G. TemplemanatImperial Chemical Industries. In 1940, he showed that "Growth substances applied appropriately would kill certain broad-leaved weeds in cereals without harming the crops." By 1941, his team succeeded in synthesizing the chemical. In the same year, Pokorny in the US achieved this as well.Independently, a team underJuda Hirsch Quastel, working at theRothamsted Experimental Stationmade the same discovery. Quastel was tasked by theAgricultural Research Council (ARC)to discover methods for improving crop yield. By analyzing soil as a dynamic system, rather than an inert substance, he was able to apply techniques such asperfusion. Quastel was able to quantify the influence of various plant hormones, inhibitors and other chemicals on the activity of microorganisms in the soil and assess their direct impact on plant growth. While the full work of the unit remained secret, certain discoveries were developed for commercial use after the war, including the 2,4-D compound. When it was commercially released in 1946, it triggered a worldwide revolution in agricultural output and became the first successful selective herbicide. It allowed for greatly enhanced weed control inwheat,maize(corn),rice, and similarcerealgrass crops, because it killsdicots(broadleaf plants), but not mostmonocots(grasses). The low cost of 2,4-D has led to continued usage today, and it remains one of the most commonly used herbicides in the world. Like other acid herbicides, current formulations use either an amine salt (oftentrimethylamine) or one of manyestersof the parent compound. These are easier to handle than the acid.Health and environmental effectsHerbicides have widely variabletoxicity. In addition toacute toxicityfrom occupational exposure levels.Some herbicides cause a range of health effects ranging from skin rashes to death. The pathway of attack can arise from intentional or unintentional direct consumption, improper application resulting in the herbicide coming into direct contact with people or wildlife, inhalation of aerial sprays, or food consumption prior to the labeled preharvest interval. Under some conditions, certain herbicides can be transported via leaching or surface runoff to contaminate groundwater or distant surface water sources. Generally, the conditions that promote herbicide transport include intense storm events (particularly shortly after application) and soils with limited capacity toadsorbor retain the herbicides. Herbicide properties that increase likelihood of transport include persistence (resistance to degradation) and high water solubility. Phenoxy herbicidesare often contaminated withdioxinssuch asTCDD; research has suggested such contamination results in a small rise in cancer risk after occupational exposure to these herbicides. Triazineexposure has been implicated in a likely relationship to increased risk ofbreast cancer, although acausalrelationship remains unclear. ClassificationHerbicides can be grouped by activity, use, chemical family, mode of action, or type of vegetation controlled.By activity: Contactherbicides destroy only the plant tissue in contact with the chemical. Generally, these are the fastest acting herbicides. They are less effective on perennial plants, which are able to regrow from rhizomes, roots or tubers. Systemicherbicides are translocated through the plant, either from foliar application down to the roots, or from soil application up to the leaves. They are capable of controlling perennial plants and may be slower-acting, but ultimately more effective than contact herbicides.

By use: Soil-appliedherbicides are applied to the soil and are taken up by the roots and/or hypocotyl of the target plant. The three main types are:1. Preplant incorporatedherbicides are soil applied prior to planting and mechanically incorporated into the soil. The objective for incorporation is to prevent dissipation throughphotodecompositionand/or volatility.2. Pre-emergent herbicidesare applied to the soil before the crop emerges and prevent germination or early growth of weed seeds.3. Postemergent herbicidesare applied after the crop has emerged.Their classification bymechanism of action(MOA) indicates the first enzyme, protein, or biochemical step affected in the plant following application. The main mechanisms of action are: ACCase inhibitorscompounds kill grasses. Acetyl coenzyme A carboxylase (ACCase) is part of the first step of lipid synthesis. Thus, ACCase inhibitors affect cell membrane production in themeristemsof the grass plant. The ACCases of grasses are sensitive to these herbicides, whereas the ACCases ofdicotplants are not. ALS inhibitors: theacetolactate synthase(ALS) enzyme (also known as acetohydroxyacid synthase, or AHAS) is the first step in the synthesis of the branched-chain amino acids (valine,leucine, andisoleucine). These herbicides slowly starve affected plants of theseamino acids, which eventually leads to inhibition of DNA synthesis. They affect grasses and dicots alike. The ALS inhibitor family includessulfonylureas, imidazolinones, triazolopyrimidines, pyrimidinyl oxybenzoates, and sulfonylamino carbonyl triazolinones. The ALS biological pathway exists only in plants and not animals, thus making the ALS-inhibitors among the safest herbicides. EPSPS inhibitors: Theenolpyruvylshikimate 3-phosphate synthase enzymeEPSPS is used in the synthesis of the amino acidstryptophan,phenylalanineandtyrosine. They affect grasses and dicots alike.Glyphosate(Roundup) is a systemic EPSPS inhibitor inactivated by soil contact. Synthetic auxinsinaugurated the era of organic herbicides. They were discovered in the 1940s after a long study of the plant growth regulatorauxin. Synthetic auxins mimic this plant hormone. They have several points of action on the cell membrane, and are effective in the control of dicot plants.2,4-Dis a synthetic auxin herbicide. Photosystem II inhibitorsreduce electron flow from water to NADPH2+ at the photochemical step in photosynthesis. They bind to the Qb site on the D1 protein, and prevent quinone from binding to this site. Therefore, this group of compounds causes electrons to accumulate onchlorophyllmolecules. As a consequence,oxidationreactions in excess of those normally tolerated by the cell occur, and the plant dies. Thetriazineherbicides (includingatrazine) and urea derivatives (diuron) are photosystem II inhibitors Photosystem I inhibitorssteal electrons from the normal pathway through FeS to Fdx toNADPleading to direct discharge of electrons on oxygen. As a result, reactive oxygen species are produced andoxidationreactions in excess of those normally tolerated by the cell occur, leading to plant death.Bipyridiniumherbicides (such asdiquatandparaquat) inhibit the Fe-S Fdx step of that chain, whilediphenyl etherherbicides (such asnitrofen,nitrofluorfen, andacifluorfen) inhibit the Fdx NADP step HPPD inhibitorsinhibit4-Hydroxyphenylpyruvate dioxygenase, which are involved intyrosinebreakdown.Tyrosine breakdown products are used by plants to makecarotenoids, which protectchlorophyllin plants from being destroyed by sunlight. If this happens, the plants turn white due to complete loss of chlorophyll, and the plants die. Mesotrioneandsulcotrioneare herbicides in this class; a drug,nitisinone, was discovered in the course of developing this class of herbicides.