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Dimethoate
Dimethoate
Dimethoate
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Dimethoate
Names
Preferred IUPAC name
O,O-Dimethyl S-[2-(methylamino)-2-oxoethyl] phosphorodithioate
Other names
O,O-dimethyl S-methylcarbamoylmethyl phosphorodithioate
Phosphorodithioic acid, O,O-Dimethyl S-(2-(methylamino)-2-oxoethylyl)ester
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
ECHA InfoCard 100.000.437 Edit this at Wikidata
KEGG
UNII
  • InChI=1S/C5H12NO3PS2/c1-6-5(7)4-12-10(11,8-2)9-3/h4H2,1-3H3,(H,6,7) checkY
    Key: MCWXGJITAZMZEV-UHFFFAOYSA-N checkY
  • InChI=1/C5H12NO3PS2/c1-6-5(7)4-12-10(11,8-2)9-3/h4H2,1-3H3,(H,6,7)
    Key: MCWXGJITAZMZEV-UHFFFAOYAB
  • O=C(NC)CSP(=S)(OC)OC
Properties
C5H12NO3PS2
Molar mass 229.26 g/mol
Appearance Grey-white crystalline solid
Density 1.3 g/cm3, solid
Melting point 43 to 45 °C (109 to 113 °F; 316 to 318 K)
Boiling point 117 °C (243 °F; 390 K) at 10 Pa
2.5 g/100 ml
Hazards
Occupational safety and health (OHS/OSH):
Main hazards
 Highly toxic
GHS labelling:
GHS07: Exclamation mark[1]
H302, H312[1]
P280[1]
Flash point 107 °C (225 °F; 380 K)
Safety data sheet (SDS) External MSDS
Related compounds
malathion
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Dimethoate is a widely used organophosphate insecticide and acaricide. It was patented and introduced in the 1950s by American Cyanamid. Like other organophosphates, dimethoate is an acetylcholinesterase inhibitor which disables cholinesterase, an enzyme essential for central nervous system function. It acts both by contact and through ingestion. It is readily absorbed and distributed throughout plant tissues, and is degraded relatively rapidly.[2] One of the breakdown products of dimethoate is omethoate, a potent cholinesterase inhibitor, is ten times more toxic than its parent compound.[3]

Uses

[edit]

Dimethoate is a general use insecticide for combatting insects such as aphids, mites, beetles, weevils, and leafhoppers. Dimethoate is formulated as emulsifiable concentrates or wettable powders to be applied primarily as foliar sprays. The majority of the approximately 800.000 kg (1.8 million pounds) of dimethoate used annually in the U.S. is accounted for by applications on alfalfa, wheat, cotton, and corn crops. In 2005, dimethoate usage was cancelled in the U.S. for use on apples, broccoli raab, cabbage, collards, grapes, head lettuce, and spinach due to being identified as significant dietary risk contributors.[4] Dimethoate also has applications as a form of botfly and mite control in livestock.[5] As of 2000, dimethoate is cancelled for usage in residential and non-agriculture applications in the U.S[4][3]

Environment

[edit]

Dimethoate is relatively non-persistent, but highly mobile in the environment due to its high solubility in water and low adsorption in soil.[4][6] The half-life of dimethoate in soil has been shown to range from 2.5 to 31 days depending on the type of soil and its moisture content.[6] The half-life of dimethoate is shorter in moist soil due the action of microbial degradation.[5] Breakdown of dimethoate by hydrolysis in water is highly dependent on temperature and pH, with the half-life ranging from 12 to 423 days.[6]

Health effects

[edit]

Routes of exposure

[edit]

Exposure of the general population to dimethoate and its breakdown product omethoate can happen through consumption of contaminated food or water. Workers involved in the application or manufacture of dimethoate are typically exposed through contact with skin, or through inhalation of aerosols and dust.[3]

Acute exposure in humans

[edit]

In mammals, dimethoate has an LD50 of 150 mg/kg bodyweight in mice and 400 mg/kg bodyweight in rats.[3] Acute exposure through oral, dermal, or inhalation routes can cause symptoms such as diarrhea, nausea, sweating, blurred vision, difficulty breathing, and slowed heartbeat. Relapse situations where the patient appears to have stabilized before getting worse have been associated with higher exposure doses. Respiratory ailments, cholinesterase inhibitor exposure, impaired cholinesterase production, or liver malfunction can play a role in potentiating toxicity.[5]

Chronic exposure in humans

[edit]

Chronic exposure to dimethoate can result in symptoms such as disorientation, irritability, impaired memory and concentration, nightmare, and speech difficulties. Chronic exposure as also been associated with nausea, loss of appetite, and malaise. Under normal conditions the chances of teratogenic, mutagenic, or carcinogenic effects from chronic exposure are low.[5]

Fruit fly control efforts

[edit]

The Queensland fruit fly, or Bactrocera tryoni, is a tephritid fly species that has caused more than $28.5 million a year in damage to Australian fruit crops. In order to combat infestation, farmers treated crops with dimethoate and fenthion.[7] In 2011 the Australian Pesticides and Veterinary Medicines Authority (APVMA) banned the use of dimethoate containing products on food producing plants in home gardens, as well as on a variety of fruits, berries, cucurbits, and vegetables.[8] In September 2023, due to concerns that dimethoate and omethoate levels were exceeding acceptable maximum residue limits on avocados and mangoes, the APVMA issued a 12-month suspension notice on the use of dimethoate containing compounds as a post-harvest dip to control fruit flies on certain tropical fruits, including avocados and mangoes.[9][10]

Trade names

[edit]

Dimethoate is sold under various trade names, including Cygon, De-fend, Destan, Rogor, Rogodan, Rogodial, Roxion, Dimetate, Devigon, Dicap, Dimet, and B-58.[6][11][12][13]

Poisoning incidents

[edit]

In late October 2020 a Bulgarian farmer, a previous jackpot winner of the national 'toto' lottery drank a glass of the Russian B-58 brand, as of early November 2020 he is hospitalised in a comatose condition, he has a history of psychiatric issues but it is currently unknown whether the incident was accidental or intentional.[14]

References

[edit]
[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Dimethoate

View on Grokipedia
from Grokipedia
Dimethoate is a synthetic organothiophosphate compound (C5H12NO3PS2) classified as an organophosphate acetylcholinesterase inhibitor, employed as a contact and systemic insecticide to control a wide array of insect pests and mites on agricultural crops. It targets species including aphids, leafhoppers, beetles, weevils, and mites through disruption of nerve impulse transmission via cholinesterase inhibition, enabling both foliar application and uptake by plant tissues for protection against sucking and chewing insects. Commonly used on crops such as broccoli, corn, soybeans, alfalfa, and fruits, dimethoate supports resistance management in integrated pest control strategies, with annual U.S. application approximating 1.8 million pounds of active ingredient. Despite its efficacy, dimethoate poses notable risks due to its toxicity profile, exhibiting acute and chronic effects in mammals through suppression, which can manifest as neurological symptoms, reproductive impairments, and developmental anomalies in exposed organisms. In humans, occupational or environmental exposure has been linked to hematological alterations, immune disruption, and potential long-term neurobehavioral changes, prompting regulatory and risk assessments by agencies like the EPA. Ecologically, it demonstrates high hazard to aquatic species, causing teratogenesis, behavioral disruptions, and mortality via and persistence in water bodies, which has led to restrictions in certain applications to mitigate off-target impacts.

Chemical Properties and Mechanism

Molecular Structure and Physical Properties

Dimethoate is an organophosphorus compound with the molecular formula C₅H₁₂NO₃PS₂ and a of 229.3 g/mol. Its systematic name is O,O-dimethyl S-[2-(methylamino)-2-oxoethyl] phosphorodithioate, featuring a central phosphorus atom bonded to two methoxy groups, a atom linked to a methylcarbamoylmethyl chain, and another completing the dithioate . This configuration distinguishes it from simpler organophosphates by incorporating both and functionalities, contributing to its stability and reactivity as an . The compound appears as a white to grey crystalline solid at . Key physical properties include a of 51–52 °C and a of 117 °C at 0.01 kPa. Its is 1.28–1.3 g/cm³, and it exhibits low volatility with a of 0.001 Pa at 25 °C.
PropertyValue
Solubility in 25 g/L at 21 °C
Partition coefficient (log Kow)0.78 at 20 °C
107 °C (closed cup)
Dimethoate shows moderate solubility and high solubility in organic solvents such as and acetone, facilitating its formulation as emulsifiable concentrates. These properties influence its environmental persistence and application efficacy in agricultural settings.

Mode of Action and Toxicology Basics

Dimethoate functions as an organophosphate insecticide primarily by inhibiting the enzyme acetylcholinesterase (AChE), which is essential for terminating nerve impulses in insects through the hydrolysis of the neurotransmitter acetylcholine. This inhibition leads to the accumulation of acetylcholine at cholinergic synapses, resulting in continuous stimulation of the postsynaptic membrane, disruption of nerve transmission, and ultimately paralysis and death of target pests such as aphids, mites, and flies. As a phosphorothionate compound, dimethoate is an indirect AChE inhibitor; it undergoes oxidative desulfuration in vivo, primarily via cytochrome P450 enzymes, to form its active metabolite omethoate, which binds covalently to the serine residue in the AChE active site, preventing enzyme reactivation. In terms of , dimethoate exhibits moderate to mammals through the same mechanism, causing overstimulation of the parasympathetic and central nervous systems. The oral LD50 for dimethoate in rats ranges from 150 to 414 mg/kg body weight, with clinical signs including piloerection, hunched posture, tremors, and lacrimation preceding death. symptoms encompass (pinpoint pupils), blurred vision, headache, excessive salivation, sweating, nausea, vomiting, diarrhea, muscle fasciculations, and in severe cases, progressing to and , even with supportive care. Dermal absorption is lower, with an LD50 exceeding 2000 mg/kg in rabbits, but or ocular exposure can still provoke effects. Chronic exposure to dimethoate may lead to delayed neuropathy due to potential inhibition of neuropathy target esterase (NTE), though this is less pronounced than with other organophosphates; subchronic studies in show effects like reduced body weight and cholinesterase depression at doses above 1-5 mg/kg/day. Antidotal treatment involves atropine to counteract muscarinic effects and to reactivate AChE, emphasizing the need for rapid and monitoring of plasma levels as a of exposure.

History and Development

Invention and Early Commercialization

Dimethoate, an , was first described in by researchers E. J. Hoegberg and J. T. Cassaday in 1951, following earlier reports of related compounds around 1950. Their work at involved the synthesis of O,O-dimethyl S-(N-methylcarbamoylmethyl) phosphorodithioate through the reaction of the sodium salt of O,O-dimethyldithiophosphoric acid with N-methylchloroacetamide, marking a key advancement in systemic insecticides capable of plant uptake and translocation to control sucking pests. This development built on post-World II research into organophosphates, aiming to create broad-spectrum agents effective against , mites, and flies while offering advantages over contact-only pesticides. The compound was patented in the early 1950s by , which recognized its potential for agricultural use due to its systemic properties and relatively low mammalian toxicity compared to earlier organophosphates like . Commercial production began shortly thereafter, with dimethoate introduced to the market in 1956 as a versatile for crops such as fruits, , and cereals. Early formulations were primarily emulsifiable concentrates, facilitating foliar application and initial adoption in the United States and , where it rapidly gained traction for managing pests resistant to older chemicals. By the late 1950s, expanded commercialization through licensing and sales under trade names like Cygon, emphasizing dimethoate's role in before that term's formalization. Global production scaled up, with early estimates indicating thousands of tons annually by the , driven by demand for effective control of leafhoppers and other sap-feeding insects in high-value crops. This period established dimethoate as a cornerstone of mid-20th-century innovation, though subsequent scrutiny revealed environmental persistence concerns not fully anticipated at launch.

Evolution of Formulations and Usage

Dimethoate was first synthesized and described in 1951, with commercial introduction occurring in 1956 as a broad-spectrum developed by . Initial formulations primarily consisted of emulsifiable concentrates (typically 40% ), wettable powders, and dusts, enabling foliar sprays at application rates of 0.3 to 0.7 kg per for control of , mites, , and leafhoppers on crops such as fruits, , , and cereals. Granular formulations and ultra-low volume (ULV) concentrates emerged shortly thereafter to facilitate soil incorporation or , reducing drift and improving systemic uptake through plant roots and leaves, which enhanced efficacy against chewing and sucking pests. By the and , usage expanded globally, including dips for grubs and applications against houseflies at concentrations of 10 to 25 g/liter, reflecting its versatility as both contact and systemic agent with a allowing residual protection of 7 to 14 days. However, early reports of acute human poisonings, such as the first documented agricultural case in 1960 involving olive orchard spraying, prompted initial precautions for protective and re-entry intervals. Formulations remained largely unchanged technically (93-95% purity with minor impurities like O,O-dimethyl S-methylphosphorodithioate), but admixture with synergists or other pesticides increased to counter emerging resistance in target . Regulatory scrutiny intensified from the 1980s onward due to concerns over acetylcholinesterase inhibition, environmental persistence, and residues exceeding tolerances, leading to phased restrictions. In the United States, all non-agricultural uses were canceled in 2000, followed by prohibitions on apple, grape, and several vegetable crops in 2005 to mitigate dietary exposure risks. Recent developments include low-volatile organic compound (VOC) liquid formulations patented in 2012 to comply with emission standards, and ongoing reviews, such as the U.S. EPA's 2024 proposed interim decision emphasizing buffer zones and pollinator protections. In Australia, suspensions for berry crops were proposed in 2023 amid health residue detections, reflecting a broader shift toward integrated pest management reducing reliance on dimethoate in favor of less toxic alternatives. These changes have curtailed overall usage volumes, with agricultural applications now limited to high-value crops under strict pre-harvest intervals of 7 to 21 days.

Uses and Efficacy

Agricultural Applications

Dimethoate serves as a systemic and applied foliarly to agricultural for controlling piercing, sucking, and certain chewing pests through contact, ingestion, and translaminar action. It is registered for use on field such as corn, soybeans, , and ; vegetable including ; fruit trees like , apples, and grapefruit; and other commodities like olives, , and grain . Approximately 1.8 million pounds of are applied annually in the United States using ground or aerial equipment, often at rates tailored to pest pressure, such as 0.25 to 1 pound per acre depending on the and target . Target pests include , leafhoppers, mites, , , psyllids, scales, leaf miners, and certain beetles or weevils that feed on crop juices, with efficacy stemming from its inhibition of in . It provides broad-spectrum control but is less effective against heavy-chewing insects like caterpillars unless sufficient tissue is ingested, limiting its utility to sap-feeding arthropods. In , dimethoate contributes to resistance mitigation by rotating with other chemical classes, as evidenced by its role in suppressing populations on soybeans and where alternatives may be costlier or less reliable. Application typically occurs at crop emergence or early infestation stages via spray equipment calibrated for uniform coverage, with pre-harvest intervals varying by —such as 7 days for or 14 days for —to minimize residues. Efficacy trials demonstrate mortality rates of 50-60% against larval stages of certain pests when applied at labeled rates, though outcomes depend on factors like pest resistance status and environmental conditions. Its cost-effectiveness supports adoption on large-acreage row , where it remains a key tool despite regulatory scrutiny on non-target impacts.

Economic Benefits and Pest Management Role

Dimethoate serves as a cost-effective tool in (IPM) for controlling economically damaging pests, including , mites, leafhoppers, asparagus beetles, and citrus psyllid, across diverse crops such as soybeans, corn, , , brassicas, melons, pears, pecans, and . Its systemic properties enable foliar or soil application with residual activity, reducing the frequency of treatments compared to contact-only and aiding resistance through its mode of action ( Group 1B). In regions like the Midwest, where 25-29% of acres receive insecticide treatments, dimethoate prevents yield losses from pests such as twospotted mites, which can devastate crops with tight profit margins. Economic advantages stem from dimethoate's lower application costs and versatility relative to alternatives; for instance, treatments cost 7.52−7.52-7.68 per acre versus 10.19−10.19-44.58 per acre for substitutes, while maintaining efficacy against broad-spectrum threats. In , particularly in , where up to 90% of bearing orange acres are treated with insecticides, dimethoate supports high-value yield protection against and leafhoppers without requiring more expensive options. Similarly, in (e.g., 88% of planted acres treated in 2022), it targets beetles and other pests, preserving marketable quality and volume. Field trials in demonstrate dimethoate's pest management efficacy, reducing thrips () populations by up to 85% at 10 days post-application and contributing to significantly higher yields compared to untreated controls, with a cost-benefit of 1.49 (each unit invested returning 1.49 units). These outcomes underscore its role in safeguarding production in labor-intensive or export-oriented , where pest outbreaks can lead to 20-50% yield reductions without intervention, though benefits vary by regional pest pressure and crop economics.

Environmental Impact

Fate in Soil, Water, and Air

Dimethoate degrades moderately in primarily through microbial oxidation, , and to a lesser extent photolysis on soil surfaces, though the latter process contributes minimally to overall dissipation. Under aerobic conditions, microbially mediated degradation yields a of approximately 2.2 days, while typical field half-lives range from 4 to 16 days, influenced by , , , , and organic content. In sterile soils lacking , persistence extends up to 206 days, highlighting microbial activity as the dominant degradation pathway. Due to its high water solubility (39.8 g/L at 20°C) and weak adsorption to soil particles (Koc values around 20-50), dimethoate exhibits moderate mobility but low overall leaching potential, as confirmed by standardized models. In water, dimethoate undergoes , photolysis, and , with persistence varying widely from 18 hours to 8 weeks based on , light exposure, temperature, and microbial presence; it remains relatively stable at pH 2-7 but degrades more rapidly under alkaline conditions or with UV . In natural river , dominates, yielding a of about 8 days, indicating non-persistence in the . Photodegradation in water is limited, and in sediment-water systems under dark aerobic conditions, dimethoate dissipates via microbial processes without significant accumulation in sediments. Its high facilitates dissolution but also promotes eventual breakdown products like omethoate, which may exhibit greater . Dimethoate displays low volatility in air, with a of 2.46 × 10^{-4} Pa at 25°C, classifying it as slightly volatile and leading to partitioning between vapor and particulate phases upon atmospheric release. In moist air, it degrades photochemically to hydrolytic and oxidation products, reducing long-range transport potential, though short-term post-application volatilization can occur during spraying. Volatilization from or surfaces is not a major dissipation route due to the compound's physicochemical properties and constant (1.42 × 10^{-6} Pa m³/mol). Atmospheric concentrations post-application decline rapidly, with dimethoate detectable for up to 10 days but at diminishing levels.

Effects on Ecosystems and Non-Target Species

Dimethoate demonstrates to pollinators, with laboratory studies showing LD50 values as low as 0.1-0.4 μg/ for honeybees (Apis mellifera), rendering it highly hazardous to bees through direct contact or contaminated and . This sensitivity extends to wild bee species, where interspecific variation in tolerance highlights risks to in pollinator-dependent ecosystems, potentially disrupting services in agricultural landscapes. Field applications have led to documented bee mortality, prompting restrictions on use during bloom periods to mitigate colony-level impacts. Aquatic ecosystems face significant threats from dimethoate runoff, where it persists in water columns and exhibits very high toxicity to invertebrates such as Daphnia spp. (96-hour EC50 ≈ 0.02-1 mg/L) and amphipods, inhibiting reproduction and survival at environmentally relevant concentrations. Fish species show moderate sensitivity, with 96-hour LC50 values ranging from 1-100 mg/L across tested taxa like common carp (Cyprinus carpio), though early life stages experience behavioral impairments and oxidative stress from sublethal exposures. These effects cascade through food webs, reducing invertebrate populations that serve as prey for fish and amphibians, thereby altering community structure in contaminated freshwater and estuarine habitats. Beneficial terrestrial arthropods, including predatory carabid beetles in agroecosystems, suffer sublethal toxicity from dimethoate residues, evidenced by reduced foraging activity and enzyme disruption at concentrations below lethal thresholds, which undermines natural pest control. Birds exhibit moderate acute toxicity (LD50 >100 mg/kg body weight for most species), but dietary exposure via contaminated insects can cause cholinesterase inhibition and reproductive impairments, posing risks to avian populations in treated fields. Overall, dimethoate's broad-spectrum action contributes to biodiversity declines by non-selectively affecting predators, decomposers, and primary consumers, with ecological risk assessments indicating high hazard quotients for sensitive non-target guilds in sprayed watersheds.

Human Health Considerations

Exposure Pathways and Risk Assessment

Human exposure to dimethoate, an , occurs via dermal absorption, of aerosols or dust, and oral . Occupational exposure predominates among agricultural handlers, mixers, loaders, and applicators, with dermal contact accounting for the majority of uptake (absorption rates of 5-11% in humans, dose-dependent) during mixing, loading, application, and post-application re-entry into treated fields. contributes during spraying, though data are limited (e.g., estimated LC50 of 1553 mg/m³ over 4 hours in rats). General exposure is primarily dietary through residues on treated crops (e.g., dimethoate and its toxic metabolite omethoate) and, less commonly, , with trace detections reported but often below 0.01 μg/L. Residential exposure is negligible absent registered uses, though incidental dermal or oral routes via spray drift or contaminated surfaces may occur rarely. Dimethoate inhibits (AChE), leading to toxicity; acute effects include , salivation, , respiratory distress, and, at high doses, or , with rapid onset (15-90 minutes post-exposure). Oral LD50 values range from 150-414 mg/kg body weight in rats and 60-168 mg/kg in mice, indicating moderate , while dermal LD50 exceeds 2000 mg/kg in rats, reflecting lower hazard. Chronic exposure causes sustained AChE inhibition, potential developmental effects (e.g., reduced pup weight and increased mortality at ≥0.5 mg/kg bw/day in rats), and organ changes (e.g., liver pigmentation, ), though no carcinogenicity or is evident in rodents. Key endpoints include no-observed-adverse-effect levels (NOAELs) of 0.04-0.2 mg/kg bw/day for AChE inhibition across , with points of departure (PODs) based on 10% brain AChE inhibition modeled via physiologically based pharmacokinetic/pharmacodynamic (PBPK-PD) approaches. Risk assessments by regulatory bodies indicate low concern with mitigations. The U.S. EPA's June 2024 revised assessment finds no human health risks exceeding levels of concern (LOC=10), with acute dietary margins of exposure (MOEs) of 44-87 and chronic MOEs of 16-35 for food plus water; occupational handler MOEs range 17-20,000 and post-application dermal MOEs 40-8,400. Acceptable daily intakes (ADIs) are set at 0.001 mg/kg bw (Australian APVMA) to 0.002 mg/kg bw (WHO), with acute reference doses (ARfD) of 0.02 mg/kg bw; WHO's guideline is 6 μg/L. Mitigations include (PPE) such as gloves, respirators, and chemical-resistant aprons for handlers, plus restricted entry intervals (REIs) of 48-72 hours post-application.

Acute Toxicity and Treatment

Dimethoate, an insecticide, causes primarily through irreversible inhibition of , leading to . In rats, the acute oral LD50 is 425 mg/kg, while the dermal LD50 exceeds 2000 mg/kg, indicating moderate oral toxicity but lower dermal absorption risk. Human case fatality from dimethoate self-poisoning reaches 20.6%, higher than comparably classified organophosphates like at 1.9%, due to factors including delayed efficacy against its omethoate. Symptoms of acute exposure manifest rapidly, within minutes to hours, and include muscarinic effects such as , lacrimation, , , gastrointestinal distress, and emesis (SLUDGE syndrome), alongside nicotinic signs like muscle fasciculations, weakness, and . involvement presents as , , seizures, , and ; severe cases often feature profound from , unresponsive to initial fluid resuscitation. In documented human incidents, moderately severe outcomes include and , with fatalities occurring 2.5–32 hours post-ingestion despite intervention. Treatment prioritizes decontamination by removing contaminated clothing and washing skin, followed by supportive care including oxygenation and if needed. Atropine, administered intravenously at 2–4 mg boluses titrated to control secretions and (up to 20–50 mg total in severe cases), antagonizes muscarinic effects but does not reverse nicotinic symptoms. (2-PAM) at 1–2 g IV over 30 minutes, repeated as needed, reactivates inhibited if given early (within hours), though efficacy diminishes with dimethoate due to aging of the enzyme-inhibitor complex. Adjunctive measures include benzodiazepines for seizures and vasopressors for refractory ; or activated charcoal may aid in ingestions, but evidence for their impact on outcomes remains limited. Despite protocol adherence, prognosis in severe dimethoate correlates with ingestion dose and timely administration, with reported survival dependent on intensive monitoring.

Chronic Exposure and Long-Term Studies

Chronic exposure to dimethoate in and dogs primarily manifests as dose-dependent inhibition of plasma, , and activity, serving as the critical toxicological endpoint without consistent evidence of other systemic organ toxicity at sub-inhibitory levels. In a 2-year chronic toxicity and carcinogenicity study in rats, the (NOAEL) was 0.04 mg/kg body weight per day, derived from and inhibition observed at 0.2 mg/kg bw/day. Similarly, chronic dog studies identified a lowest-observed-adverse-effect level (LOAEL) of 1 mg/kg bw/day based on inhibition, with no-observed-effect levels around 0.1 mg/kg bw/day for erythrocyte effects in offspring from reproductive studies. The omethoate exhibits greater potency in eliciting these inhibitory effects compared to the parent compound. Long-term animal carcinogenicity bioassays have yielded equivocal results, with the U.S. Environmental Protection Agency (EPA) classifying dimethoate as a Group C possible human carcinogen due to limited evidence of increased liver adenomas, thyroid follicular cell tumors, and stromal sarcoma in female rats at doses exceeding 10 mg/kg bw/day, though no such effects were consistently observed in mice or dogs. The International Agency for Research on Cancer (IARC) has not classified dimethoate for carcinogenicity, citing inadequate human data and inconsistent animal findings. Mutagenicity tests show dimethoate to be weakly genotoxic in some in vitro assays but negative in most in vivo studies, suggesting any carcinogenic potential may involve non-genotoxic mechanisms like cholinesterase-mediated endocrine disruption rather than direct DNA damage. Reproductive and developmental toxicity studies in multiple species reveal adverse outcomes primarily at maternally toxic doses causing inhibition. In multi-generation studies, the NOAEL for parental systemic toxicity and was 0.65 mg/kg bw/day, with a LOAEL of 2.3 mg/kg bw/day linked to reduced rates and reproductive organ effects; NOAEL was 0.1 mg/kg bw/day based on inhibition without impacts on viability or development. In mice, dietary exposure at 60 ppm reduced mating success, pup survival, and growth, while and lactational exposure impaired adult reproductive function, including altered pituitary-testicular axis and . Developmental assessments in rats indicate potential behavioral deficits from early-life exposure, but only at doses inducing inhibition, with no qualitative differences from adults. Human epidemiological data on long-term occupational or environmental exposure remain limited and inconclusive, with no robust evidence establishing causal links to chronic diseases, cancer, or reproductive outcomes beyond acute cholinesterase-related symptoms. Reviews of available cohort and case-control studies, including those among agricultural workers, find insufficient evidence of associations with , , or , though some report elevated risks confounded by co-exposures to other organophosphates. Regulatory assessments emphasize that points of departure derived from animal data provide protective margins for human chronic risks, incorporating uncertainty factors for interspecies and sensitive subpopulations.

Regulations and Policy

National and International Standards

The (WHO), through its International Programme on (IPCS), classifies dimethoate as moderately hazardous (Class II) based on acute oral LD50 values in rats ranging from 150 to 400 mg/kg body weight, emphasizing risks of cholinesterase inhibition when mishandled. The Commission sets international maximum residue limits (MRLs) for dimethoate and its omethoate, measured and reported separately for compliance purposes but summed for dietary risk assessments; examples include 0.02 mg/kg for pome fruits and 0.01 mg/kg for tomatoes, with many commodities at the limit of quantification (0.001–0.01 mg/kg). In the United States, the Environmental Protection Agency (EPA) establishes tolerances (equivalent to MRLs) for dimethoate residues in raw agricultural commodities under 40 CFR Part 180, such as 0.2 mg/kg for citrus fruits and 2.0 mg/kg for grain, with ongoing registration reviews as of June 2024 proposing risk mitigations like buffer zones and reduced application rates to address ecological and human health concerns without full cancellation. The did not renew approval for dimethoate under Commission Implementing Regulation (EU) 2019/1090, citing unacceptable , neurodevelopmental risks, and exposure concerns for operators, residents, and consumers, leading to a de facto ban on its use and authorization in plant protection products effective from July 2020, with MRLs reduced to default levels of 0.01 mg/kg or lower for most commodities. In , the Australian Pesticides and Veterinary Medicines Authority (APVMA) permits dimethoate for specific agricultural uses but suspended post-harvest applications on mangoes, avocados, and certain berries in September 2023 after detecting residues exceeding MRLs (e.g., up to 10 mg/kg in berries), mandating 14-day withholding periods where allowed and classifying it under an of 0.02 mg/kg body weight. India's Central Insecticides Board and Registration Committee restrict dimethoate to non-raw-consumed crops, banning its use on fruits and eaten raw via S.O. 4294(E) effective October 3, 2023, due to risks, while enforcing MRLs up to 2.0 mg/kg under and Standards Authority guidelines for permitted applications.

Recent Developments and Registration Reviews

In June 2024, the U.S. Environmental Protection Agency (EPA) issued its Proposed Interim Registration Review Decision (PID) for dimethoate under the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA), determining no risks of concern to human health from dietary, residential, or aggregate exposures when applied per label instructions and existing mitigation measures, such as for handlers. The assessment identified potential ecological risks to terrestrial and aquatic organisms, prompting proposals to cancel registrations for dimethoate use on specific crops like , , and certain fruit trees where protections could not be ensured through refined application rates or buffers. Public comments on the PID highlighted tensions between pest control benefits and risk mitigation; agricultural groups, including the Kansas Ag Retailers Association, argued in August 2024 for retaining registrations on key crops due to limited alternatives for managing pests like aphids and leafhoppers, emphasizing economic impacts on producers without sufficient data on viable substitutes. Conversely, the expressed concerns in late August 2024 over dimethoate's potential as an , citing studies on developmental effects in animal models and urging further evaluation of low-dose exposures despite the EPA's hazard characterization. The EPA's final decision remains pending, with opportunities for rebuttal comments and potential adjustments based on new data. In the , dimethoate's approval was not renewed under Commission Implementing Regulation (EU) 2019/1090, effective July 31, 2020, following assessments identifying genotoxic risks to consumers from omethoate residues (dimethoate's primary metabolite) and unacceptable operator exposure levels, leading to revocation of all plant protection product authorizations containing the substance. Australia's Pesticides and Veterinary Medicines Authority proposed suspension of specific dimethoate products on August 5, 2025, targeting non-compliant labels or formulations amid ongoing compliance reviews, with a one-year deemed permit for continued use under strict conditions if approved, reflecting heightened scrutiny of residues in exports. In , the Pest Management Regulatory Agency's July 2024 cumulative assessment of 10 organophosphates, including dimethoate, confirmed alignment with the 2015 re-evaluation decision (RVD2015-04) that retained registrations with label amendments for reduced application rates and buffer zones to protect aquatic life, but noted ongoing monitoring for aggregate risks without proposing immediate changes.

Controversies and Incidents

Poisoning Cases and Safety Data

Dimethoate exerts toxicity primarily through inhibition of , leading to accumulation of and overstimulation. Acute oral exposure in humans can cause symptoms including , excessive sweating, , , , loss of coordination, , convulsions, and , potentially progressing to fatal . In animal models, the oral LD50 for rats ranges from 60 to 425 mg/kg, classifying it as moderately toxic (EPA Toxicity Category II). Dermal LD50 in rats exceeds 2,000 mg/kg, indicating lower acute skin absorption risk, though skin irritation and eye irritation are reported. No specific occupational exposure limits have been established by agencies like OSHA, emphasizing the need for in handling. Human poisoning cases predominantly involve intentional self-ingestion, particularly in agricultural regions, with dimethoate exhibiting a case fatality rate approximately three times higher than chlorpyrifos due to rapid progression to hypotensive shock. Several suicidal ingestions have been documented, often resulting in profound peripheral vasodilation, distributive shock, and death despite atropine and pralidoxime administration. Accidental occupational exposures, such as dermal contact or inhalation during application, have also occurred, though less frequently fatal; one reported case involved a gardener's ingestion leading to severe symptoms requiring prolonged skin decontamination and supportive care. In severe instances, dimethoate poisoning uniquely features refractory hypotension unresponsive to standard fluids, prompting adjunctive treatments like methylene blue to restore hemodynamic stability. Treatment follows organophosphate protocols: immediate decontamination, atropine (initially 2-4 mg IV for adults, titrated to control secretions), and (1-2 g IV, repeatable) to reactivate , alongside supportive measures for ventilation and seizures. Early intervention improves outcomes, but delayed presentation in self-poisoning cases correlates with higher mortality, as dimethoate's metabolite omethoate exacerbates inhibition. Recent EPA assessments (2024) indicate no anticipated human health risks from registered uses with protective measures, though incident data underscores risks in misuse scenarios.

Debates on Benefits Versus Risks

Dimethoate offers agricultural benefits primarily through its systemic action as a broad-spectrum , effectively controlling pests such as , spider mites, leaf s, and grasshoppers on crops including soybeans, , , and various fruits and vegetables, thereby protecting yields and supporting programs. Its relatively low application cost—e.g., approximately $7.52 per acre for soybeans—and flexibility in timing allow fewer treatments compared to some alternatives, while aiding resistance management by reducing dependence on pyrethroids or neonicotinoids. In specific contexts, such as U.S. asparagus production where up to 88% of Michigan acreage relies on it for aphid and control, or fields as the sole Group 1B option against transmitting barley yellow dwarf virus, termination could elevate pest pressure and economic losses without equivalent substitutes. Agricultural stakeholders argue these benefits justify continued registration, particularly in regions lacking affordable, equally efficacious alternatives. Conversely, risks center on dimethoate's high acute oral toxicity (LD50 around 150-400 mg/kg in mammals), potential genotoxicity, and inhibition of cholinesterase leading to neurological effects, with chronic exposure linked to DNA damage, mitochondrial dysfunction, reproductive interference (e.g., reduced testosterone), and multi-organ impacts including liver, kidney, and brain toxicity. Environmentally, it poses elevated hazards to non-target species, including birds, mammals, aquatic invertebrates, bees, and earthworms, with persistence in soil and potential groundwater leaching exacerbating ecosystem disruption and bioaccumulation. Regulatory bodies like the European Food Safety Authority (EFSA) have identified insufficient data to exclude mutagenic risks, precluding safe reference values and prompting a 2006 EU-wide prohibition, as benefits were deemed insufficient against residue and ecological threats. Debates intensify in regulatory contexts, where U.S. EPA assessments for registration (initiated 2009, interim decisions ongoing as of 2024) weigh low-to-moderate benefits for certain minor crops against high ecological and worker exposure risks, proposing mitigations or cancellations despite industry pushback citing costlier alternatives (up to 480% more expensive) and yield vulnerabilities. Environmental advocates, including petitions from groups like , assert that long-term societal costs—from health burdens like potential carcinogenicity to biodiversity loss—outweigh gains, especially with emerging IPM and options reducing reliance. In developing regions, economic imperatives sustain use for staple crop protection despite bans elsewhere, highlighting tensions between immediate and precautionary principles, though studies suggest overall pesticide expenses often exceed yield benefits when externalities are factored. These conflicts underscore issues, as industry submissions emphasize agronomic data while peer-reviewed and EFSA evaluations prioritize empirical risk metrics over short-term economic claims.

Commercial Aspects

Trade Names and Manufacturers

Dimethoate is commercially available under numerous trade names, reflecting its formulation as emulsifiable concentrates (typically 30-48% ) or other systemic products targeted at agricultural pests. , key products include Dimethoate 400 EC manufactured by for broad-spectrum control on crops like fruits and vegetables. Drexel Chemical Company produces Dimethoate 2.67 and Dimethoate 4EC, both formulations providing contact and systemic activity against sucking and chewing insects. Loveland Products offers Dimethoate 400 , registered for use on nonbearing trees, vineyards, and nursery stock. Other established trade names historically associated with dimethoate include Cygon 400, De-Fend, and Rogor, often produced by firms for global markets, though specific registrations vary by region due to regulatory restrictions. In , formulations such as Cygon 480-Ag (FMC dimethoate 480 g/L EC) and Diamante 4 remain listed for agricultural applications. Internationally, Rallis markets Tafgor (Dimethoate 30% EC) for crops including , mustard, and potatoes. Production occurs primarily in countries with active manufacturing sectors, such as the , , and , where companies like Aceagrochem supply Dimethoate 40% EC for export. Availability has diminished in some markets following voluntary cancellations and use terminations, as documented in 2005 U.S. EPA orders affecting products from Drexel and Loveland.

Alternatives and Phase-Out Efforts

The declined to renew approval for dimethoate as a plant protection product, citing unacceptable risks to operators, workers, and consumers from exposure to the substance and its omethoate, classified as mutagenic category 2 by the ; the ban took effect on July 17, 2020, for most crops including olives, with a until October 17, 2020, for cherries. This measure primarily targeted its use against pests like the , prompting concerns among conventional olive growers in countries such as , where dimethoate had already been restricted, over potential yield losses and price increases absent direct substitutes of comparable efficacy. In the United States, the Environmental Protection Agency issued a Proposed Registration Review Interim Decision for dimethoate in June 2024 as part of ongoing evaluations of insecticides, incorporating risk mitigation measures such as buffer zones and to address acute and ecological hazards, though full phase-out proposals from prior administrations remain unfinalized. Australia's Pesticides and Veterinary Medicines Authority proposed suspension of certain dimethoate products in August 2025 due to reevaluated risks, allowing continued labeled use during consultation but signaling a shift toward reduced reliance. Export-related restrictions, such as France's extension of safeguards on U.S. cherries citing dimethoate residues exceeding maximum residue limits, underscore enforcement challenges in . Alternatives to dimethoate emphasize (IPM) frameworks, incorporating biological controls like augmentation of natural enemies (e.g., parasitic wasps or predatory insects), cultural practices such as and habitat diversification to support , and physical barriers like netting or bagging for fruit crops. Biopesticides, including microbial agents like (Bt) for lepidopteran pests or spinosad for sucking insects, offer targeted efficacy with lower persistence and reduced non-target impacts compared to broad-spectrum organophosphates. For quarantine treatments in , non-chemical options such as cold disinfestation, heat treatments, or have replaced dimethoate in protocols for fruit fly control in exports from regions like . Chemical replacements vary by and pest but often include pyrethroids like zeta-cypermethrin (e.g., Mustang Max) or formulations (e.g., Lorsban Advanced) for and leafminer suppression in , though these may require sequential applications and face their own regulatory scrutiny for toxicity. Neonicotinoids such as provide systemic control for in like and peas, with application costs ranging from $14.22 per acre versus dimethoate's $1.59, potentially increasing economic burdens without fully matching spectrum or residue tolerance profiles. In cases like olive production, IPM adoption has mitigated gaps left by the ban, though farmers report variable efficacy against high-pressure infestations, highlighting trade-offs between risk reduction and pest management reliability.

References

  1. https://pubchem.ncbi.nlm.nih.gov/compound/Dimethoate
  2. https://cameochemicals.noaa.gov/chemical/4958
  3. https://www.epa.gov/pesticides/epa-releases-updates-organophosphate-pesticides-dicrotophos-dimethoate-and
  4. https://sitem.herts.ac.uk/aeru/ppdb/en/Reports/244.htm
  5. https://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=P10049N4.TXT
  6. https://pmc.ncbi.nlm.nih.gov/articles/PMC7009644/
  7. https://pubmed.ncbi.nlm.nih.gov/35132945/
  8. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0321848
  9. https://downloads.regulations.gov/EPA-HQ-OPP-2009-0059-0073/content.pdf
  10. https://www.researchgate.net/publication/383166630_Dimethoate-induced_toxicity_a_comprehensive_review_of_its_aquatic_environmental_hazards
  11. https://webbook.nist.gov/cgi/cbook.cgi?ID=60-51-5
  12. https://www.inchem.org/documents/ehc/ehc/ehc90.htm
  13. https://www.chemicalbook.com/ChemicalProductProperty_US_CB0459837.aspx
  14. https://chemicalsafety.ilo.org/dyn/icsc/showcard.display?p_card_id=0741
  15. https://www.osha.gov/chemicaldata/510
  16. https://www.sciencedirect.com/topics/neuroscience/dimethoate
  17. https://pubmed.ncbi.nlm.nih.gov/17897769/
  18. https://www.apvma.gov.au/sites/default/files/publication/15166-dimethoate_human_health_tox.pdf
  19. https://www.sciencedirect.com/topics/medicine-and-dentistry/dimethoate
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC2635059/
  21. https://www.inchem.org/documents/jmpr/jmpmono/v84pr19.htm
  22. https://www.apvma.gov.au/sites/default/files/dimethoate-phase-8-human-health.pdf
  23. https://patents.google.com/patent/US20120053151A1/en
  24. https://www.apvma.gov.au/news-and-publications/public-consultations/dimethoate-proposed-suspension
  25. https://www.fao.org/fileadmin/templates/agphome/documents/Pests_Pesticides/Specs/Dimethoate2012_2.pdf
  26. https://downloads.regulations.gov/EPA-HQ-OPP-2009-0059-0111/attachment_3.pdf
  27. https://www.canada.ca/content/dam/hc-sc/migration/hc-sc/cps-spc/alt_formats/pdf/pubs/pest/_decisions/rvd2015-04/RVD2015-04-eng.pdf
  28. https://labelsds.com/images/user_uploads/Dimethoate%2520400%2520Label%25202-6-14.pdf
  29. https://cdn.nufarm.com/wp-content/uploads/sites/22/2018/05/06182542/Dimethoate104879180116.pdf
  30. https://assets.greenbook.net/L98457.pdf
  31. https://ipmil.cired.vt.edu/wp-content/uploads/2019/02/insects-10-00045-1-002.pdf
  32. https://academicjournals.org/journal/AJAR/article-full-text/62FF06369813
  33. http://extoxnet.orst.edu/pips/dimethoa.htm
  34. https://www.mdpi.com/2305-6304/13/3/219
  35. https://efsa.onlinelibrary.wiley.com/doi/pdf/10.2903/j.efsa.2006.84r
  36. https://cdn.who.int/media/docs/default-source/wash-documents/wash-chemicals/dimethoate-bd.pdf?sfvrsn=e0965069_4
  37. https://www.wfduk.org/sites/default/files/Media/dimethoate.pdf
  38. https://pubmed.ncbi.nlm.nih.gov/26613988/
  39. https://pmc.ncbi.nlm.nih.gov/articles/PMC5043368/
  40. https://www.waterquality.gov.au/anz-guidelines/guideline-values/default/water-quality-toxicants/toxicants/dimethoate-2000
  41. https://www.tandfonline.com/doi/full/10.1080/11250003.2011.571222
  42. https://pubmed.ncbi.nlm.nih.gov/27454845/
  43. https://labelsds.com/images/user_uploads/Dimethoate%2520400%2520SDS%252010-4-16.pdf
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC2964340/
  45. https://nj.gov/health/eoh/rtkweb/documents/fs/0733.pdf
  46. https://www.ncbi.nlm.nih.gov/books/NBK470430/
  47. https://chemm.hhs.gov/countermeasure_pralidoxime.htm
  48. https://www.tandfonline.com/doi/full/10.1080/15563650802172063
  49. https://www.fao.org/fao-who-codexalimentarius/codex-texts/dbs/pestres/pesticide-detail/en/?p_id=27
  50. https://www.fao.org/fao-who-codexalimentarius/codex-texts/dbs/pestres/commodities-detail/en/?c_id=320
  51. https://www.ecfr.gov/current/title-40/chapter-I/subchapter-E/part-180
  52. https://eur-lex.europa.eu/legal-content/EN/TXT/PDF/?uri=CELEX:32019R1090
  53. https://www.efsa.europa.eu/en/efsajournal/pub/4647
  54. https://www.apvma.gov.au/news-and-publications/news/suspension-specific-dimethoate-products
  55. https://www.abc.net.au/news/2023-09-23/dimethoate-use-suspended-on-mangoes-avocados-post-harvest/102758696
  56. https://ppqs.gov.in/sites/default/files/list_of_pesticides_which_are_banned_refused_registration_and_restricted_in_use_0.pdf
  57. https://www.fssai.gov.in/upload/uploadfiles/files/Contaminants_Regulations.pdf
  58. https://www.federalregister.gov/documents/2024/06/24/2024-13807/pesticide-registration-review-proposed-decisions-for-several-pesticides-notice-of-availability
  59. https://www.ksagretailers.org/regulatory/kara-submits-comment-to-epa-on-importance-of-maintaining-dimethoate-registration/
  60. https://www.endocrine.org/-/media/endocrine/files/advocacy/society-letters/2024/august/endocrine-society-comments-dimethoate.pdf
  61. https://www.epa.gov/pesticide-reevaluation/upcoming-registration-review-actions
  62. https://eur-lex.europa.eu/eli/reg_impl/2019/1090/oj/eng
  63. https://efsa.onlinelibrary.wiley.com/doi/full/10.2903/j.efsa.2016.4647
  64. https://www.apvma.gov.au/news-and-publications/news/proposed-suspension-specific-dimethoate-products-0
  65. https://www.apvma.gov.au/news-and-publications/public-consultations/proposed-suspension-of-dimethoate-products
  66. https://publications.gc.ca/collections/collection_2024/sc-hc/h113-5/H113-5-2024-2-eng.pdf
  67. https://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=90190700.TXT
  68. https://cdn.caymanchem.com/cdn/msds/24246m.pdf
  69. https://pubmed.ncbi.nlm.nih.gov/19003596/
  70. https://www.researchgate.net/publication/347722377_A_Case_of_Dimethoate_Poisoning_Requiring_Prolonged_Skin_Decontamination
  71. https://apjmt.mums.ac.ir/article_4915_deea4d2b4e18a291f78db150c6fa369c.pdf
  72. https://www.inchem.org/documents/hsg/hsg/hsg020.htm
  73. https://www.sciencedirect.com/science/article/pii/S0140673607612021
  74. https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/dimethoate
  75. https://downloads.regulations.gov/EPA-HQ-OPP-2009-0059-0102/attachment_1.pdf
  76. https://pmc.ncbi.nlm.nih.gov/articles/PMC7712428/
  77. https://www.sciencedirect.com/science/article/abs/pii/B9780128190920000078
  78. https://www.researchgate.net/publication/285048696_Environmental_Fate_and_Toxicology_of_Dimethoate
  79. https://journal-jbv.apub.kr/articles/article/EKeb/
  80. https://www.efsa.europa.eu/en/efsajournal/pub/5454
  81. https://nepis.epa.gov/Exe/ZyPURL.cgi?Dockey=P100WFTO.TXT
  82. https://earthjustice.org/document/organophosphate-petition
  83. https://beyondpesticides.org/dailynewsblog/2024/02/health-savings-outweigh-cost-of-banning-pesticides-linked-to-parkinsons-disease-according-to-study/
  84. https://www.slowfood.com/blog-and-news/banned-at-home-sold-abroad-the-eus-pesticide-hypocrisy/
  85. https://beyondpesticides.org/dailynewsblog/2021/12/pesticides-expenses-significantly-outweigh-economic-benefits/
  86. https://ag.fmc.com/us/en/insecticides-miticides/dimethoate-400-ec
  87. https://www.drexchem.com/products/dimethoate-2-67/
  88. https://www.drexchem.com/products/dimethoate-4ec/
  89. https://www.lovelandproducts.com/content/loveland/us/en/products/crop-protection/insecticide/dimethoate-400-insecticide.html
  90. https://www.gov.mb.ca/agriculture/crops/guides-and-publications/pubs/trade-names-guide-2024.pdf
  91. https://www.rallis.com/international-business/Dimethoate
  92. https://aceagrochem.com/pesticide/insecticide/single/Dimethoate%2520400%2520EC.html
  93. https://www.federalregister.gov/documents/2005/07/20/05-14070/dimethoate-product-cancellation-order-and-amendments-to-terminate-uses
  94. https://eur-lex.europa.eu/legal-content/EN/TXT/PDF/?uri=CELEX:32019R1090&from=EN
  95. https://www.efsa.europa.eu/en/efsajournal/pub/rn-84
  96. https://www.oliveoiltimes.com/production/use-of-dimethoate-to-be-banned-in-eu/68689
  97. https://apps.fas.usda.gov/newgainapi/api/Report/DownloadReportByFileName?fileName=France%20extends%20ban%20on%20US%20cherries%20over%20dimethoate%20use%20despite%20new%20EU%20rules_Paris_France_05-19-2020
  98. https://z.umn.edu/HomeownersIPM
  99. https://pmc.ncbi.nlm.nih.gov/articles/PMC9978502/
  100. https://extension.arizona.edu/sites/default/files/2024-08/az1765-2018.pdf
  101. https://ausveg.com.au/app/uploads/technical-insights/VG11031-Final-Report-AUSVEG.pdf
  102. https://www.cdfa.ca.gov/files/pdf/EmulsifiableConcentrateAlternativesAnalysis.pdf
  103. https://cales.arizona.edu/crop/vegetables/insects/aphid/insecticidealts.html
  104. https://westernipm.org/index.cfm/searchable-data-sources/docPull?ID=DIMETH_23
  105. https://californiaagriculture.org/article/110465-alternatives-to-targeted-pesticides-the-danr-database/attachment/215402.pdf
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