Many plants and minerals have insecticidal properties; that is, they are toxic to insects. Botanical insecticides are naturally occurring chemicals (insect toxins) extracted or derived from plants or minerals. They are also called natural insecticides. Organic gardeners will choose these insecticides, in some cases, over synthetic organic materials.
In general, they act quickly, degrade rapidly and have, with a few exceptions, low mammalian toxicity. Products containing ingredients derived from plants (Table 1) are considered pesticides . However, products containing these active ingredients must be registered for use by the Environmental Protection Agency (EPA) and used in accordance with the provisions of the Federal Insecticide, Fungicide and Rodenticide Act (FIFRA). In order to market these products in Texas, they must also be registered by the Texas Department of Agriculture.
| Generic Name | Oral LD50 | Dermal LD50 | Signal Word |
|---|---|---|---|
| Pyrethrins | 1,200-1,500 | >1,800 | Caution |
| Rotenone | 60-1,500* | 940-3,000 | Caution |
| Sabadilla | 4,000 | — | Caution |
| Ryania | 750-1,200 | 4,000 | Caution |
| Nicotine | 50-60 | 50 | Danger |
| d-Limonene | >5,000 | — | Caution |
| Linalool | 2,440-3,180 | 3,578-8,374 | Caution |
| Neem | 13,000 | — | Caution |
* Toxicity varies greatly depending on type of solvent used as carrier
Pyrethrum and Pyrethrins
Structure.
| cinerin I cinerin II cinerin III jamolin I jamolin II pyerethrin I pyrethrin II |
C20H28O3 C21H28O5 C21H30O3 C21H30O3 C22H30O5 C21H28O3 C22H28O5 |
Source. Pyrethrum is the powdered, dried flower head of the pyrethrum is daisy, Chrysanthemum cinerariaefolium. Most of the world’s pyrethrum crop is grown in Kenya. The term “pyrethrum” is the name for the crude flower dust itself, and the term “pyrethrins” refers to the six related insecticidal compounds that occur naturally in the crude material, the pyrethrum flowers. They are extracted from crude pyrethrum dust as a resin that is used in the manufacture of various insecticidal products.
Mode of action. Pyrethrins exert their toxic effects by disrupting the sodium and potassium ion exchange process in insect nerve fibers and interrupting the normal transmission of nerve impulses. Pyrethrins insecticides are extremely fast acting and cause an immediate “knockdown” paralysis in insects. Despite their rapid toxic action, however, many insects are able to metabolize (break down) pyrethrins quickly. After a brief period of paralysis, these insects may recover rather than die. To prevent insects from metabolizing pyrethrins and recovering from poisoning, most products containing pyrethrins also contain the synergist, piperonyl butoxide (PBO). Without PBO the effectiveness of pyrethrins is greatly reduced.
Mammalian toxicity. Pyrethrins are low in mammalian toxicity (see Table), and few cases of human poisonings have ever been reported. Cats, however, are highly susceptible to poisoning by pyrethrins, and care must be taken to follow label directions closely when using products containing pyrethrins to treat cats for fleas.
When ingested, pyrethrins are not readily absorbed from the digestive tract, and they are rapidly hydrolyzed under the acid conditions of the gut and the alkaline conditions of the liver. Pyrethrins are more toxic to mammals by inhalation than by ingestion because inhalation provides a more direct route to the bloodstream. Exposure to high doses may cause nausea, vomiting, diarrhea, headaches, and other nervous disturbances. Repeated contact with crude pyrethrum dusts may cause skin irritation or allergic reactions. The allergens that cause these reactions are not present in products containing refined pyrethrins. Tests indicate that chronic exposure to pyrethrins does not cause genetic mutations or birth defects.
There is no single antidote for acute pyrethrin poisoning. Treatment of poisoning is symptomatic, i.e., the various symptoms of poisoning are treated individually as they occur because there is no way to counteract the source of the poisoning directly.
Rotenone
Structure.C23H228O6
Source. Rotenone is insecticidal compound that occurs in the roots of Lonchocarpus species in South America, Derris species in Asia, and several other related tropical legumes. Commercial rotenone was at one time produced from Malaysian Derris. Currently the main commercial source of rotenone is Peruvian Lonchocarpus, which often is referred to as cube root.
Rotenone is extracted from cube roots in acetone or ether. Extraction produces a 2-40% rotenone resin which contains several related but less insecticidal compounds known as rotenoids. The resin is used to make liquid concentrates or to impregnate inert dusts or other carriers. Most rotenone products are made from the complex resin rather than from purified rotenone itself. Alternatively, cube roots may be dried, powdered and mixed directly with an inert carrier to form an insecticidal dust.
Mode of action. Rotenone is a powerful inhibitor of cellular respiration, the process that converts nutrient compounds into energy at the cellular level. In insects rotenone exerts its toxic effects primarily on nerve and muscle cells, causing rapid cessation of feeding. Death occurs several hours to a few days after exposure. Rotenone is extremely toxic to fish, and is often used as a fish poison (piscicide) in water management programs. It is effectively synergized by PBO or MGK 264.
Mammalian toxicity. Although rotenone is a potent cell toxin, mammals detoxify ingested rotenone efficiently via liver enzymes. As with pyrethrins, rotenone is more toxic by inhalation than by ingestion. Exposure to high doses may cause nausea, vomiting, muscle tremor, and rapid breathing. Very high doses may cause convulsions followed by death from respiratory paralysis and circulatory collapse. Direct contact with rotenone may be irritating to skin and mucous membranes. Treatment of poisoning is symptomatic. Chronic exposure to rotenone may lead to liver and kidney damage. Although some rodent testing has shown that chronic dietary exposure to rotenone may induce tumor formation,the most recent US EPA registration standard considers rotenone to be noncarcinogenic.
Rotenone is one of the more acutely toxic botanicals. As a matter of comparison, pure, unformulated rotenone is more toxic than pure carbaryl (Sevin®) or malathion, two commonly used synthetic insecticides. In the form of a 1% dust, rotenone poses roughly the same acute hazard as the commonly available 5% Sevin dust. Commercial rotenone products have presented little hazard to man over many decades. Neither fatalities nor systemic poisonings in humans have been reported in relation to ordinary use.
Sabadilla (veratrine alkaloids)
Structure.
Cevadine: C32H49NO9
Veratridine: C36H51NO11
Source. Sabadilla is derived from the ripe seeds os Schoenocaulon officinale, a tropical lily plant which grows in Central and South America. Sabadilla is also sometimes known as cevadilla or caustic barley.
When sabadilla seeds are aged, heated, or treated with alkali, several insecticidal alkaloids are formed or activated. Alkaloids are physiologically active compounds that occur naturally in many plants. In chemical terms they are a heterogeneous class of cyclic compounds that contain nitrogen in their ring structures. Caffeine, nicotine, cocaine, quinine, and strychnine are some of the more familiar alkaloids. The alkaloids in sabadilla are known collectively as veratrine or as the veratrine alkaloids. They constitute 3-6% of aged, ripe sabadilla seeds. Of these alkaloids, cevadine and veratridine are the most active insecticidally.
European white hellebore (Veratrum album) also contains veratridine in its roots. Hellebore was once commonly used in Europe and the U.S. for insect control, but is now unavailable commercially and is not registered by the US EPA.
Mode of action. In insects, sabadilla’s toxic alkaloids affect nerve cell membrane action, causing loss of nerve cell membrane action, causing loss of nerve function, paralysis and death. Sabadilla kills insects of some species immediately, while others may survive in a state of paralysis for several days before dying. Sabadilla is effectively synergized by PBO or MGK 264.
Mammalian toxicity. Sabadilla, in the form or dusts made from ground seeds, is the least toxic of the registered botanicals. Purified veratrine alkaloids are quite toxic, however, and are considered on a par with the most toxic synthetic insecticides. Sabadilla can be severely irritating to skin and mucous membranes, and has a powerful sneeze-inducing effect when inhaled. Ingestion of small amounts may cause headaches, severe nausea, vomiting, diarrhea, cramps and reduced circulation. Ingestion of very high doses may cause convulsions, cardiac paralysis, and respiratory failure. Sabadilla alkaloids can be absorbed through the skin or mucous membranes. Systemic poisoning by sabadilla preparations used as insecticides has been very rare or nonexistant.
Ryania
Structure. None
Source. Ryania comes from the woody stems of Ryania speciosa, a South American shrub. Powdered Ryania stem wood is combined with carriers to produce a dust or is extracted to produce a liquid concentrate. The most active compound in ryania is the alkaloid ryanodine, which constitutes approximately 0.2% of the dry weight of stem wood.
Mode of action. Ryania is a slow-acting stomach poison. Although it does not produce rapid knockdown paralysis, it does cause insects to stop feeding soon after ingesting it. Little has been published concerning its exact mode of action in insect systems. Ryania is effectively synergized by PBO and is reported to be most effective in hot weather.
Mammalian toxicity. Ryania is moderately toxic to mammals by ingestion and only slightly toxic by dermal exposure. Ingestion of large doses causes weakness, deep and slow respiration, vomiting, diarrhea, and tremors, sometimes followed by convulsions, coma, and death. Purified ryanodine is approximately 700 times more toxic than the crude ground or powdered wood and causes poisoning symptoms similar to those of synthetic organophosphate insecticides. (Depending on exposure, organophosphate poisoning symptoms may include sweating, headache, twitching, muscle cramps, mental confusion, tightness in chest, blurred vision, vomiting, evacuation of bowels and bladder, convulsions, respiratory collapse, coma, and death.)
Nicotine
Structure. C10H16N2O4S
Source. Nicotine is a simple alkaloid derived from tobacco, Nictiana tabacum, and other Nicotiana species. Nicotine contitutes 2-8% of dried tobacco leaves. Insecticidal formulations generally contain nicotine in the form of 40% nicotine sulfate and are currently imported in small quantities from India.
Mode of action. In both insects and mammals, nicotine is an extremely fast-acting nerve toxin. It competes with acetylcholine, the major neurotransmitter, by bonding to acetylcholine receptors at nerve synapses and causing uncontrolled nerve firing. This disruption of normal nerve impulse activity results in rapid failure of those body systems that depend on nervous input for proper functioning. In insects, the action of nicotine is fairly selective, and only certain types of insects are affected.
Mammalian toxicity. Despite the fact that smokers regularly inhale small quantities of nicotine in tobacco smoke, nicotine in pure form is extremely toxic to mammals and is considered a Class I (most dangerous) poison. Nicotine is particularly hazardous because it penetrates skin, eyes, and mucous membranes readily both inhalation and dermal contact may result in death. Ingestion is slightly less hazardous due to the effective detoxifying action of the liver.
Symptoms of nicotine poisoning are extreme nausea, vomiting, excess salivation, evacuation of bowels and bladder, mental confusion, tremors, convulsions, and finally death by respiratory failure and circulatory collapse. Poisoning occurs very rapidly and is often fatal. Treatment for nicotine poisoning is symptomatic, and only immediate treatment, including prolonged artificial respiration, may save a victim of nicotine poisoning. Nicotine has been responsible for numerous serious poisonings and accidental deaths because of its rapid penetration of skin and mucous membranes and because of the concentrated form in which it is used.
Neem
Structure. Azadiractin
Source. Neem products are derived from the neem tree, Azadirachta indica, that grows in arid tropical and subtropical regions on several continents. The principle active compound in neem is azadirachtin, a bitter, complex chemical that is both a feeding deterrent and a growth regulator. Meliantriol, salannin, and many other minor components of neem ar also active in various ways. Neem products include teas and dusts made from leaves and bark, extracts from whole fruits, seeds, or seed kernels, and an oil expressed from the seed kernel.
The product known as “neem oil” is more like a vegetable or horticultural oil and acts to suffocate insects. Neem and neem oil are often confused.
Mode of action. Neem is a complex mixture of biologically active materials, and it is difficult to pinpoint the exact modes of action of various extracts or preparations. In insects, neem is most active as a feeding deterrent, but in various forms it also serves as a repellent, growth regulator, oviposition (egg deposition) suppressant, sterilant, or toxin.
As a repellent, neem prevents insects from initiating feeding. As a feeding deterrent, it causes insects to stop feeding. As a feeding, either immediately after the first “taste” (due to the presence of deterrent taste factors), or at some point soon after ingesting the food (due to secondary hormonal or physiological effects of the deterrent substance). As a growth regulator, neem is thought to disrupt normal development interfering with chitin synthesis. Susceptibility to the various effects of neem differs by species.
Citrus Oil Extracts: Limonene and Linalool
Source. Crude citrus oils and the refined compounds d-limonene (hereafter referred to simply as limonene) and linalool are extracted from orange and other citrus fruit peels. Limonene, a terpene, constitutes about 90% of crude citrus oil, and is purified from the oil by steam distillation. Linalool, a terpene alcohol, is found in small quantities in citrus peel and in over 200 other herbs, flowers, fruits, and woods.
Terpenes and terpene alcohols are among the major components of many plant volatiles or essential oils. Other components of essential oils are ketones, aldehydes, esters, and various alcohols. Essential oils are the volatile compounds responsible for most of the tastes and scents of plants. Many of the essential oils also have some physiological activity.
Mode of action. The modes of action of limonene and linalool in insects are not fully understood. Limonene is thought to cause an increase in the spontaneous activity of sensory nerves. This heightened activity sends spurious information to motor nerves and results in twitching, lack of coordination, and convulsions. The central nervous system may also be affected, resulting in additional stimulation of motor nerves. Massive over stimulation of motor nerves leads to rapid knockdown paralysis. Adult fleas and other insects may recover from knockdown, however, unless limonene is synergized by PBO. Linalool is also synergized by PBO. Little has been published regarding the mode of action of linalool in insects.
Mammalian toxicity. Both limonene and linalool were granted GRAS (Generally Regarded As Safe) status by the United States Food and Drug Administration in 1965, and are used extensively as flavorings and scents in foods, cosmetics, soaps, and perfumes. Both compounds are considered safe when used for these purposes because they have low oral and dermal toxicities. At higher concentrations, however, limonene and linalool are physiologically active and may be irritating or toxic to mammals.
When applied topically, limonene is irritating to skin, eyes, and mucous membranes. Both limonene and linalool may be allergenic. Limonene acts as a topical vasodilator and a skin sensitizer; it was also shown to promote tumor formation in mouse skin that had been previously sensitized to tumor initiation. Linalool is more active as a systemic toxin than as a skin irritant.
Both compounds affect the central nervous system, and moderate to high doses applied topically to cats and other laboratory animals cause tremors, excess salivation, lack of coordination, and muscle weakness. Even at the higher doses, however, these symptoms are temporary (lasting several hours to several days), and animals recover fully. Some cats may experience minor tremors and excess salivation for up to one hour after applications of limonene or linalool at recommended rates.
Crude citrus peel oils and products prepared with the crude oils may be more toxic to animals than products containing purified limonene or linalool. Adequate research on the toxicity of crude citrus oils has not been conducted, and they are not recommended for use on animals.
Other Essential Plant Oils: Herbal Repellents and Insecticides
Essential oils are volatile, odorous oils derived from plant sources. Although they are used mainly as flavorings and fragrances in foods, cosmetics, soaps, and perfumes, some of them also have insect repellent or insecticidal properties. Many essential oils have GRAS (Generally Regarded As Safe) status; however, when applied topically at high concentrations they tend to be irritating to skin and mucous membranes. They are sometimes used as topical counterirritant to relieve or mask pain. Many of the essential oils that have low dermal toxicity may be toxic by ingestion.
The most common essential oils used as repellents are the oils of cedar, lavender, eucalytus, pennyroyal, and citronella. They are used mostly on pets and humans to repel fleas and mosquitoes. With the exception of pennyroyal, these essential oils are thought to pose little risk to people or pets, though they should not be used above recommended rates. Some herbal pest products that contain essential oils recommend use daily or “as often as needed.” These products should be used moderately and with careful observation of the pet to spot early signs of skin irritation or possible toxic effects.
Oil of pennyroyal contains pulegone, a potent toxin that can cause death in humans at doses as low as one tablespoon when ingested. At lower internal doses it may cause abortion, liver damage, and renal failure. Although the dermal toxicity of pennyroyal is fairly low, some cats are susceptible to poisoning by topical application of oil of pennyroyal, possibly because they ingest it during grooming.
Citronella is sold mainly in the form of candles to be burned outdoors to repel mosquitoes from back yards or other small areas. It is also contained in some “natural” mosquito repellent lotions. Before the development of synthetic repellents, citronella was the most effective mosquito repellent available. Despite its wide usage, there is little scientific information available regarding its efficacy or mammalian toxicity.
Related
Organic Gardening – Natural Insecticides – New Mexico State University Extension
Botanical Insecticides – NC State University Extension
Botanical Insecticides in the Home Garden – Iowa State University Extension
References
Extracted and modified from T. Henn and R. Weinzieri, 1989; Larson, L.L., et al., 1985; and Morgan, D.P., 1989
Gates, J. P. 1989 (mimeo). “Organic gardening”, Agri-Topics, National Agricultural Library, USDA:
Henn, T. and R. Weinzieri. 1989. Botanical insecticides and insecticidal soaps. Circular 1296. Cooperative Extension Service. University of Illinois, Urbana-Champaign. 18 pp.
Henn, T. and R. Weinzieri. 1990. Beneficial insects and mites. Circular 1298. Cooperative Extension Service. University of Illinois, Urbana-Champaign. 24 pp.
Larson, L. L., E. E. Kenaga and R.W. Morgan. 1985. Commercial and experimental organic insecticides. Entomological Society of America. 105 pp.
Morgan, D. P. 1989. Recognition and management of pesticide poisonings. EPA-540/9-88-001. U.S. Environmental Protection Agency, Washington, D.C. 205 pp.
Weinzieri, R. and T. Henn. 1989. Microbial insecticides. Circular 1295. Cooperative Extension Service. University of Illinois, Urbana-Champaign. 24 pp.
Whitcomb, C. E. 1983. Know It and Grow It, Lacebark Publications, Stillwater, Oklahoma, 739 pp.
Mother Earth News (eds.). 1989. The Healthy Garden Handbook. Simon & Shuster Inc., New York. 192 pp.
Gates, J. P. (1989) lists a number of additional references on organic gardening. The following are extracted from this listing and appear to specifically address pest management:
Evans, B. R., J.D. Gay and F. Bullock. 1989. Organic gardening and pest control. University of Georgia, Athens, GA, Bull. 1007. 20 pp.
Overdahl, C. J., O. C. Turnquist, G. R. Miller, F. L. Pfleger, M. E. Ascerno and V. S. Packard. 1977. Organic gardening: an integrated approach. Bull. Agric. Ext. Serv. Minn. #377, 18 pp.
Stranberg, M. 1976. Food growing without poisons. Turnstone Press, Ltd., 96 pp.
Tyler, H. A. 1970. Organic gardening without poisons. Van Nostrand Reinhold, New York, 111 pp.
Yepsen, R. B. 1984. The encyclopedia of natural insect & disease control: the most comprehensive guide to protecting plants–vegetables, fruit, flowers, trees, and lawns–without toxic chemicals. Rodale Press, Emmaus, PA, 490 pp.
Texas AgriLife Extension Service has produced several publications addressing organic production:
Sauls, J. W., M. Baker, S. Helmers, J. Lipe, C. Lyons, G. McEachern, L. Shreve, and L. Stein. 1991. Producing Texas fruits and nuts organically. B-5024. Texas Agric. Ext. Serv., College Station, TX 12 pp.
Turney, H. A. and G. McIlveen. 1983. Insect control guide for organic gardeners. B-1252. Texas Agric. Ext. Serv., College Station, TX 12 pp.