How honey is made — making, used, processing, parts, composition, procedure, product, industry

Honey

Honey is a sweet syrupy substance produced by honeybees from the nectar of flowers and used by humans as a sweetener and a spread. Honey is comprised of 17-20% water, 76-80% glucose, and fructose, pollen, wax, and mineral salts. Its composition and color is dependent upon the type of flower that supplies the nectar. For example, alfalfa and clover produce a white honey, heather a reddish-brown, lavender an amber hue, and acacia and sainfoin a straw color.

Background

Honey, golden and sweet, has always been held in high regard. The Bible refers to heaven as the «Land of Milk and Honey.» In ancient times, honey was considered the food of the gods and the symbol of wealth and happiness. It was used as a form of sustenance and offered in sacrifice. In the Middle Ages, honey was the basis for the production of mead, an alcoholic beverage. Because of its antiseptic qualities, physicians found it a perfect covering for wounds before the advent of bandages. Even Napoleon was enchanted by it, choosing the honeybee for his personal crest.

Beekeeping is one of oldest forms of animal husbandry. Early beekeepers encouraged the establishment of bee colonies in cylinders of bark, reed, straw, and mud. However, when the honeycomb was removed from the cylinders, the colony was destroyed.

Honeybees were brought to North America in the mid-1600s. Although there were bees on the continent, they were not honeybees. Early settlers took note of the bees’ penchant for hollow logs. They developed a «bee gum,» by placing sticks crosswise over the opening of the logs to support the honeycombs. This not only allowed for the comb to be removed from one end, but also kept the comb intact so that the colony could use it again.

In Europe, beekeepers working toward a similar goal, developed a device called a skep. It was essentially a basket placed upside-down over the beehive. The full honeycombs were removed from underneath. A further innovation called for cutting a hole in the top of the hive and placing a straw or wooden box over the hole. The box would eventually fill with honey as well. It could then be removed without harming the comb.

In the mid-nineteenth century, an American named Moses Quimby improved upon the beekeeping system by layering a number of boxes over the main chamber. But it was the Reverend Langstroth who was responsible for creating the basis for the method that is currently used. Langstroth’s moveable frame hive allowed for easy extraction and reinsertion of the combs. It consisted of a base, a hive body fitted with frames that contained the brood chamber, one or more removable sections (called supers) that were also fitted with frames for honey storage. The entire system is protected with waterproof covers.

Another popular type of hive is the leaf hive. This is a wooden box divided by means of a metal grid into an upper (honey) chamber and a lower (brood) chamber. Just above the floor and above the grid are racks of horizontal metal bars. Frames that hold the hanging honeycombs slide onto the racks.

Raw Materials

An average bee colony produces 60-100 lb (27.2-45.4 kg) of honey each year. Colonies are divided by a three-tier organization of labor: 50,000-70,000 workers, one queen, and 2,000 drones. Worker bees only live for three to six weeks, each one collecting about one teaspoon of nectar. One pound (0.454 kg)of honey requires 4 lb (1.8 kg) of nectar, which requires two million flowers to collect.

When the worker bees are about 20 days old, they leave the hive to collect nectar, the sweet secretion produced by the glands of flowers. The bee penetrates the flower’s petals and sucks the nectar out with its tongue and deposits the nectar into its honey sac or abdomen. As the nectar journeys through the bee’s body, water is drawn out and into the bee’s intestines. The bee’s glandular system emits enzymes that enrich the nectar.

Pollen attaches to the bee’s legs and hairs during the process. Some of it falls off into subsequent flowers; some mixes with the nectar.

When the worker bee cannot hold anymore nectar, she returns to the hive. The processed nectar, now on its way to becoming honey, is deposited into empty honeycomb cells. Other worker bees ingest the honey, adding more enzymes and further ripening the honey. When the honey is fully ripened, it is deposited into a honeycomb cell one last time and capped with a thin layer of beeswax.

The Manufacturing
Process

Full honeycombs removed from
hive

  • 1 To remove the honeycombs, the beekeeper dons a veiled helmet and protective gloves. There are several methods for removing the combs. The beekeeper may simply sweep the bees off the combs and guide them back into the hive. Alternately, the beekeeper injects a puff of smoke into the hive. The bees, sensing the presence of fire, gorge themselves on honey in an attempt to take as much as they can with them before fleeing. Somewhat tranquilized by engorgement, the bees are less likely to sting when the hive is opened. A third method employs a separator board to close the honey chamber off from the brood chamber. When the bees in the honey chamber discover that they have been separated from their queen, they move through a hatch that allows them to enter the brood chamber, but not reenter the honey chamber. The separator board is inserted approximately two to three hours before the honeycomb is to be removed.

The majority of the cells in the comb should be capped. The beekeeper tests the comb by shaking it. If honey spurts out, the comb is reinserted into the honey chamber for several more days. Approximately one-third of the honey is left in the hive to feed the colony.

Uncapping the honeycombs

  • 2 Honeycombs that are at least two-thirds capped are placed into a transport box and taken to a room that is completely free of bees. Using a long-handled uncapping fork, the beekeeper scrapes the caps from both sides of the honeycomb onto a capping tray.

Extracting the honey from the
combs

  • 3 The honeycombs are inserted into an extractor, a large drum that employs centrifugal force to draw out the honey. Because the full combs can weigh as much as 5 lb (2.27 kg), the extractor is started at a slow speed to prevent the combs from breaking.

As the extractor spins, the honey is pulled out and up against the walls. It drips down to the cone-shaped bottom and out of the extractor through a spigot. Positioned under the spigot is a honey bucket topped by two sieves, one coarse and one fine, to hold back wax particles and other debris. The honey is poured into drums and taken to the commercial distributor.

Processing and bottling

  • 4 At the commercial distributor, the honey is poured into tanks and heated to 120°F (48.9°C) to melt out the crystals. Then it is held at that temperature for 24 hours. Any extraneous bee parts or pollen rise to the top and are skimmed off.
  • 5 The majority of the honey is then flash-heated to 165°F (73.8°C), filtered through paper, then flash cooled back down to 120°F (48.9°C). This procedure is done very quickly, in approximately seven seconds.

A small percentage, perhaps 5%, is left unfiltered. It is merely strained. The honey is darker and cloudier, but there is some market for this unprocessed honey.

  • 6 The honey is then pumped into jars or cans for shipment to retail and industrial customers.
  • Quality Control

    The maximum USDA moisture content requirement for honey is 18.6%. Some distributors will set their own requirements at a percent or more lower. To accomplish this, they often blend the honey received from various beekeepers to produce honey that is consistent in moisture content, color, and flavor.

    Beekeepers must provide proper maintenance for their hives throughout the year in order to assure the quality and quantity of honey. (pest prevention, health of the hive, etc.) They must also prevent overcrowding, which would lead to swarming and the development of new colonies. As a result, bees would spend more time hatching and caring for new workers than making honey.

    Byproducts/Waste

    Four major byproducts of the honey-making process: beeswax, pollen, royal jelly, and propolis. Beeswax is produced in the bee’s body as the nectar is transforming into honey. The bee expels the wax through glands in its abdomen. The colony uses the wax to cap the filled honeycomb cells. It is scrapped off the honeycomb by the beekeeper and can be sold to commercial manufacturers for use in the production of drugs, cosmetics, furniture polish, art materials, and candles.

    Pollen sticks on the worker bee’s legs as she collects flower nectar. Because pollen contains large amounts of vitamin B 12 and vitamin E, and has a higher percentage of protein than beef, it is considered highly nutritious and is used to the dietary supplement. To collect it, the beekeeper will force the bees through a pollen trap—an opening

    Royal jelly is a creamy liquid produced and secreted by the nurse bees to feed the queen. Nutrient rich with proteins, amino acids, fatty acids, sugars, vitamins, and minerals, it is valued as a skin product and as a dietary supplement. Proponents believe it prolongs youthfulness by improving the skin, increases energy, andhelps to reduce anxiety, sleeplessness, and memory loss.

    Propolis is plant resincollected by the bees from the buds of plants and then mixed with enzymes, wax and pollen. Bees use it as a disinfectant, to cover cracks in the hive, and to decrease the hive opening during the winter months. Commercially it is used as a disinfectant, to treat corns, receding gums, and upper respiratory disease, and to varnish violins.

    The Future

    In the latter part of the twentieth century, the honeybee industry has been hard hit by two factors: parasitic mites and Africanized bees. Mites, primary the tracheal and varroa types, have destroyed thousands of bee colonies. The destruction of bee colonies not only affects honey sales, but the fruit and vegetable farmers who depend on bees to pollinate their crops. It is estimated that the value of bee pollination reaches $10 billion annually. At the close of the century, researchers were exploring ways to prevent the mite infestation without chemical intervention.

    Africanized bees were first detected in North America in the early 1990s. Their presence has been detected in Texas, southern California, New Mexico, and Arizona, but further migration has not been detected. As a subspecies of honeybee, Africanized bees can only be distinguished from the European honeybee by its more aggressive stinging behavior. Hence, they have earned the appellation «killer bees.» Africanized honeybees can mated with the European honeybee, creating a hybrid with the more aggressive stinging behavior. By the early 1990s, almost 100% of honeybees in Mexico carried the aggressive gene. In tropical climates, the aggressiveness gene is a dominant trait. Scientists have isolated five genes linked to the aggressiveness, one of which triggers stinging behavior. The goal is to use such findings to limit the spread of the Africanized trait throughout the Western Hemisphere and the U.S. honeybee population.

    Although it has long been known that the antioxidants in honey prevent the growth of bacteria, the use of honey to retard food spoilage has not garnered widespread support. In the late 1990s, proponents began to gather statistical evidence to support their case.

    Where to Learn More

    Books

    Bonney, Richard E. Hive Management. Pownal, VT: Garden Way Publishing, 1990.

    Diemer, Irmgard. Bees and Beekeeping. London: Merehurst Press, 1988.

    Melzer, Werner. Beekeeping: A Complete Owner’s Guide. Hauppage, NY: Barron’s Educational Services, Inc. 1986.

    Other

    International Bee Research Association. 10 North Road, Cardiff CFI 3DY, UK. (+44)1222 372409. [email protected]

    Sioux Honey Association. Sioux City, IA. (712)259-0638.

    www.madehow.com

    Processing bees from ticks: the use of chemical, folk methods

    Ticks belong to a group called arachnids and related to spiders and mites. There are hundreds of species of ticks found worldwide and more than 25 species occur in Arizona. Of that number, most people are likely to encounter only a few species. The most common in Arizona is the Brown Dog Tick, Rhipicephalus sangiuneus.

    Ticks have four stages in their life cycle: egg, larva, nymph, and adult. Once hatched, a tick needs to have a blood meal before it can develop into the next stage. The larvae, or “seed ticks” are less than 1/16 inch long and have six legs. After a meal of blood it will molt and enter the nymph stage. Nymphs are still small, less than1/8 inch long, and have eight legs. In the final adult stage a blood meal allows the female to lay eggs. She will deposit as many 5,000 eggs and then die. Ticks at any stage of development can live many months without feeding; an adult brown dog tick can survive for as long as two years without a blood meal.

    See also:  Mite Infestation (Mange, Acariasis, Scabies) in Dogs - Dog Owners - Merck Veterinary Manual

    Because ticks feed on blood, they can transmit disease from animal host to animal host, which makes them a health concern. Tick-borne diseases are rare in Arizona, but they can be serious. Different types of ticks transmit different diseases. Rocky Mountain Spotted Fever (RMSF) is the most common tick-borne disease in Arizona, although there are usually less than a dozen cases per year. In Arizona, the brown dog tick can be a “vector,” transmitting the bacteria that cause RMSF from host to host. The brown dog tick is found worldwide. It has adapted to living both indoors and out, so it can survive cold climates by staying inside a house. Its principal hosts are dogs, but if there is a large population, they may also feed on humans.

    Control of ticks on pets and in the local environment is the best prevention for RMSF. The Rocky Mountain wood tick, Dermacentor andersoni, can also transmit RMSF. This tick is only known in the very northern part of Arizona in brushy areas. The first symptoms of Rocky Mountain spotted fever are fever, chills, muscle ache, and headache. A spotted rash often develops two to five days later. Early treatment for RMSF is effective. If a tick bite is suspected it should be mentioned to the doctor so the disease can be diagnosed quickly and treated with the appropriate antibiotic.

    One other disease of concern is known to be vectored by ticks in Arizona. Tick-Borne Relapsing Fever is very rare, but is transmitted by a “soft tick,” genus Ornithodorus. These ticks are occasionally encountered in rustic cabins and woodpiles. The ticks are night feeders and only remain attached for a short time, 15 to 30 minutes.

    Lyme disease is a serious problem in many parts of the U.S. However, as of 2007, no one has contracted Lyme disease as the result of a tick bite that occurred in Arizona. The vector for disease in the west is the Western black-legged tick, Ixodes pacificus. This family of ticks needs high humidity to survive and usually cannot live in the arid Arizona climate. In Arizona the western black-legged tick has a very limited distribution. It is only known in the higher elevations of the Hualapai Mountains and only in late winter and early spring.

    If a tick is found on the skin it should be removed immediately. A tick normally needs to be attached for at least several hours before it will transmit disease to its host; so prompt removal dramatically reduces the likelihood of infection. Removal should be done with fine tweezers. Grasp the tick as close to the skin as possible and gently pull it straight up. Do not twist the tick or the mouthparts may break off and be left in the skin. Also be careful not to squeeze the tick’s body, which can cause it to release fluids into the tissue. After removal, clean the bite area with soap and water, disinfect the tweezers and wash your hands. Preserve any tick taken from a human in a small leak-proof container in rubbing alcohol and label with the date, contact information, and area of origin.

    There are a number of chemical ways to provide protection for pets, including collars, dips, sprays, shampoo, and “spot-on” methods. Some tick treatments that are suitable for dogs can be toxic to cats. Your veterinarian can provide information on appropriate applications considering the age and health of your pet. The information above was excerpted from the Yavapai County Cooperative Extension publication titled “Ticks in Arizona” by Master Gardener Debbie Allen. The entire publication is linked to the on-line version of this column.

    Follow the Backyard Gardener on Twitter – use the link on the BYG website. If you have other gardening questions, call the Master Gardener line in the Camp Verde office at 928-554-8999 Ext. 3 or e-mail us at [email protected] and be sure to include your name, address and phone number. Find past Backyard Gardener columns or provide feedback at the Backyard Gardener web site: http://cals.arizona.edu/yavapai/anr/hort/byg/.

    Link to Yavapai County Bulletin #77: Ticks in Arizona, by Debbie Allen, Yavapai County Master Gardener Click Here

    cals.arizona.edu

    Spreads from spider mite on indoor plants: drugs and folk methods

    • Preparations from spider mite
    • Folk remedies from spider mite

    Spider mite — a frequent resident of plants in the house and on the farmyard. We know several subspecies of this arachnoid, but you can often encounter a common spider mite. This is an

    pest up to 2 mm in size, milky or yellowish. Female branches during reproduction are red or pink. In the presence of a parasite on the surface of the leaves or near the stem there are small points of white or spider web.

    First, the traces of the spider mite can be detected on the inside of the leaves, as the colony’s points develop, the points appear on the entire surface of the plant.

    Preparations from spider mite

    Before deciding what to do with indoor flowers, estimate the extent of damage to the plant and its neighbors with dandruff. Next, the plant is treated with one of the chemicals called acaricides. These remedies against the spider mite are specific, kill only ticks, and nonspecific, valid and other parasites.

    Preparations for the control of spider mites are biological and synthetic. Active substance of biological means is avermectins — products of vital activity of a soil fungus. These natural toxins affect the nervous system of the spider mite, after which the pest loses its ability to eat and dies quickly. Preparations of biological origin are good in that the ticks do not get used to them. In addition to the antiparasitic effect, the composition of these agents include amino acids and vitamins, stimulating the growth of the plant and strengthen it. Biological products include: Aktofit, Akarin, Vertimek, Agravertin, Fitomer and Kleshchevit.

    Synthetic remedies from spider mite on indoor plants are diverse. It is difficult to choose the best remedy, as ticks quickly get used to drugs of this type. To improve the effectiveness of repeated appearance of mites, chemicals are replaced.

    Some synthetic drugs:

    • Neron — the product includes bromopropylate, which has a neurotoxic effect. Effective only when in direct contact with spider-shaped.
    • Nissoran — the active substance of the drug is a homonoid substance hextitiazox. The remedy destroys mites, their eggs and young larvae. Adult mites do not kill the drug, but sterilizes
    • Omajet — a powerful drug, which includes propargitis. It has a wide range of effects, destroying mites and other pests.

    To effectively get rid of spider mites using chemical agents, you need to follow a few simple rules:

    • Before the treatment, the flower is washed with soap and well watered.
    • The plant is treated completely regardless of the location of the spots from the mite.
    • You can use the same tool no more than 3 times in a row. Then the drug is changed to a vehicle with another mechanism of action. For example, Akarin on Nissoran.
    • For complete destruction of pests, treatment is carried out 3 times at intervals of 7 days.
    • Biological agents with neurotoxic action are used in non-living well-ventilated premises. During the treatment, use gloves and a bandage on the face.

    Folk remedies from spider mite

    Traditionally, the first methods of controlling parasites on plants are folk. They are environmentally friendly, but they are not always effective in isolation and require patience and attention. How to successfully get rid of spider mite by popular means? These techniques are effective in the simultaneous use of chemicals.

    • Green soap. This biologically pure product is used against a wide range of pests on plants.40-50 g of soap are dissolved in 1 liter of hot water, after cooling to 50 degrees in a mixture add 2 liters of kerosene. Probably simultaneous application with chemicals.
    • Diptyne soap. To get rid of mites on indoor plants, 100 g of powdered soap is dissolved in 10 liters of water. Spray the plant 2-3 times a day for a week.
    • Alcohol solution.30 ml of ammonia dissolve in 10 liters of water. Several times a day the plant and pot are processed.
    • Broths of herbs. To combat the spider mite, folk remedies use the root of cyclamen, wormwood, horseradish, cook an infusion of wood or potato wedges. An effective and easy recipe is to cook infusion from the roots of a dandelion: 40 g of crushed root insist in a liter of boiling water. Infusion is prepared for several hours, then the plant is treated several times a day for 10-14 days.

    A spider mite — an insidious pest that can be tricky to fight. The key to success is the early detection of parasites and the careful implementation of instructions when applying chemicals and folk remedies.

    dumpor.com

    Brazilian Red Propolis—Chemical Composition and Botanical Origin

    1 Department of Food Science, College of Food Engineering, State University of Campinas, PO Box 6177, Campinas, SP, Brazil

    Abstract

    Propolis contains resinous substances collected by honey bees from various plant sources and has been used as a traditional folk medicine since ca 300 BC. Nowadays, the use of evidence-based complementary and alternative medicine (CAM) is increasing rapidly and so is the use of propolis in order to treat or support the treatment of various diseases. Much attention has been focused on propolis from Populus sp. (Salicaceae) and Baccharis dracunculifolia (Asteracea), but scientific information about the numerous other types of propolis is still sparse. We gathered six samples of red propolis in five states of Northeastern Brazil. The beehives were located near woody perennial shrubs along the sea and river shores. The bees were observed to collect red resinous exudates on Dalbergia ecastophyllum (L) Taub. (Leguminosae) to make propolis. The flavonoids of propolis and red resinous exudates were investigated using reversed-phase high-performance liquid chromatography and reversed-phase high-performance thin-layer chromatography. We conclude that the botanical origin of the reddish propolis is D. ecastophyllum. In areas where this source (D. ecastophyllum) was scarce or missing, bees were collecting resinous material from other plants. Propolis, which contained the chemical constituents from the main botanical origin, showed higher antimicrobial activity.

    Copyright

    Copyright © 2008 Andreas Daugsch et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

    www.hindawi.com

    Imidacloprid

    Technical Fact Sheet

    As of 2011, NPIC stopped creating technical pesticide fact sheets. The old collection of technical fact sheets will remain available in this archive, but they may contain out-of-date material. NPIC no longer has the capacity to consistently update them. To visit our general fact sheets, click here. For up-to-date technical fact sheets, please visit the Environmental Protection Agency’s webpage.

    Molecular Structure —
    Imidacloprid

    Laboratory Testing: Before pesticides are registered by the U.S. EPA, they must undergo laboratory testing for short-term (acute) and long-term (chronic) health effects. Laboratory animals are purposely given high enough doses to cause toxic effects. These tests help scientists judge how these chemicals might affect humans, domestic animals, and wildlife in cases of overexposure.

    Chemical Class and Type:

    • Imidacloprid is a neonicotinoid insecticide in the chloronicotinyl nitroguanidine chemical family. 1,2 The International Union of Pure and Applied Chemistry (IUPAC) name is 1-(6-chloro-3- pyridylmethyl)-N-nitroimidazolidin-2-ylideneamine and the Chemical Abstracts Service (CAS) registry number is 138261-41-3. 2
    • Neonicotinoid insecticides are synthetic derivatives of nicotine, an alkaloid compound found in the leaves of many plants in addition to tobacco. 3,4,5
    • Imidacloprid was first registered for use in the U.S. by the United States Environmental Protection Agency (U.S. EPA) in 1994. 6 See the text box on Laboratory Testing.

    Physical / Chemical Properties:

    • Imidacloprid is made up of colorless crystals with a slight but characteristic odor. 2
    • Vapor pressure 7 : 3 x 10 -12 mmHg at 20 °C
    • Octanol-Water Partition Coefficient (Kow) 2 : 0.57 at 21 °C
    • Henry’s constant 2 : 1.7 x 10 -10 Pa·m 3 /mol
    • Molecular weight 2 : 255.7 g/mol
    • Solubility (water) 2 : 0.61 g/L (610 mg/L) at 20 °C
    • Soil Sorption Coefficient (Koc) 8,9 : 156-960, mean values 249-336
    • Imidacloprid is used to control sucking insects, some chewing insects including termites, soil insects, and fleas on pets. In addition to its topical use on pets, imidacloprid may be applied to structures, crops, soil, and as a seed treatment. 2,10 Uses for individual products containing imidacloprid vary widely. Always read and follow the label when applying pesticide products.
    • Signal words for products containing imidacloprid may range from Caution to Danger. The signal word reflects the combined toxicity of the active ingredient and other ingredients in the product. See the pesticide label on the product and refer to the NPIC fact sheets on Signal Words and Inert or «Other» Ingredients.
    • To find a list of products containing imidacloprid which are registered in your state, visit the website http://npic.orst.edu/reg/state_agencies.html select your state then click on the link for «State Products.»

    Mode of Action:

    Target Organisms

    • Imidacloprid is designed to be effective by contact or ingestion. 2 It is a systemic insecticide that translocates rapidly through plant tissues following application. 2,10
    • Imidacloprid acts on several types of post-synaptic nicotinic acetylcholine receptors in the nervous system. 11,12 In insects, these receptors are located only within the central nervous system. Following binding to the nicotinic receptor, nerve impulses are spontaneously discharged at first, followed by failure of the neuron to propagate any signal. 13,14 Sustained activation of the receptor results from the inability of acetylcholinesterases to break down the pesticide. 12 This binding process is irreversible. 5
    See also:  Nematode Diseases of Plants, Ohioline

    Non-target Organisms

    • Imidacloprid’s mode of action is similar on target and non-target beneficial insects including honeybees, predatory ground beetles and parasitoid wasps. 10 However, imidacloprid is ineffective against spider mites and nematodes. 2
    • Mammalian nicotinic receptors are made up of a number of subtypes. 14 In contrast to insects, these receptors are present at neuromuscular junctions as well as in the central nervous system. 14 However, the binding affinity of imidacloprid at the nicotinic receptors in mammals is much less than that of insect nicotinic receptors. 15 This appears to be true of other vertebrate groups including birds. 16,17
    • The blood-brain barrier in vertebrates blocks access of imidacloprid to the central nervous system, reducing its toxicity. 14

    Acute Toxicity:

    • Imidacloprid is moderately toxic if ingested. 18 Oral LD50 values in rats were estimated to be 450 mg/kg for both sexes in one study and 500 and 380 mg/kg in males and females, respectively in another study. 2,19 In mice, LD50 values were estimated at 130 mg/kg for males and 170 mg/kg for females. 19,20 See the text boxes on Toxicity Classification and LD50/LC50.

    LD50/LC50: A common measure of acute toxicity is the lethal dose (LD50) or lethal concentration (LC50) that causes death (resulting from a single or limited exposure) in 50 percent of the treated animals. LD50 is generally expressed as the dose in milligrams (mg) of chemical per kilogram (kg) of body weight. LC50 is often expressed as mg of chemical per volume (e.g., liter (L)) of medium (i.e., air or water) the organism is exposed to. Chemicals are considered highly toxic when the LD50/LC50 is small and practically non-toxic when the value is large. However, the LD50/LC50 does not reflect any effects from long-term exposure (i.e., cancer, birth defects or reproductive toxicity) that may occur at levels below those that cause death.

    Dermal

    • Imidacloprid is very low in toxicity via dermal exposure. 18 The dermal LD50 in rats was estimated at greater than 5000 mg/kg. 2,19
    • Researchers did not observe eye or skin irritation in rabbits. 19,20 Imidacloprid is not considered a skin sensitizer 20 although reports of hypersensitivity in skin following exposure to imidacloprid have been reported in companion animals. 1

    Inhalation

    • Imidacloprid is variable in toxicity if inhaled. The inhalation LC50 was estimated to be greater than 5323 mg/m 3 for dust and 69 mg/m 3 for aerosol exposure in rats. 2,20 Imidacloprid dust is considered slightly toxic but the aerosol form is highly toxic. 18
    TOXICITY CLASSIFICATION — IMIDACLOPRID
    High Toxicity Moderate Toxicity Low Toxicity Very Low Toxicity
    Acute Oral LD50 Up to and including 50 mg/kg
    (≤ 50 mg/kg)
    Greater than 50 through 500 mg/kg
    (>50-500 mg/kg)
    Greater than 500 through 5000 mg/kg
    (>500-5000 mg/kg)
    Greater than 5000 mg/kg
    (>5000 mg/kg)
    Inhalation LC50 Up to and including 0.05 mg/L
    (≤0.05 mg/L)
    Greater than 0.05 through 0.5 mg/L
    (>0.05-0.5 mg/L)
    Greater than 0.5 through 2.0 mg/L
    (>0.5-2.0 mg/L)
    Greater than 2.0 mg/L
    (>2.0 mg/L)
    Dermal LD50 Up to and including 200 mg/kg
    (≤200 mg/kg)
    Greater than 200 through 2000 mg/kg
    (>200-2000 mg/kg)
    Greater than 2000 through 5000 mg/kg
    (>2000-5000 mg/kg)
    Greater than 5000 mg/kg
    (>5000 mg/kg)
    Primary Eye Irritation Corrosive (irreversible destruction of ocular tissue) or corneal involvement or irritation persisting for more than 21 days Corneal involvement or other eye irritation clearing in 8 — 21 days Corneal involvement or other eye irritation clearing in 7 days or less Minimal effects clearing in less than 24 hours
    Primary Skin Irritation Corrosive (tissue destruction into the dermis and/or scarring) Severe irritation at 72 hours (severe erythema or edema) Moderate irritation at 72 hours (moderate erythema) Mild or slight irritation at 72 hours (no irritation or erythema)
    The highlighted boxes reflect the values in the «Acute Toxicity» section of this fact sheet. Modeled after the U.S. Environmental Protection Agency, Office of Pesticide Programs, Label Review Manual, Chapter 7: Precautionary Labeling. http://www.epa.gov/oppfead1/labeling/lrm/chap-07.pdf

    Signs of Toxicity — Animals

    • Salivation and vomiting have been reported following oral exposure. 1,6 Very high oral exposures may lead to lethargy, vomiting, diarrhea, salivation, muscle weakness and ataxia, which are all indicative of imidacloprid’s action on nicotinic receptors. 1 Other signs of exposure at high doses are uncoordinated gait, tremors, and reduced activity. 20
    • Hypersensitivity reactions in skin have been reported following dermal applications of products containing imidacloprid. 1
    • Onset of signs of toxicity is rapid following acute exposure. In rats, clinical signs of intoxication occurred within 15 minutes of oral exposure. 14,21 Signs of toxicity disappear rapidly, with most resolving within 24 hours of the exposure. Lacrimation and urine staining may persist for up to four days after exposure to some neonicotinoids. Death occurred within 24 hours following administration of lethal doses. 21
    • Neither persistent neurotoxic effects nor effects with a delayed onset have been reported for imidacloprid. 21

    Signs of Toxicity — Humans

    • Three case reports of attempted suicides described signs of toxicity including drowsiness, dizziness, vomiting, disorientation, and fever. 22,23,24 In two of these cases, the authors concluded that the other ingredients in the formulated product ingested by the victims were more likely to account for many of the observed signs. 22,23
    • A 69-year-old woman ingested a formulated product containing 9.6% imidacloprid in N-methyl pyrrolide solution. The woman suffered severe cardiac toxicity and death 12 hours after the exposure. 25 Signs of toxicity soon after the ingestion included disorientation, sweating, vomiting, and increased heart and respiratory rates. 25
    • A 24-year-old man who accidentally inhaled a pesticide containing 17.8% imidacloprid while working on his farm was disoriented, agitated, incoherent, sweating and breathless following the exposure. 26
    • Pet owners have reported contact dermatitis following the use of veterinary products containing imidacloprid on their pets. 19
    • Always follow label instructions and take steps to minimize exposure. If any exposure occurs, be sure to follow the First Aid instructions on the product label carefully. For additional treatment advice, contact the Poison Control Center at 1-800- 222-1222. If you wish to discuss an incident with the National Pesticide Information Center, please call 1-800-858-7378.

    Chronic Toxicity:

    Animals

    • Rats consumed imidacloprid in their diet for three months at doses of 14, 61, and 300 mg/kg/day for males and 20, 83, and 420 mg/ kg/day for females. Researchers noted reductions in body weight gain, liver damage, and reduced blood clotting function and platelet counts at 61 mg/kg/day in males and 420 mg/kg/day in females. Liver damage disappeared after exposure ended, but abnormalities in the blood were not entirely reversible. Researchers estimated the NOAEL at 14 mg/kg/day. 27 See the text box on NOAEL, NOEL,LOAEL, and LOEL.

    NOAEL: No Observable Adverse Effect Level

    NOEL: No Observed Effect Level

    LOAEL: Lowest Observable Adverse Effect Level

    LOEL: Lowest Observed Effect Level

    Humans

    • No studies were found involving human subjects chronically exposed to imidacloprid. See the text box on Exposure.

    Exposure: Effects of imidacloprid on human health and the environment depend on how much imidacloprid is present and the length and frequency of exposure. Effects also depend on the health of a person and/or certain environmental factors.

    Endocrine Disruption:

    • No data were found evaluating the potential of imidacloprid to disrupt endocrine function.
    • Imidacloprid is included in the draft list of initial chemicals for screening under the U.S. EPA Endocrine Disruptor Screening Program (EDSP). 32 The list of chemicals was generated based on exposure potential, not based on whether the pesticide is a known or likely potential endocrine disruptor.

    Carcinogenicity:

    Animals

    • Researchers concluded that Scottish terriers treated with topical flea and tick products, including those containing imidacloprid, did not have a greater risk of developing urinary bladder cancer compared with control dogs. 33 Rats were fed imidacloprid for 18 or 24 months at unspecified concentrations. Although signs of toxicity were noted, researchers concluded that imidacloprid showed no evidence of carcinogenic potential. 20
    • A range of studies using both in vitro and in vivo techniques concluded that imidacloprid did not damage DNA. 19

    Humans

    • The U.S. EPA has classified imidacloprid into Group E, no evidence of carcinogenicity, based on studies with rats and mice. 20,31 See the text box on Cancer.

    Cancer: Government agencies in the United States and abroad have developed programs to evaluate the potential for a chemical to cause cancer. Testing guidelines and classification systems vary. To learn more about the meaning of various cancer classification descriptors listed in this fact sheet, please visit the appropriate reference, or call NPIC.

    Reproductive or Teratogenic Effects:

    Animals

    • Rats were fed imidacloprid at doses of 10, 30, or 100 mg/kg/day on days 6 to 15 of their pregnancies. 20 On day 21 of the pregnancy, rats at the highest doses showed reduced embryo development and signs of maternal toxicity. In addition, wavy ribs were observed in the fetuses. 20,34
    • Researchers fed rabbits doses of imidacloprid at 8, 24, or 72 mg/kg/day during days 6-18 of pregnancy. On day 28 of pregnancy, researches noted maternal toxicity including death in the highest dose group, and the animals that survived in this group carried embryos with reduced rates of growth and bone ossification. In some of these rabbits, the young were aborted or resorbed. 20,35
    • In a two-generation study of reproductive toxicity, researchers dosed rats with 100, 250, or 700 ppm of imidacloprid in their diet for 87 days until rats mated. This was equivalent to 6.6, 17.0, and 47.0 mg/kg/day. Mother rats exhibited increased Odemethylase activity at doses of 17 mg/kg/day and greater. Reduced body weight gains were noted in pups at doses of 47 mg/kg/day. No effects on reproductive behavior or success were observed. 20,36

    Humans

    • No human data were found on the reproductive effects of imidacloprid.

    Fate in the Body:

    Absorption

    • The gastrointestinal tract of rats absorbed 92% of an unspecified dose. Plasma concentrations peaked 2.5 hours after administration. 19
    • Little systemic absorption through the skin occurs following dermal exposure in pets. 1
    • Researchers tested imidacloprid absorption using human intestinal cells. Cells rapidly absorbed imidacloprid at a very high rate of efficiency. Researchers concluded that an active transport system was involved. 37

    Distribution

    • Researchers administered a single oral dose of radio-labeled imidacloprid at 20 mg/kg to male rats. One hour after dosing, imidacloprid was detected throughout the bodies with the exception of fatty tissues and the central nervous system. 38
    • No studies were found examining the distribution of imidacloprid in humans.

    Metabolism

    • Mammals metabolize imidacloprid in two major pathways discussed below. Metabolism occurs primarily in the liver. 20
    • In the first pathway, imidacloprid may be broken by oxidative cleavage to 6-chloronicotinic acid and imidazolidine. Imidazolidine is excreted in the urine, and 6-chloronicotinic acid undergoes further metabolism via glutathione conjugation to form mercaptonicotinic acid and a hippuric acid. 20,39
    • Imidacloprid may also be metabolized by hydroxylation of the imidazolidine ring in the second major pathway. 20,39 Metabolic products from the second pathway include 5-hydroxy and olefin derivatives. 40

    Excretion

    • The metabolic products 5-hydroxy and olefin derivatives resulting from hydroxylation of the imidazolidine ring are excreted in both the feces and urine. 39,41
    • Metabolites found in urine include 6-chloronicotinic acid and its glycine conjugate, and accounted for roughly 20% of the original radio-labeled dose. 42
    • Metabolites in the feces accounted for roughly 80% of the administered dose in rats and included monohydroxylated derivatives in addition to unmetabolized imidacloprid, which made up roughly 15% of the total. Olefin, guanidine, and the glycine conjugate of methylthionicotinic acid were identified as minor metabolites. 2,42
    • Rats excreted 96% of radio-labeled imidacloprid within 48 hours following an unspecified oral dosing, with 90% excreted in the first 24 hours. 40 Radio-labeled imidacloprid was present in low amounts in organs and tissues 24 hours after male rats were orally dosed with 20 mg/kg. 38
    • No information was found on the specific metabolism of imidacloprid in humans.

    Medical Tests and Monitoring:

    • Researchers have tested for imidacloprid exposure in farm workers by evaluating urine samples with high performance liquid chromatography. 43 The method has not been well studied in humans and the clinical significance of detected residues is unknown.

    The «half-life» is the time required for half of the compound to break down in the environment.

    1 half-life = 50% remaining
    2 half-lives = 25% remaining
    3 half-lives = 12% remaining
    4 half-lives = 6% remaining
    5 half-lives = 3% remaining

    Half-lives can vary widely based on environmental factors. The amount of chemical remaining after a half-life will always depend on the amount of the chemical originally applied. It should be noted that some chemicals may degrade into compounds of toxicological significance.

    Environmental Fate:

    • Soil half-life for imidacloprid ranged from 40 days in unamended soil to up to 124 days for soil recently amended with organic fertilizers. 44 See the text box on Half-life.
    • Researchers incubated three sandy loams and a silt loam in darkness following application of [ 14 C-methylene]-imidacloprid for a year. The degradation time required for imidacloprid to break down to half its initial concentration (DT50) in non-agricultural soil was estimated to be 188-997 days. In cropped soils, the DT50 was estimated to be 69 days. 42 Metabolites found in the soil samples included 6-chloronicotinic acid, two cyclic ureas, olefinic cyclic nitroguanidine, a cyclic guanidine, and its nitroso and nitro derivatives. After 100 days, metabolites each accounted for less than 2% of the radiocarbon label. 42
    • Sorption of imidacloprid to soil generally increases with soil organic matter content. 45,46 However, researchers have demonstrated that sorption tendency also depends on imidacloprid concentration in the soil. Sorption is decreased at high soil concentrations of imidacloprid. As imidacloprid moves away from the area of high concentration, sorption again increases, limiting further movement. 46
    • Imidacloprid’s binding to soil also decreases in the presence of dissolved organic carbon in calcareous soil. The mechanism may be through either competition between the dissolved organic carbon and the imidacloprid for sorption sites in the soil or from interactions between imidacloprid and the organic carbon in solution. Such interactions suggest that the potential for imidacloprid to leach into ground water would increase in the presence of dissolved organic carbon. 47
    • Researchers found no imidacloprid residue in soil 10-20 cm under or around sugar beets grown from treated seeds, and concluded that no leaching had occurred. 48
    • Metabolites found in agricultural soils used for growing sugar beets from imidacloprid-treated seed included 6-hydroxynicotinic acid, (1-[(6-chloro-3-pyridinyl)methul]-2-imidazolidone), 6-chloronicotinic acid, with lesser amounts of a fourth compound, 2-imidazolidone. 48
    • In another laboratory study of soil and imidacloprid, researchers determined that half lives varied by both product formulation and soil type. Metabolites were first detected 15 days after imidacloprid was applied. 49
    • Imidacloprid residues became increasingly bound to soil with time, and by the end of the one year test period, up to 40% of the radio-label could not be extracted from the soil samples. 42
    • In a water-sediment system, imidacloprid was degraded by microbes to a guanidine compound. The time to disappearance of one-half of the residues (DT50) was 30-162 days. 42
    • Photodegradation at the surface of a sandy loam soil was rapid at first in a laboratory test, with a measured DT50 of 4.7 days, but the rate slowed after that time. Metabolites included 5-hydroxy-imidacloprid, which was the major product, and lesser amounts of an olefin, nitroso derivative, a cyclic urea, and 6-chloronicotinic acid in addition to two unidentified products. 42
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    Water

    • Imidacloprid is broken down in water by photolysis. 45 Imidacloprid is stable to hydrolysis in acidic or neutral conditions, but hydrolysis increases with increasing alkaline pH and temperature. 50
    • Researchers determined that hydrolysis of imidacloprid produced the metabolite 1-[(6-chloro-3-pridinyl)methyl]-2-imidazolidone. 50 This may be further broken down via oxidative cleavage of the N-C bond between the pyridine and imidazolidine rings, and the resulting compounds may be broken down into C02, N03 — , and Cl — . 45
    • When imidacloprid was added to water at pH 7 and irradiated with a xenon lamp, half of the imidacloprid was photolyzed within 57 minutes. 42 Nine metabolites were identified in the water, of which five were most prominent. These included a cyclic guanidine derivative, a cyclic urea, an olefinic cyclic guanidine, and two fused ring products. These metabolites accounted for 48% of the radio carbon label following two hours of radiation, and the parent compound accounted for 23% of the label. 42
    • Although hydrolysis and photodegradation proceeded along different metabolic pathways in aqueous solution, the main metabolite was imidacloprid-urea in both cases. 45
    • At pH 7, only 1.5% of the initial concentration of 20 mg/L of imidacloprid was lost due to hydrolysis in three months, whereas at pH 9, 20% had been hydrolyzed in samples that were kept in darkness for the same time period. 50
    • The presence of dissolved organic carbon in calcareous soil may decrease the sorption potential of imidacloprid to soil, and thus increase the potential for imidacloprid to leach and contaminate groundwater. 47
    • A total of 28.7% of imidacloprid applied to a 25 cm soil column in the laboratory was recovered in leachate. Formulated products showed greater rates of leaching likely due to the effects of carriers and surfactants. Under natural conditions, soil compaction and rainfall amount may also affect leaching potential. 51
    • Imidacloprid is not expected to volatilize from water. 7
    • Volatilization potential is low due to imidacloprid’s low vapor pressure. 7
    • Imidacloprid is metabolized by photodegradation from soil surfaces and water. 42

    Plants

    • Imidacloprid applied to soil is taken up by plant roots and translocated throughout the plant tissues. 2 Freshly cut sugar beet leaves contained 1 mg/kg imidacloprid residues up to 80 days following sowing of treated seed although residues were undetectable at harvest 113 days after sowing. 44 In a similar study, sugar beet leaves harvested 21 days after the sowing of treated seeds contained an average of 15.2 μg/g imidacloprid. 52
    • Researchers grew tomato plants in soil treated with 0.333 mg active ingredient per test pot, and monitored the plants and fruits for 75 days. Plants absorbed a total of 7.9% of the imidacloprid over the course of the experiment, although absorption of imidacloprid declined with time since application. 53
    • More than 85% of the imidacloprid taken up by the tomato plants was translocated to the shoots, and only small quantities were found in the roots. Shoot concentrations declined towards the top of the plant. These patterns were also seen in sugar beets grown from treated seed. 52 The tomato fruits also contained imidacloprid, although tissue concentrations were not related to the position of the fruits on the plant. 53
    • Although tomato fruits contained primarily unmetabolized imidacloprid, the plants’ leaves also included small quantities of the guanidine metabolite, a tentatively identified olefin metabolite, and an unidentified polar metabolite in addition to the parent compound. 53 However, sugar beets grown from treated seed appeared to rapidly metabolize imidacloprid in the leaves. On day 97 after sowing, the majority of the radio-label was associated with metabolites, not the parent compound. 52
    • Researchers sprayed imidacloprid on eggplant, cabbage, and mustard crops at rates of 20 and 40 g/ha when the crops were at 50% fruit formation, curd formation, and pod formation, respectively. 54 The researchers calculated foliar half-lives of 3 to 5 days based on the measured residues. 54
    • Metabolites detected in the eggplant, cabbage, and mustard plants included the urea derivative [1-(6-chloropyridin-3- ylmethil)imidazolidin-2-one] and 6-chloronicotinic acid 10 days after foliar application. Residues of 2.15-3.34 μg/g were detected in the eggplant fruit. 54
    • Three plant metabolites of imidacloprid, the imidazolidine derivative, the olefin metabolite and the nitroso-derivative, were more toxic to aphids than imidacloprid itself. 55

    Indoor

    • No information regarding indoor half-life or residues was found for imidacloprid.
    • Researchers measured residue transfer of a commercial spot-on product containing imidacloprid on dogs’ fur to people. Gloves worn to pat the dogs contained an average of 254 ppm of imidacloprid 24 hours following application of the product. Residues from the fur declined to an average of 4.96 ppm by the end of the first week. 56

    Food Residue

    • The United States Department of Agriculture (USDA) Pesticide Data Program monitored imidacloprid residues in food and published their findings in 2006. Imidacloprid was detected in a range of fresh and processed fruits and vegetables. It was detected in over 80% of all bananas tested, 76% of cauliflower, and 72% of spinach samples. In all cases, however, the levels detected were below the U.S. EPA’s tolerance levels. Imidacloprid was also found in 17.5 % of applesauce and 0.9% raisin samples, although percentage of detections were greater in the fresh unprocessed fruit (26.6% of apples sampled, and 18.1% of grapes sampled). 57
    • Imidacloprid was not one of the compounds sampled for the 2006 Food and Drug Administration (FDA) Center for Food Safety and Applied Nutrition’s Pesticide Residue Monitoring Program. 57

    Ecotoxicity Studies:

    Birds

    • The acute LD50 for birds varies by species; it was determined to be 31 mg/kg in Japanese quail but 152 mg/kg in bobwhite quail. However, dietary LC50 values for a five-day interval were 2225 mg/kg/day for bobwhite quail and in excess of 5000 mg/kg for mallard ducks. 2

    Fish and Aquatic Life

    • LC50 values for a 96-hour exposure were 237 mg/L for golden orfe (Leuciscus idus) and 21 mg/L for rainbow trout (Oncorhyncus mykiss). 2
    • Researchers determined LC50 values of 85 mg/L for Daphnia with a 48-hour exposure. A concentration of greater than 100 mg/L for 72 hours was required to reduce the growth rate of the alga Pseudokirchneriella subcapitata by 50%. 2
    • The EC50 of imidacloprid for Daphnia magna was 96.65 mg/L. However, the EC50 declined to 90.68 mg/L when predator cues were added to the water as an additional stress. Sublethal exposures reduced feeding and increased respiration rates in Daphnia. Exposed Daphnia did not respond to predator cues as quickly as did control animals, and failed to mature as quickly or produce as many young. These changes led to reduced population growth rate following exposure. 58 See the text box on EC50.

    EC50: The median effective concentration (EC50) may be reported for sublethal or ambiguously lethal effects. This measure is used in tests involving species such as aquatic invertebrates where death may be difficult to determine. This term is also used if sublethal events are being monitored.

    Newman, M.C.; Unger, M.A. Fundamentals of Ecotoxicology; CRC Press, LLC.: Boca Raton, FL, 2003; p 178.

    Terrestrial Invertebrates

    • Oral LD50 values for bees range from 3.7 to 40.9 ng per bee, and contact toxicity values ranged from 59.7 to 242.6 ng per bee. 59 Based on these values, imidacloprid is considered to be highly toxic to bees. 18 Colonies of bees (Apis mellifera) appeared to vary in their sensitivity to imidacloprid, perhaps due to differences in oxidative metabolism among colonies. The 5-hydroxyimidacloprid and olefin metabolites were more toxic to honeybees than the parent compound. 60
    • Bees were offered sugar solution spiked with imidacloprid at nominal concentrations of 1.5, 3.0, 6.0, 12.0, 24.0, 48.0, or 96.0 μg/kg for 14 days. The experiment was repeated with bees that matured in July (summer bees) and between December and February (winter bees). Summer bees died at greater rates than controls in the 96 μg/kg treatment, whereas winter bees demonstrated increased mortality at 48 μg/kg. Reflex responses of summer bees decreased at 48 μg/kg, whereas the reflex responses of winter bees were unaffected. Learning responses in summer bees were decreased following exposures of 12 μg/kg imidacloprid, and winter bees demonstrated reduced learning responses at doses of 48 μg/kg. 61
    • Surveys of pollen collected by bees from five locations in France revealed detectable residues of imidacloprid or its metabolite 6-chloronicotinic acid in 69% of the samples. Maximum detected concentrations were 5.7 μg/kg and 9.3 μg/kg for imidacloprid and the metabolite, respectively. 62
    • Researchers performed 10-day chronic exposure tests on honeybees and found that mortality increased over controls at doses as low as 0.1 μg/L of imidacloprid and six metabolites. 60
    • Researchers fed bumblebees (Bombus terrestris) nectar and pollen spiked with either 10 μg/kg or 25 μg/kg imidacloprid in syrup and 6 μg/kg or 16 μg/kg in pollen. Worker survival rates declined by 10% in both treatment groups and brood production was reduced in the low-dose group. 63
    • Researchers grew sunflowers from seeds treated with 0.7 mg imidacloprid per seed and found imidacloprid residue in nectar (1.9 ± 1 ppt) and pollen (3.3 ± 1 ppt). No metabolites were found in nectar or pollen. They also grew sunflowers from untreated seeds in soil with imidacloprid residues at concentrations up to 15.7 ppt. In that test, neither imidacloprid nor its metabolites were found in nectar or pollen. 59
    • Researchers have found that bees avoided feeding on a sugar solution spiked with imidacloprid at 24 μg/kg concentrations, and that this avoidance appeared to be due to a repellent or antifeedant effect. 64
    • The predatory insect Hippodamia undecimnotata experienced reduced survival, delayed and reduced egg production, reduced longevity, and reduced population growth rate following exposure to aphids raised on potted bean plants which had been treated 10 days earlier with imidacloprid applied at 0.0206 mg active ingredient per pot or 1/14 the label rate. 65
    • Adult green lacewings (Chrysoperla carnea) exhibited reduced survival rates after feeding on the nectar of greenhouse plants that had been treated with granules of a commercial product containing 1% imidacloprid. Treatments were done with imidacloprid-containing products mixed at label rates and at twice the label rate three weeks prior to the experiment. Insects fed on the treated plants even when untreated plants were present. 66
    • The LC50 for the earthworm Eisenia foetida was determined to be 10.7 mg/kg in dry soil. 2 In a separate study, two earthworm species (Aporrectodea nocturna and Allolobophoria icterica) were placed in soil cores treated with 0.1 or 0.5 mg/kg imidacloprid. At the highest dose, both species of worms produced shorter burrows. A. nocturna also produced fewer surface casts at the highest dose, and gas diffusion through the soil cores was reduced by approximately 40% compared to controls. 67

    Regulatory Guidelines:

    • The reference dose (RfD) is 0.057 mg/kg/day. 31 See the text box on Reference Dose (RfD).

    Reference Dose (RfD): The RfD is an estimate of the quantity of chemical that a person could be exposed to every day for the rest of their life with no appreciable risk of adverse health effects. The reference dose is typically measured in milligrams (mg) of chemical per kilogram (kg) of body weight per day.

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