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About Chemical Pesticides (Overview)

  

Numerous now-banned pesticides were once thought safe, but have since been implicated in many cases of cancer and other health issues. For this reason, pesticide regulatory listings should be evaluated with some scepticism.

 

Take a recent example (2009) where the EU Assembly voted overwhelmingly to ban and/or phase out over 20 widely used pesticides. Most of the pesticides concerned are/were produced by Bayer or BASF, and include Amitrol, Ioxynil, Tepraloxydim, Epoxiconazole, Iprodion, Metconazole, Tebuconazole and Thiacloprid. The substances that were banned are linked to cancer, damage of the reproductive and nervous systems, and/or are endocrine (hormone) disrupters.

 

Many of these chemicals are still widely available and used in countries outside of the EU. These countries include Australia, the UK, and North America.

 

As of today, industrialized countries are facing an increase of diseases attributable to an alteration of the immune system function (reduced immune system function), and concern is growing that this trend could be at least partially attributable to new and modified patterns of exposure to chemicals. Among the chemicals of concern, pesticides are included.1

 

Research conducted by Renate Stiller-Winkler et al (1999) showed:

 

[Quote]

  

Immune parameters were examined in 224 non-exposed controls and in 304 pesticide applicators in the agricultural environment. In comparison to the control group pesticide applicators showed significant increased odds ratios for neopterin and soluble tumor necrosis factor receptor (sTNF RII) and a decreased odds ratio for immunoglobulin M. Obtained results indicate an enhanced macrophage activation and an impaired humoral defense. These alterations have been found to correlate with exposure duration in the group of pesticide applicators in agriculture. For subjects who worked in indoor pest control an inverse correlation for sTNF RII with exposure duration was obtained indicating impairment of cell mediated immune function. It can be concluded that exposure to pesticides in the agricultural environment may contribute to modulation of the immune system. Since immune modulating agents can potentially lead to adverse health consequences the involvement of immune biomarkers in pesticide-related health studies seems to be of considerable value for risk assessment studies.2

 

[End Quote]

 

Over the past 40 years, a substantial rise in the incidence of non-Hodgkin lymphoma (NHL) has been observed. Epidemiologic studies aimed at understanding this rise have revealed some association with occupational exposure to pesticides. NHL is common among farmers, where pesticides have been described as the culprit. The association between pesticides and NHL has been demonstrated mainly in case-control studies, while retrospective cohorts have been less convincing. Pesticides including chlorphenol and phenoxyacetic acid herbicides, organochlorines, and organophosphate insecticides, carbamates, and fungicides have been associated with NHL.

 

Organochlorines, organophosphates, and carbamates—act on the nervous system to prevent the normal flow of nerve impulses to muscles that control both voluntary movement, such as walking, and involuntary movement, such as breathing and heart beat.

 

Pesticides in all three classes are absorbed to varying degrees through inhalation, ingestion, and skin contact. Exposure to amounts of these pesticides that exceed levels set by EPA could result in immediate and lifethreatening effects, such as respiratory failure, or conditions that do not appear immediately, such as cancer.

 

Both human and animal studies have demonstrated that pesticides during pregnancy can be transferred to the fetus by crossing the placenta. Further, toxic environmental contaminants can be transferred from mother to infant via breastfeeding.

 

Harmful pesticides may be absorbed or remain residual on the surface of the plant after cultivation and then enter the human body through various modes of ingestion.

 

Repeated exposure to unknown chemical poisons may build to toxic levels in a user’s system. This means that med users who often purchase from multiple sources and consume cannabis on a regular basis are at risk of long-term and regular exposure.

 

Given this information, it seems absurd that argued to be medicine should be produced using products which suppress the human immune system and are linked to cancer, neurological diseases, and other health implications.

 

REFS

 

  1. C.Colosio, S,Brindle, E.Corsini, C.L. Galli, M. Maroni (2004) Low level exposure to chemicals and immune system
  2. Renate Stiller-Winkler, Wolfgang Hadnagy, Gabriele Leng, Evamarie Straub, Helga Idel (1999) Immunological parameters in humans exposed to pesticides in the agricultural environment

 

Pests and Resistance to Chemical Pesticides

 

Because of the rapid reproductive rate of many pests a generation of many insects can take place in a few weeks and many generations can be produced in a single season or year.

 

Repeated use of the same class of pesticides to control a pest can cause undesirable changes in the gene pool of a pest leading to another form of artificial selection, pesticide resistance. When a pesticide is first used, a small proportion of the pest population may survive exposure to the material due to their distinct genetic makeup. These individuals pass along the genes for resistance to the next generation. Subsequent uses of the pesticide increase the proportion of less-susceptible individuals in the population. Through this process of selection, the population gradually develops resistance to the pesticide. The faster the development rate of the pest species and the faster the pesticide resistance occurs.

 

Multiple resistance —resistance to more than one pesticide and to pesticides in more than one chemical class— Is increasing rapidly. There are over 1,000 insect/insecticide resistance combinations, and at least 17 species of insects that are resistant to all major classes of insecticides.1

 

For instance, the twospotted spider mite is a pest of many crops and is notorious for rapidly developing resistance to pesticides.

 

Chemical control of spider mites generally involves pesticides that are specifically developed for spider mite control (miticides or acaricides). Few insecticides are effective for spider mites and many may aggravate problems. Additionally, strains of spider mites resistant to pesticides frequently develop (most spider mites become resistant to new pesticides within two to four years2), making chemical control difficult. Because most miticides do not affect eggs, a repeat application at an approximately 10- to 14-day interval is usually needed for control. Rapid reproductive rate and dispersal behavior are factors that contribute to the ability of twospotted spider mite populations to develop resistance to pesticides.

 

Twospotted spider mites (TSSM) have been shown to have resistance to organophosphates, organochlorines, carbamates, and recently there has been anecdotal evidence of widespread TSSM resistance to abermectin/avermechtin based insecticides such as Avid.3 This is likely due to near total reliance on this chemical to control mites in many crops instead of rotating chemical groups.

 

REFS

 

1. Robert G. Bellinger (1996) Department of Entomology, Clemson University

2. Spider mite’s secrets revealed (Press release). Instituto Gulbenkian de Ciencia. November 24, 2011.

3. J K Clark, J G Scott, F Campos, and J R Bloomquist (1995) Resistance to Avermectins: Extent, Mechanisms, and Management Implications

 

 

Pesticides Types – The So-So, The Ugly and The Very Ugly

 

 

Avermechtins/Abamectins: eg. Avid and Vertimec

 

Active Ingredient: AVID contains 18 g/litre ABAMECTIN in the form of an emulsifiable concentrate. Also contains: 265 g/litre 2-Pyrrolidinone, 1-methyl and 9.5 g/litre Phenol, 2,6-bis(1,1-dimethylethyl)-4-methyl.

 

Contrary to some claims, abamectin (Avid) is classed as non-systemic. This said it remains residual on leaf surfaces for extended periods (dependent on crop type and environmental factors etc) and is banned for use on most consumable crops.

 

This said, it is widely used by cannabis cultivators for control of spidermite.

 

In one example from Hayward California, a well-known marijuana patient with an unusual immune disease died from repeated exposure to the miticide “Avid”. Other anecdotal information exists about patients becoming ill after being exposed to Avid contaminated cannabis.

 

Avid’s active ingredient is Abamectin. Abamectin comes from the soil bacterium Streptomyces avermitilis.

 

Microbial based pesticides effect neural transmissions. Exposure to high doses can debilitate the central nervous system resulting in incoordination and trembling. The Avermectins block the transmittance of electrical activity in nerves and muscle cells. This cause’s a rush of chloride ions into the cells leading to hyperpolarization and eventual paralysis of the neuromuscular system.

 

In more simple terms abamectin has been shown to have central nervous system effects on animals.

 

It is not shown to be carcinogenic. However, toxicity of other components found in Avid, Butylated Hydroxytoluene (BHT) listed as a (Group 3) carcinogen is stated as “carcinogen not classifiable as human (‘No Data Available”) with limited animal evidence.

 

Different countries have different legislation around Avid. In some countries it is registered for use on consumable crops while in other countries or states of countries it registered for use on ornamental crops only.

 

Abamectin is registered for single applications on apples in Australia at 0.014 kg ai/ha with harvest after an interval of 14 days. In three trials corresponding to this use pattern the abamectin residues were 0.002, 0.003 and 0.005 mg/kg.

 

Abamectin is permitted for use on pome fruit in New Zealand with one application at 0.027 kg ai/ha and a PHI of 14 days. Abamectin residues on apples were 0.004 and 0.007 mg/kg in two New Zealand studies.

 

Avid is shown to have withholding periods in at least one crop (Kiwifruit) for 120 days, 14 days for apples and pears, 3 days for tomatoes, 3 days for strawberries, and 28 days for hops. In research evaluated by the FAO The mean processing factor for abamectin residues during the conversion of fresh hops to dry hops was 4.09, suggesting that approximately 80% of the abamectin survived the drying process. As Cannabis is very similar to hops (hops and Cannabis are the only two genera in the family Cannabinaceae and there are many similarities between hemp (Cannabissativa) and the cultivated hop) and while no qualitive research exists on withholding periods of abamectin in cannabis this provides some insight into the fact that abamectin will remain residual in indoor grown cannabis for at least 28 days (4 weeks). However, what must also be noted is that residual activity of abamechtin is likely to decrease more quickly in outdoor environments than indoor environments (Wright et al, 1984). Therefore, it is safe to say that withholding periods in indoor crops is well above 28 days.

 

Avid use should therefore be strongly discouraged at any point during the bloom cycle (better yet, discouraged at all times).

 

Floramite

 

Active Ingredient: Bifenazate: Hydrazine carboxylic acid, 2-(4-methoxy-[1,1-biphenyl]-3-yl) 1-methylethyl ester

 

Floramite is a non-systemic miticide that kills mites by disrupting the nervous system.

 

Although Floramite is primarily active against the adults and nymphs of spider mites, it also has activity against eggs. Floramite kills mites by contact activity within three days and persists on the plant surface for up to between 21-28 days. Again however, it must be stressed that residual activity of Floramite is likely to decrease more quickly in outdoor environments than indoor environments.

 

Floramite SC is a very effective contact miticide that is registered for the Canadian ornamental industry. Other than this, Floramite is food crop safe on peppers and tomatoes according to the Ontario Ministry of Agriculture.

 

The active ingredient in Floramite, Bifenazate, when trialed did not cause cancer in animals and was not genotoxic.

 

In the US it has registration for ornamentals, non- bearing fruit trees that will not bear fruit for a minimum of 12 months, and greenhouse tomatoes with varieties greater than 1” diameter when mature.

 

It is also widely used among some indoor growers for control of Spider Mite.



Pyethoids/Pyrethroids

 

Pyethoids/Pyrethroids are a group of synthetic pesticides very similar to the organic pesticide which is produced by flowers (pyrethrum). Pyrethoids now control a major part of the synthetic insecticide market. Toxicity will occur at high concentrations , but repeated exposure will increase health risks at a lower concentration. Pyrethoids are allergenic and have caused asthema in patients. This group includes Cypermethrin , Cyfluthrin , Permethrin , Resmethrin , and Tetramethrin.

 

Pyrethroids are some 2250 times more toxic to insects than mammals because insects have increased sodium channel sensitivity, smaller body size and lower body temperature.1

 

Synthetic pyethroids affect an insect through the organism’s nervous system. As a neurotoxin, this chemical makes the host nervous system hypersensitive to stimuli from the sensory organs, and affects this channel through binding to sodium ions, blocking their movement. This can lead to repetitive nerve impulses, the inhibition of certain enzymes, and increases in body temperature.

 

Studies have demonstrated that this process, of slowing down the nervous system, is negatively linked with temperature, and therefore permethrin more strongly affects cold-blooded organisms such as insects and frogs, than it does warm-blooded animals. In mammals, the breakdown products of permethrin, the metabolites, do not persist in tissues. Instead, the animal quickly excretes these by-products. In studies of oral administration to rats, within several days the mammals almost completely eliminated the compound from their bodies, with only three to sex percent of the original doses remaining. The only exception is that permethrin persists slightly longer in fatty tissues, and has a half-life of four to five days in the brain and in body fat.

 

Opinions differ as to whether eg. cypermethrin is a carcinogen or not. Cypermethrin is classified by the US EPA as a weak category C oncogen – a possible human carcinogen with limited evidence of carcinogenicity in animals but no evidence of carcinogenicity in humans: it produced benign lung adenomas (tumours) at the highest dose level in female mice and has potential for liver carcinogenicity in rodents. However, the view of WHO is that as there was no evidence of carcinogenicity in male mice and as the results of mutagenic studies have been mainly negative it is concluded that there is no evidence for the carcinogenic potential of cypermethrin.



Testing on rats has suggested that pyrethroids in general may have an immuno-suppressive effect. WHO concludes that, “more attention should be paid to this aspect, but at present, no opinion can be given about its relevance in the extrapolation of these data for man.”

 

Additionally, in resesearch conducted by Jolanta Łukowicz-Ratajczak et al (1991) the influence of deltamethrin on the immune system in mice was investigated. The results indicated that deltamethrin exhibits an immunosuppressive effect.2

 

Recent studies show that the health effects of cypermethrin and pyrethroids in general may be more severe than previous toxicological evaluations suggest.

 

Previous studies conducted with tobacco cigarettes have positively identified the transfer of pesticides such as pyrethroid residues into the smoke stream around 2-16%. However, in recent cannabis specific trials conducted by the WERC Shop (2012) s simulated experiment was set up to represent the pot smoking behaviour of a typical adult. Their findings showed 52.3% pyrethroid residue was found in combusted cannabis smoked through a glass pipe, 38.9% through a unfiltered water pipe, and 8.5% through a triple filtered water pipe.3

 

REFS

 

  1. Bradberry, Sally M; Cage, Sarah A; Proudfoot, Alex T; Vale, J Allister (2005) Poisoning due to Pyrethroids
  2. Jolanta Łukowicz-Ratajczak, and Jerzy Krechniak (1991) Effects of deltamethrin on the immune system in mice
  3. The Werc Shop (2012) Summary Report to Scientific Inhalations Regarding McFinn’s Triple-Filtered Waterpipe With Pesticides

 

 

 

Organophosphates (eg. Diazinon, Cygon, Mocap. Malithon) and Carbamates (eg. Bendocarb, Propoxur)

 

These refer to a group of insecticides that are neurotoxins. Exposure at any dose can effect the central nervous system and the brain. Some of these are highly toxic and are responsible for many cases of poisonings throughout the world.

 

Most members of the OP/Carbamate families of pesticides share a common mode of insecticidal activity; interference with the enzyme acetylcholinesterase. The primary human health concerns are possible neurotoxic effects in humans.  This toxicity may manifest acutely, or with long-term consumer exposure to residues on food.

 

Let’s Break this down a bit…..

 

Organophosphates (eg. Diazinon, Cygon, Mocap. Malithon)

 

OPs were first recognised in 1854, but their general toxicity was not established until the 1930s. Tetraethyl pyrophosphate (TEPP) was the first OP insecticide, which was developed in Germany during World War Two as a by-product of nerve gas development.



OPs are all derived from phosphoric acid. They are generally among the most acutely toxic of all pesticides to vertebrate animals. They are also unstable and therefore break down relatively quickly in the environment.



OPs are nerve poisons which kill the target pest. Most Ops are insecticides, although there are also a number of related herbicide and fungicide compounds.

 

OPs work by inhibiting important enzymes of the nervous system which play a vital role in the transmission of nerve impulses. Nerve impulses usually travel along neurons (nerve cells) by way of electrical signals. However, at a junction between two neurons (a synapse) and between a neuron and a muscle (neuromuscular junction) the impulse is transmitted in the form of a chemical substance (neurotransmitter). The neuro-transmitter operating in the autonomic nervous system, neuromuscular junctions and parts of the central nervous system is acetylcholine which is released by cholinergic neurons. It is broken down and inactivated in milliseconds by the enzyme cholinesterase. With exposure to OPs, the enzyme is unable to function and a build-up of acetylcholine occurs, which causes interference with nerve impulse transmission at nerve endings.

 

OPs are one of the most common causes of poisoning worldwide, and are frequently intentionally used in suicides in agricultural areas. Organophosphorus pesticides can be absorbed by all routes, including inhalation, ingestion, and dermal absorption.

 

Even at relatively low levels organophosphates may be hazardous to human health. They can be absorbed through the lungs or skin or by eating them on food.

 

OPs in Food


OPs are regularly detected at low levels in a range of food items. Usually residue levels are below the statutory maximum residue levels. OP residues found in UK carrots has proved an exception. Ministry of Agriculture, Fisheries and Food figures for 1995 showed that 1-2% of carrots contain OP residues up to 25 times higher than expected. OPs implicated included chlorfenvinphos, quinalophos and triazophos. In the higher residue samples, the acceptable daily intake was exceeded by up to three times.



According to a 2008 report from the U.S. Department of Agriculture, in a representative sample of produce tested by the agency, 28 percent of frozen blueberries, 20 percent of celery, 27 percent of green beans, 17 percent of peaches, 8 percent of broccoli and 25 percent of strawberries contained traces of organophosphate.1

 

Possible Effects to Human Health




Psychiatric effects: Research reports have suggested that exposure to agricultural use of OPs produces depression, a major risk factor in suicides. Research from Spain has shown that suicide rates are higher in areas of greater OP use.

 

Cardiac effects: A number of studies have drawn attention to cardiac effects associated with occupational exposure to OPs. In a Health and Safety Executive publication (MS 17 December 1980) there is mention of “slowing of the heart with decreased cardiac output.”

 

Teratogenicity (birth defects): There is conflicting evidence concerning the teratogenic effects of OPs in animals. Data on the effects of OP occupational exposure on pregnant women and their foetuses are not available.

 

Cancer: There is little evidence of strong mutagenic or carcinogenic effects in mammals from exposure to OPs. The exception is dichlorvos classifies in its C category as a possible human carcinogen, in which there is limited evidence of carcinogenicity in animals in the absence of human data.

 

Eye defects: Research from Japan and the US has found OP exposure during use in agriculture is related to an increase incidence of myopia (short-sightedness) and a more advanced ocular disease syndrome, Saku disease.

 

Areas of further research: There may be other chronic effects associated with OP exposure which are receiving current research interest. Firstly, there may be important but as yet un-characterised protein targets of OPs. Secondly, OP exposure may be affecting bone cells. The hypothesis is that chronic exposure to OPs carries the risk of developing severe metabolic bone disease.

 

REFS

 

1. Study: ADHD linked to pesticide exposure”CNN. 17 May 2010.

 

Carbamates

 

Carbamate insecticides, used to kill or control insects, are made from carbamic acid. There are many forms of carbamates, each different in the way they work and in their poisonous effects. Carbamates break down in the environment within weeks or months.

 

Several carbamates have systemic use in plants because they have a high water solubility which allows them to be taken up by the roots and into the leaves of plants.

 

There is no evidence of carbamates causing delayed neurotoxicity as is seen with some of the organophosphate compounds.

 

Carbamates are not regarded as mutagenic, carcinogenic or teratogenic substances.

 

Low-level exposure to residues in foods may occur wherever carbamates are used on crops.

 

Most carbamates are classified as Schedule 5 and 6 poisons depending on the relative concentrations. A few carbamates, such as methomyl and some concentrations of bendiocarb, are classified as Schedule 7 poisons.

 

Recent epidemiological studies have suggested an increased risk of non-Hodgkin lymphoma (NHL) from carbamate insecticide use among farmers. Compared with nonfarmers, farmers who had ever used carbamate pesticides had a 30% to 50% increased risk of NHL, whereas farmers without carbamate pesticide use showed no increased risk. Carbanates such as carbofuran have been shown to be immune system suppressants.

 

Organochlorine Insecticides (OCI)

 

The OCIs are a heterogenous group of insecticides that encompass DDT,DDD, toxaphene, dieldrin, and aldrin among others. The OCIs exert their toxic effect by virtue of opening sodium channels and hence generating steady action potentials. Due to their long half-lives the OCIs have a strong tendency for bioaccumulation in adipose (fat) tissues. Most of the OCI compounds are banned in the US because laboratory studies on rodents revealed carcinogenicity. Others that remain in use include lindane, endosulfan, dicofol, methoxychlor and pentachlorophenol.

 

Studies have found a correlation between organochlorine exposure and various types of cancer, neurological damage (several organochlorines are known neurotoxins), Parkinson’s disease, birth defects, respiratory illness, and abnormal immune system function.

 

Many organochlorines are known or suspected hormone disruptors, and recent studies show that extremely low levels of exposure in the womb can cause irreversible damage to the reproductive and immune systems of the developing fetus.

 

In research conducted by Lino CM et al (1999) on medicinal plants sold in Portugal, levels of 14 organochlorine pesticide residues were evaluated in 127 samples of medicinal plants collected in pharmacies (78 samples) and herb stores (49 samples) in 1996. Samples were divided between 15 national brands and 7 foreign brands. Maximum organochlorine residue levels were exceeded in 38 (48.7%) pharmacy samples and in 26 (53.1%) of the medicinal herb store samples.1

 

REF

 

  1. Lino CM, Guarda LM, Silveira MI (1999) Determination of organochlorine pesticide residues in medicinal plants sold in Coimbra, Portugal.

 

 

CHLORONICOTINYL/NEONICOTINOID INSECTICIDES (eg. Imidacloprid)

 

The chloronicotinyl pesticides were released in the 1990’s by Bayer for use against a variety of insects in salad vegetables.  They are a group of systemic insecticides that are registered for use in greenhouses. These include imidacloprid (Marathon), acetamiprid (Tristar), and thiamethoxam (Flagship). These materials are transported throughout the plant in the transpiration stream and provide a certain degree of residual activity after application. EPA lists them as schedule II (moderately toxic; moderately irritating) or shedule III (slightly toxic; slightly irritating).

 

Chloronicotinyls have a different mode of action, compared to organophosphates (Orthene and Duraguard), carbamates (Mesurol), pyrethroids (Talstar, Decathlon, and Mavrik), and macrocyclic lactone (Avid).

 

Chloronicotinyl insecticides kill target pests in a similar manner as the natural product nicotine, by acting on the central nervous system, causing irreversible blockage of the postsynaptic nicotinergic acetylcholine receptors. These insecticides disrupt nerve transmission in insects, causing uncontrolled firing of nerves. This results in rapid pulses from the steady influx of sodium, leading to hyperexcitation, convulsions, paralysis, and death. A general characteristic of chloronicotinyl insecticides is that they are highly effective in controlling phloem-feeding or sucking insects, including aphids, whiteflies, and mealybugs; however, they are not effective for spider mites ((that is, twospotted spider mite). In fact, research by David G James et al (2002) found that imidacloprid increased the production rates of twospotted spider mite.1

 

Chloronicotinyl insecticides have been shown in some studies to have limited effects on honey bees2 and are claimed to have low environmental persistence.

 

However, According to the EPA, clothianidin’s (a neonicotinoid insecticide) major risk concern is to nontarget insects (honey bees). Although EPAs Environmental Fate and Effects Division does not conduct risk assessments on non-target insects, information from standard tests and field studies, as well as incident reports involving other neonicotinoid insecticides (e.g., imidacloprid) suggest the potential for long term toxic risk to honey bees and other beneficial insects. 3

 

Christian H. Krupke et al (2012) found high levels of neonicotinoids in planter exhaust material produced during the planting of treated maize seed. They also found neonicotinoids in the soil of field tests, including unplanted fields. Plants visited by foraging bees (dandelions) growing near these fields were found to contain neonicotinoids as well. This indicates deposition of neonicotinoids on the flowers, uptake by the root system, or both. Dead bees collected near hive entrances during the spring sampling period were found to contain neonicotinoids, although whether exposure was oral (consuming pollen) or by contact (soil/planter dust) is unclear. Also detected was the insecticide neonicotinoids in pollen collected by bees and stored in the hive. When maize plants in the field reached anthesis, maize pollen from treated seed was found to contain neonicotinoids and other pesticides; and honeybees collected this maize pollen.4

 

These and other findings suggest that neonicotinoid insecticides may be far more persistent and environmentally unfriendly than once thought. 

 

REFS

 

  1. David G James, Tanya S Price: Fecundity in twospotted spider mite (Acari: Tetranychidae) is increased by direct and systemic exposure to imidacloprid. In Journal of Economic Entomology (2002) Volume: 95, Issue: 4, Pages: 729-732
  2. Hazards of Pesticides to Bees: Avignon (France), September 07-09, 1999: International Commission for Plant-Bee Relationships. Bee Protection Group. International Symposium, Colette Pélissier, Gavin B. Lewis
  3. Congressional Research Service Honey Bee Colony Collapse Disorder
  4. Christian H. KrupkeGreg J. Hunt, Brian D. Eitzer,Gladys AndinoKrispn Given (2012) Multiple Routes of Pesticide Exposure for Honey Bees Living Near Agricultural Fields

 

SPINOSAD

 

Spinosad (spinosyn A and spinosyn D) are a new chemical class of insecticides that are registered by the United States Environmental Protection Agency‎ (EPA) to control a wide variety of insects. The active ingredient is derived from a naturally occurring soil dwelling bacterium called Saccharopolyspora spinosa. The bacteria produce compounds (metabolites) while in a fermentation broth. The first fermentation-derived compound was formulated in 1988.

 

Spinosad causes excitation of the insect nervous system, leading to involuntary muscle contractions, prostration with tremors, and finally paralysis. These effects are consistent with the activation of nicotinic acetylcholine receptors by a mechanism that is clearly novel and unique among known insecticidal compounds. Spinosad also has effects on GABA receptor function that may contribute further to its insecticidal activity.

 

Spinsosad can control a variety of insect pests, including fruit flies, caterpillars, leafminers, thrips, sawflies, fire ants, and leaf beetle larvae.

 

Spinosad works by contact and by ingestion. Contact occurs either by direct application to the insect or by movement of the insect onto a treated surface. Ingestion occurs as insects feed on treated substrate (such as foliage). While control via contact is effective, control via ingestion is 5 – 10 times more effective.

 

Spinosad is relatively fast acting. The insect dies within one to two days after ingesting the active ingredient.

 

Spinosad is principally toxic to plant-eating insects in the orders Lepidoptera (caterpillars), Coleoptera (beetles), Thysanoptera (thrips), and Diptera (flies). It is not a plant systemic, but will penetrate leaves to some extent and therefore has activity against some leafminers. Spinosad is shown not effective at controlling mites at normal use rates (Thompson et al., 2000; Cowles et al., 2000; Tjosvold and Chaney, 2001), although at high rates or in combination with some adjuvants it has miticidal activity (Gilrein 2004).

 

An EPA factsheet issued February 1997 classifies spinosad as Category III (slightly toxic) due to the acute dermal LD50 in rabbit of >2000 mg/kg. For all other acute toxicological categories it is listed as Category IV (Practically non-toxic; not an irritant). The Dow MSDS issued in 2001 shows EPA classification as Category IV even for dermal toxicity. Due to its low toxicity and perceived low impact on the environment, EPA registered spinosad as a reduced-risk material (DOW, 2001; EPA, 1997; Jachetta, 2001).  EPA sets tolerances for residues of spinosad in food crops and livestock products at 40 CFR 180.495. These range from 0.02 ppm for grain corn, 1.0 ppm for hay, 0.2 ppm for apples, 10 ppm for brassica leafy greens, 0.02 ppm for eggs and poultry meat, 0.15 for beef meat, 7.0 ppm for forage grass, and 20 ppm for milk fat (EPA, 40 CFR 180.495).

 

Spinosad in Hydroponics

 

Research by Van Leeuwen (2005) found that when spinosad was applied to the roots of tomato plants in rock wool, “excellent” control of two spotted spider mites was obtained. Apparently, spinosad has systemic properties and quantities in root uptake and as low as 1 mg/plant could protect tomato plants from a mite infestation.

 

Sounds great! However, the authors go onto state:

 

[Quote]

 

“Root uptake of spinosad seemed to be limited to the rockwool substrate in this study, since far lower control percentages were achieved in other substrate types. Soil sorption probably contributes to lower systemicity, especially the back earth and peat/sand substrates. It was previously shown that strong sorption of spinosad occurs on fine textured soil with higher organic matter content (Thompson 2002). Systemicity might be directly related to the cation exchange capacity of the different substrates.” 1

 

[End Quote]

 

What this means is that, in all likelihood, is Spinosad use in rockwool, clayballs and water based systems (eg. Deep tank, aero system etc) is effective for controlling twospotted mite. On the other hand, Spinosad will not be effective in soils or coco substrate.

 

Potential Toxicity of Spinosad

 

Juan Cisneros et al (2002) point out:

 

[Quote]

 

“The fact that Spinosad is obtained from a naturally occurring soil organism does not automatically mean that it is safe and innocuous.”

 

(And)

 

“Judging by the results of the present study, in which low to moderate concentrations of Spinosad caused substantial mortality to insect natural enemies, we disagree with the assertion, by representatives of Dow AgroScience (Thompson and Hutchins,1999), that Spinosad has a safety profile similar to benign biological pesticides.”2

 

[End Quote]

 

The fact that Spinosad has also been shown to have systemic qualities in hydroponics and is a potential neurotoxin raises further questions.

 

Studies show that spinosad residues degrade quickly in the field with little toxicity at 3- 7 days post-application. However, in laboratory studies, spinosad was reported to be highly stable and capable of causing a high prevalence of mortality rate to insects, up to 1 month, after being applied to foliage or artificial surfaces. 3

 

When considering this, keep in mind that field-grown crops are exposed to environmental conditions such as rain etc, whereas indoor crops face very different conditions. For this reason, the residual activity of pesticides are shown to decrease more quickly in field environments than in indoor crops.

 

Conclusion re Spinosad   

 

Comparatively to other classes of pesticides, research shows that while spinosad may be potentially more toxic than deemed by regulatory bodies it, for now, offers a reduced-risk material for control of pests in the growroom.

 

However, more research is needed regarding safe application rates and times, withholding periods in growroom settings, byproducts of combustion, and harms it may pose to medical consumers – particularly those who are exposed to spinosad on a regular basis.

 

Spinosad Containing Product Names: Spinosad is produced by Dow AgroSciences. Products containing Spinosad are  Monterey Garden Insect Spray (commonly available through gardening centres), Conserve SC. If you cannot find Spinosad locally it can be purchased online from Amazon etc.

 

Spinosad OMRI Listed Products:

 

Conserve® Fire Ant Bait XT

Conserve® Fire Ant Bait

Entrust® Naturalyte® Insect Control

Entrust® SC

GF-120® NF Naturalyte® Fruit Fly Bait

Green Light Fire Ant Killer with Spinosad

Green Light® Fire Ant Control with Conserve®

Green Light® Lawn & Garden Spray with Spinosad®

Green Light® Lawn & Garden Spray with Spinosad® 2 (Concentrate)

Green Light® Lawn & Garden Spray with Spinosad® 2 (Ready-to-Spray)

Justice™ Insect Control

Monterey Garden Insect Spray

Natular T30

Natular XRT

Natular™ G

Natular™ G30

Neudorff Bug Bait

Ortho® ecosense™ brand fire ant bait granules

Regard™ Insecticide

Seduce® Insect Bait

Spinosad 0.5% SC

 

Spinosad Non OMRI -Listed Products:

Conserve® (Dow AgroSciences)
GF-120® Fruit Fly Bait (Dow AgroSciences)
Success® Naturalyte (Dow AgroSciences)
SpinTor® (Dow AgroSciences)
Tracer® (Dow AgroSciences)
Spinosad® Home and Garden (Dow AgroSciences)

 

REFS

 

  1. T. van Leeuwen, W. Dermauw,  M. Van De Veire and L. Tirry (2005) Systemic Use of Spinosad to Control the Two-spotted Spider Mite (Acari: Tetranychidae) on Tomatoes Grown in Rockwool
  2. Juan Cisneros, Dave Goulson, Lara C. Derwent, Dora I. Penagos, Olivia Hernandez, and Trevor Williams (2002) Toxic Effects of Spinosad on Predatory Insects
  3. TREVOR WILLIAMS, JAVIER VALLE and ELISA VIN˜ UELA (2003) Is the Naturally Derived Insecticide Spinosad Compatible with Insect Natural Enemies?