Avid remains active in your plants for 28 days. Although it does not kill mite eggs, it remains lethal so all the eggs that do hatch, those new mites become paralyzed as soon as they feed and the entire population expires. Ideally, you want to eliminate any mite population during the veg period, but you can still apply Avid if needed during the first three weeks of flowering (I've never had to do that. If there are any signs of mites when I'm ready to flower I deal with it then. Avid is very reliable. What bad things have you heard about it? If you mishandle it it will make you sick, but it breaks down rapidly in the environment. Also, the active ingredient in Avid, Abamectin, is derived from a soil microbe. Here is some real information:
ACUTE TOXICITY
Abamectin is a highly toxic material, however most formulated products containing abamectin are of low toxicity to mammals (
5,
7). Emulsifiable concentrate formulations may cause moderate eye irritation and mild skin irritation (
1). Symptoms of poisoning observed in laboratory animals include pupil dilation, vomiting, convulsions and/or tremors, and coma (
5). Abamectin acts on insects by interfering with neural and neuromuscular transmission. It acts on a specific type of synapse located only within the brain and is protected by the blood-brain barrier. However, at very high doses, the mammalian blood-brain barrier can be penetrated, causing symptoms of CNS depression such as incoordination, tremors, lethargy, excitation and pupil dilation. Very high doses have caused death from respiratory failure (
2).
Abamectin is not readily absorbed through skin. Tests with monkeys show that less than 1% of dermally applied abamectin was absorbed into the bloodstream through the skin (
5). Abamectin does not cause allergic skin reactions (
7).
The amount of a chemical that is lethal to one-half (50%) of experimental animals fed the material is referred to as its acute oral lethal dose fifty, or LD50. The oral LD50 for abamectin in rats is 11 mg/kg, and in mice range from 14 (
5) to > 80 mg/kg (
7). The dermal LD50 for technical abamectin on rats and rabbits is > 330 mg/kg (
4). The oral LD50 for the product Affirm 0.011% Fire Ant Bait in rats is > 5,000 mg/kg, and its dermal LD50 on rabbits is > 2,000 mg/kg (
1). The oral LD50 for the 1.8% w/v Abamectin EC product in rats is 300 mg/kg, and the dermal LD50 for this product on rabbits is > 2,000 mg/kg (
8).
CHRONIC TOXICITY
In a 1-year study with dogs given oral doses of 0, 0.25, 0.5, or 1 mg/kg/day, there were no changes in tissue at any dose level. However, some dogs at the 0.5 and 1 mg/kg/day levels had pupillary dilation, weight loss, lethargy, tremors and recumbency. The NOEL for this study was 0.25 mg/kg/day (
5,
8). Similar results were seen in a 2-year study with rats fed 0, 0.75, 1.5, or 2 mg/kg/day. No changes in the nervous or muscular systems were observed, but rats in all the dosage levels exhibited body weight gains significantly higher than the controls. A few individuals in the high dose group exhibited tremors (
5). When mice were fed 8 mg/kg/day, the highest dose tested, for 94 weeks, the males developed dermatitis and changes in blood formation in the spleen, while females exhibited tremors and weight loss (
7).
Reproductive Effects
In rats, the pup toxicity NOEL was 0.12 mg/kg/day. At 0.40 mg/kg/day, there were increased stillbirths, decreased pup viability, decreased lactation, and decreased pup weights (
7).
Teratogenic Effects
Abamectin has produced cleft palate in the offspring of treated mice and rabbits, but only at doses that were also toxic to the mothers (
5). There were no birth defects in the offspring of rats given up to 1 mg/kg/day (
7).
Mutagenic Effects
Abamectin is not mutagenic. The microbial mutagenesis and mutagenicity tests in live mice were negative. One test on rat liver cell cultures was positive (
7).
Carcinogenic Effects
Abamectin was not carcinogenic in rats or mice fed the maximum tolerated doses. The rats were fed dietary doses of 0.75, 1.5, or 2 mg/kg/day for 24 months, and the mice were fed 2, 4 or 8 mg/kg/day for 22 months (
5).
Fate in Humans and Animals
Tests with laboratory animals show that ingested avermectin B1a is absorbed into the bloodstream by mammals and that it is rapidly eliminated from the body within 2 days via the feces (
7,
8). Rats given single oral doses of radio-labeled avermectin B1a excreted most of the dose (69 to 82%) unchanged in the feces. The half-life of avermectin B1a residues in rat tissues averaged 1.2 days (
4). Similarly, when monkeys were given a single intravenous injection of avermectin B1a, more than 90% of the dose was excreted in the feces within 7 days of the dosing (
5,
8). Lactating goats given daily oral doses for 10 days excreted 89% of the administered avermectin, mainly in the feces. Less than 1% was recovered in the urine (
4).
ECOLOGICAL EFFECTS
Effects on Birds
Abamectin is relatively non-toxic to birds (
7). The LD50 for abamectin in Bobwhite quail is 2,000 mg/kg. When exposed to abamectin in their feed for 5 days, the LC50 for bobwhite quail was 3,102 ppm, and for mallard ducks was 383 ppm. There were no adverse effects on reproduction when mallard ducks were fed dietary doses of 3, 6 or 12 ppm for 18 weeks (
6).
Effects on Aquatic Organisms
Abamectin is highly toxic to fish and aquatic invertebrates (
7). Its 96-hour LC50 in rainbow trout is 3.2 ppb, 9.6 ppb in bluegill sunfish, 15 ppb in sheepshead minnow, 24 ppb in channel catfish, and 42 ppb in carp. Its 48-hour LC50 in Daphnia magna, a small freshwater crustacean, is 0.34 ppb. The 96-hour LC50 for abamectin in pink shrimp (Panaeus duorarum) is 1.6 ppb, 0.022 ppb in mysid shrimp, 430 ppb in eastern oysters, and 153 ppb in blue crab (
6). While the above LC50 values are quite low, indicating a high level of toxicity to aquatic organisms, actual concentrations of abamectin in surface waters (fresh water) adjacent to treated areas are expected to be low. Application rates of 0.025 pounds of abamectin per acre (the highest recommended rate) should result in concentrations no higher than 26 parts per trillion in adjacent surface waters one day after the application. Rapid photodegradation and adsorption to sediments should produce even lower concentrations within days. The degradation products of abamectin are less toxic to aquatic organisms than abamectin itself (
6).
Abamectin did not bioaccumulate in bluegill sunfish exposed to 0.099 ppb for 28 days in a flow-through tank. On day 28, the concentration of residues in the fish was 6.8 ppb, but this rapidly decreased to 0.32 ppb by day 42. The BCF value calculated from this study is 52, indicating that abamectin does not accumulate or persist in fish (
6).
Effects on Other Animals (Nontarget species)
Abamectin is highly toxic to bees, with a 24-hour contact LC50 of 0.002 ug/bee and an oral LD50 of 0.009 ug/bee. Rapid degradation of abamectin will reduce the risk of bee deaths. Citrus and alfalfa foliage was not toxic to bees 24 to 48 hours after treatment with abamectin (
6).
The 28-day LC50 for abamectin in earthworms is 28 ppm. Earthworms will not be adversely affected by use of abamectin at recommended application rates.
ENVIRONMENTAL FATE
Breakdown of Chemical in Soil and Groundwater
Because abamectin is nearly insoluble in water and has a strong tendency to bind to soil particles, it is therefore immobile in soil and unlikely to leach or contaminate groundwater (
6,
7). Compounds produced by the degradation of abamectin are also immobile and unlikely to contaminate groundwater (
6). Abamectin is rapidly degraded in soil. At the soil surface, it is subject to rapid photodegradation, with half-lives of 8 and 21 hours (
6) or 1 day (
7) reported. When applied to the soil surface and not shaded, its soil half-life was about 1 week. Under dark, aerobic conditions, the soil half-life was 2 weeks to 2 months (
7). The half-life for avermectin B1a in fine sandy loam, clay and construction grade sand was 20 to 47 days. Loss of abamectin from these soils is thought to be due to microbial degradation because abamectin remained undegraded in sterile soil. The rate of degradation was significantly decreased under anaerobic conditions (
6).
Breakdown of Chemical in Surface Water
Abamectin is rapidly degraded in water. After an initial distribution, its half-life in artificial pond water was 4 days. Its half- life in pond sediment was 2 to 4 weeks (
6). It undergoes rapid photodegradation, with a half-life of 12 hours in water (
6,
7). When tested at pH levels common to surface and groundwater (pH 5, 7, and 9), abamectin did not hydrolyze (
6).
Breakdown of Chemical in Vegetation
Plants do not absorb abamectin from the soil (
6). Abamectin is subject to rapid degradation when present as a thin film, as on treated leaf surfaces. Under laboratory conditions and in the presence of light, its half-life as a thin film was 4 to 6 hours (
6).
Pyrethrins are two chemicals which are extracted from the chrysanthemum flower's seed casings. They are the common ingredient in Raid, Doktor Doom, etc. Really ineffective on mites and can burn your plant's foliage.
I spray mist with water twice a day, once in the morning and once at lunch time.
In the evening, 2 hours before they go to sleep, I give them a neem treatment.
Question is, Will GONATS also work at keeping mite population controlled or bringing them down over a series of different pesticides, all of course omori listed organic. does pyrethirns come from the chrysanthemum flower?
I would like to know what other regimen I should add with my NEEM OIL treatments.
So far I am using every day to every other, neem oil and cedar oil.
Must I add avid to my mix once or twice?
I hear bad things about it when it comes to smoke and health but for getting mites out i hear good things.??