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Caution when using "Hot Shot No-Pest Strips." Thread Tools Search this Thread
Old 05-24-2010, 01:21 AM #121
rocdiesel
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Originally Posted by yesum View Post
So I use these in the room I have the grow tent in or the tent itself? I have to turn off the fan in the tent while this is working?
Finally, a day or so of this will do it? I want to use the least amount of time.
that is what I am trying, I threw it in the tent and shut off my inline fan and such while it's in the dark period, hopefully problem for me will be resolved in a few days I figure having the strips in the room won't cause to much of a problem, I can rinse my flowering girls as all of them have only been in flower for 3 weeks or so.

I think it's working I looked and saw some bugs on one of my plants a day or two ago and they havent moved..
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Old 05-26-2010, 07:53 PM #122
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have seen plants die from over exposure. in a sealed space too long
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Old 06-08-2010, 03:00 PM #123
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Good info
Thanks
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Old 06-08-2010, 10:42 PM #124
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have seen plants die from over exposure. in a sealed space too long
I highly doubt this.
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Old 06-27-2010, 07:04 AM #125
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Originally Posted by 9240GrnMachine View Post
have seen plants die from over exposure. in a sealed space too long

had this happen to me...placed two SR cuts in a clone quarantine chamber with a new pest strip and several days later I pulled them out to check them and the cuts were beginning to turn black from the top down...they were able to be saved...but I believe if I would have left them in there for a few more days they would have crapped out...I still use the traps but in more of a controlled manner...now i break open the pest strip and cut into smaller pieces for the quarantine chamber, no issue after modifying the amount of strip...like anything, to much can be a bad thing...

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yeah.. that point you feel like every molecule in your body is melting down into the couch, and you're wondering if you've shit your pants or you just can't feel your ass, and you think your teeth might have fallen out... that's when you've had too much edibles.
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Old 06-27-2010, 01:26 PM #126
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Something else did that to your cuts, Grass Lands. The dichlorvos didn't do it.
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Old 06-30-2010, 08:07 PM #127
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I have to agree, I had one sitting next to a plant in the first few weeks in flower. That side of the plant started to shrivel and have problems. When I moved the No-Pest Strip away, the plant started to do better and look healthy again.

:shrug: Not complaining, just an observation.
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Old 06-30-2010, 09:08 PM #128
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i have never had any issues and i use 2 strips in a 4.5 x4.5 x 7 tent
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Old 06-30-2010, 11:36 PM #129
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I never have either, sml. That is why I even bother with this thread. It is a good product that gets unfounded bad rep from the occasional fly-by story.

I don't much like to have anything in my flower chamber, but in veg I have used countless strips and have never ever seen anything like a rare few describe.

But like anything...never say never, and there may well be plants that do not like the gas emitted. Hell, feed one a bit too much or have the pH all out and it can go south on you, so anything can happen. But for general use they are safe with no chronic effects reported in plants, and safe to use for us.
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Old 06-30-2010, 11:46 PM #130
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* Summary of toxicology

1. Effects on Animals: Dichlorvos is an anticholinesterase agent and may cause excessive salivation, eye tearing, sweating, constricted pupils, respiratory distress, anorexia, vomiting, diarrhea, weakness, twitching, paralysis, a slow and irregular heartbeat, convulsions, coma, and death [Hathaway et al. 1991]. Dichlorvos also has reproductive effects and causes malformed offspring in rodents. The acute toxicity of dichlorvos for laboratory animals is significantly high; the dermal LD(50) for rabbits is 107 mg/kg and 80 mg/kg in rats; and the acute oral LD(50) in rats is 25 mg/kg [NIOSH 1995; ACGIH 1991; Sax and Lewis 1989]. The lowest single oral dose that causes observable behavioral changes is 10 mg/kg in calves [NLM 1995]. The neurotoxic effect of dichlorvos on the central and peripheral nervous system was investigated in acute and subchronic experiments using male rats. The acute group received a single oral dose of 88 mg/kg and the two subchronic groups received a daily oral dose of 1.6 mg/kg or 0.8 mg/kg for a period of 6 weeks. Both the acute and subchronic groups exhibited significant changes in the functions of the central nervous system, increase of EEG mean frequency, decrease of EEG amplitude, and peripheral nervous system decrease of conduction velocity, and increase of relative and absolute refractory periods. In one of two studies on the long-term effects of dichlorvos by oral exposure, an increased but not statistically significant number of squamous-cell tumors were found in mice [ACGIH 1991]. However, the International Agency for Research on Cancer (IARC) has concluded that the evidence for the carcinogenicity of dichlorvos in animals is inadequate [IARC 1987]. Administered intraperitoneally during pregnancy, dichlorvos produced developmental abnormalities in rat fetuses [NIOSH 1995]. Dichlorvos is mutagenic in bacterial and mammalian test systems [NIOSH 1995; NLM 1995].

2. Effects on Humans: Dichlorvos is an organophosphorus pesticide and is therefore a cholinesterase inhibitor. Overexposure to this substance causes symptoms that vary by route of exposure. Inhalation causes ocular and respiratory symptoms. Ingestion causes gastrointestinal effects, while skin absorption causes localized sweating and muscle twitching in the area where entry occurred. If exposure is severe, muscle weakness, twitching, fasciculation, and paralysis may occur. Paralysis of the respiratory muscles may cause death. Cardiac irregularities, including complete heart block, may also occur [Hathaway et al. 1991]. Dichlorvos is easily absorbed through the skin, gastrointestinal tract, and lungs because of its high volatility [Parmeggiani 1983]. It is rapidly inactivated by the liver, and persons with liver disease may be less tolerant of the toxic effects than normal persons [Gosselin 1984]. Human volunteers exposed for 30 minutes/hour each hour, 10 hours/day for 14 days at concentrations of 0.14 to 0.33 mg/m(3) had no changes in cholinesterase levels, airway resistance, or vision. At a concentration of 1 mg/m(3) for 7.5 to 8.5 hours, volunteers experienced a 20- to 25-percent reduction in cholinesterase levels [ACGIH 1991]. Thirteen workers exposed over a period of a year to an average concentration of 0.7 mg/m(3) showed decreases of 35 percent and 60 percent, respectively, in red blood cell and plasma cholinesterase levels [Hathaway et al. 1991]. At a level of 0.1 ppm, the plasma cholinesterase is reported to drop by 20 percent [ACGIH 1991]. Daily exposure to dichlorvos at levels insufficient to produce results on a single-dose basis may produce symptoms after several days exposure. Continuing exposure after symptoms appear can produce increasingly severe effects [Hathaway et al. 1991]. Dichlorvos has also been reported to cause allergic contact dermatitis [ACGIH 1991]. Dichlorvos causes methylation of DNA in vitro, but there is no evidence of mutagenicity in humans [Hathaway et al. 1991]. IARC has concluded that there is no adequate data for evaluating the carcinogenicity of dichlorvos in humans [IARC 1987].

* Signs and symptoms of exposure

1. Acute exposure: Symptoms and signs usually appear within minutes of exposure but they may be delayed for as long as 12 hours. After inhalation, the initial symptoms and signs are a feeling of tightness in the chest, wheezing due to bronchospasm, blurring of vision, tearing, runny nose, and frontal headache. Ingestion causes sweating, nausea, vomiting, diarrhea, cramps, urination and defecation, and anorexia within 15 minutes to 2 hours of exposure. Skin absorption can produce local sweating and muscle fasciculations within 15 minutes to 2 hours after exposure. Death is usually caused by respiratory muscle paralysis and consequent asphyxiation.

2. Chronic exposure: Continued exposure to dichlorvos may cause headache, weakness, decreased memory, easy fatigability, disturbed sleep, loss of sensation in the skin, and paralysis. Delayed neurological symptoms are reversible after exposure ceases, but recovery is low and may not be complete.
...

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Abstract
This study was designed to determine if commercial preparations of the pesticides Folpet, Captan, Guthion®, and Dichlorvos, have a significant effect on genetic recombination in maize (Zea mays L.). The pesticides were applied in aqeous solutions of 1.5% dimethyl sulfoxide with 0.04% X-77 Spreader®. Premeiotic treatment s to heterozygous females were applied as a foliar spray. Testcrosses were analyzed for changes in frequencies of recombination between loci 1g−g12 and a-et on chromosomes 2 and 3, respectively. Sib-crosses were analyzed for changes in frequencies of recombination between the 1g−g12 loci and the a2−bt loci on chromosomes 2 and 5, respectively. Between the a-et markers, significant increases in genetic recombination were produced by the 0.17 M level of Folpet, the 0.50 M level of Captan, the 0.50 M level of Guthion®, and the 0.66% v/v and 1.00% v/v levels of Dichlorvos. Between the a2−bt markers, significant increases in recombination were produced by the 0.33 and the 0.50 M levels of Guthion®. Analysis of variance for simple regression was conducted on each pesticide/marker group combination to determine possible linear dose responses. Significant increases in genetic recombination were induced linearly in the a−et linkage group with increasing levels of Captan, Guthion®, and Dichlorvos. Genetic recombination also was increased linearly in the a2−bt linkage group with increasing concentrations of Captan and Guthion®. The conclusion from this study is that commercial preparations of the pesticides Captan, Guthion®, Dichlorvos, and possibly Folpet, have the ability to increase the frequency of genetic recombination between markers of maize. This study therefore supports the consensus that certain pesticides, at abnormally high rates of application, are genetically active, environmental recombinagens.
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