Ερώτηση για γεωργικό φάρμακο

• Acute toxicity: Dichlorvos is highly toxic by inhalation, dermal absorption, and ingestion [2,8]. Because dichlorvos is volatile, inhalation is the most common route of exposure. As with all organophosphates, dichlorvos is readily absorbed through the skin. Acute illness from dichlorvos is limited to the effects of cholinesterase inhibition. Compared to poisoning by other organophosphates, dichlorvos causes a more rapid onset of symptoms, which is often followed by a similarly rapid recovery [2,8]. This occurs because dichlorvos is rapidly metabolized and eliminated from the body. Persons with reduced lung function, convulsive disorders, liver disorders, or recent exposure to cholinesterase inhibitors will be at increased risk from exposure to dichlorvos. Alcoholic beverages may enhance the toxic effects of dichlorvos. High environmental temperatures or exposure of dichlorvos to light may enhance its toxicity [2,8]. Dichlorvos is mildly irritating to skin [8]. Concentrates of dichlorvos may cause burning sensations, or actual burns [2]. Application of 1.67 mg/kg dichlorvos in rabbits' eyes produced mild redness and swelling, but no injury to the cornea [8]. Symptoms of acute exposure to organophosphate or cholinesterase-inhibiting compounds may include the following: numbness, tingling sensations, incoordination, headache, dizziness, tremor, nausea, abdominal cramps, sweating, blurred vision, difficulty breathing or respiratory depression, slow heartbeat. Very high doses may result in unconsciousness, incontinence, and convulsions or fatality. Some organophosphates may cause delayed symptoms beginning 1 to 4 weeks after an acute exposure that may or may not have produced immediate symptoms. In such cases, numbness, tingling, weakness, and cramping may appear in the lower limbs and progress to incoordination and paralysis. Improvement may occur over months or years, but some residual impairment may remain [8]. The oral LD50 for dichlorvos is 61 to 175 mg/kg in mice, 100 to 1090 mg/kg in dogs, 15 mg/kg in chickens, 25 to 80 mg/kg in rats, 157 mg/kg in pigs, and 11 to 12.5 mg/kg in rabbits [2,8,13]. The dermal LD50 for dichlorvos is 70.4 to 250 mg/kg in rats, 206 mg/kg in mice, and 107 mg/kg in rabbits [2,8,13]. The 4-hour LC50 for dichlorvos is greater than 0.2 mg/L in rats [8].
• Chronic toxicity: Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure, including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking, and drowsiness or insomnia. An influenza like condition with headache, nausea, weakness, loss of appetite, and malaise has also been reported [8]. Repeated, small doses generally have no effect on treated animals. Doses of up to 4 mg/kg of a slow release formulation, given to cows to reduce flies in their feces, had no visibly adverse effects on the cows; but blood tests of these cows indicated cholinesterase inhibition [2]. Feeding studies indicate that a dosage of dichlorvos very much larger than doses which inhibit cholinesterase are needed to produce illness. Rats tolerated dietary doses as high as 62.5 mg/kg/day for 90 days with no visible signs of illness, while a dietary level of 0.25 mg/kg/day for only 4 days produced a reduction in cholinesterase levels [2]. Rats exposed to air concentrations of 0.5 mg/L of dichlorvos over a 5-week period exhibited significantly decreased cholinesterase activity in the plasma, red blood cells, and brain. Dogs fed dietary doses of 1.6 or 12.5 mg/kg/day for 2 years showed decreased red blood cell cholinesterase activity, increased liver weights, and increased liver cell size occurred [10]. Chronic exposure to dichlorvos will cause fluid to build up in the lungs (pulmonary edema). Liver enlargement has occurred in pigs maintained for long periods of time on high doses [2]. Dichlorvos caused adverse liver effects, and lung hemorrhages may occur at high doses in dogs [8]. In male rats, repeated high doses caused abnormalities in the tissues of the lungs, heart, thyroid, liver, and kidneys [8].
• Reproductive effects: There is no evidence that dichlorvos affects reproduction. When male and female rats were given a diet containing 5 mg/kg/day dichlorvos just before mating, and through pregnancy and lactation for females, there were no effects on reproduction or on the survival or growth of the offspring, even though severe cholinesterase inhibition occurred in the mothers and significant inhibition occurred in the offspring. The same results were observed in a three-generation study with rats fed dietary levels up to 25 mg/kg/day [2]. Once in the bloodstream, dichlorvos may cross the placenta [8].
• Teratogenic effects: There is no evidence that dichlorvos is teratogenic. A dose of 12 mg/kg/day was not teratogenic in rabbits and did not interfere with reproduction in any way. There was no evidence of teratogenicity when rats and rabbits were exposed to air concentrations of up to 6.25 mg/L throughout pregnancy. Dichlorvos was not teratogenic when given orally to rats [2].
• Mutagenic effects: Dichlorvos can bind to molecules such as DNA. For this reason, there has been extensive testing of dichlorvos for mutagenicity. Several studies have shown dichlorvos to be a mutagen [10]; for example, dichlorvos is reported positive in the Ames mutagenicity assay and in other tests involving bacterial or animal cell cultures. However, no evidence of mutagenicity has been found in tests performed on live animals. Its lack of mutagenicity in live animals may be due to rapid metabolism and excretion [2].
• Carcinogenic effects: Dichlorvos has been classified as a possible human carcinogen because it caused tumors in rats and mice in some studies but not others [11]. When dichlorvos was administered by gavage (stomach tube) to mice for 5 days per week for 103 weeks at doses of 20 mg/kg/day in males and 40 mg/kg/day in females, there was an increased incidence of benign tumors in the lining of the stomach in both sexes. When rats were given doses of 4 or 8 mg/kg/day for 5 days per week for 103 weeks, there was an increased incidence of benign tumors of the pancreas and of leukemia in male rats at both doses. At the highest dose, there was also an increased incidence of benign lung tumors in males. In female rats, there was an increase in the incidence of benign tumors of the mammary gland [10]. However, no tumors caused by dichlorvos were found in rats fed up to 25 mg/kg/day for 2 years, or in dogs fed up to 11 mg/kg/day for 2 years. No evidence of carcinogenicity was found when rats were exposed to air containing up to 5 mg/L for 23 hours/day for 2 years [11]. A few tumors were found in the esophagus of mice given dichlorvos orally, even though tumors of this kind are normally rare [8]. In sum, current evidence about the carcinogenicity of dichlorvos is inconclusive.
• Organ toxicity: Dichlorvos primarily affects the nervous system through cholinesterase inhibition, the blockage of an enzyme required for proper nerve functioning.

• Fate in humans and animals: Among the organophosphates, dichlorvos is remarkable for its rapid metabolism and excretion by mammals. Exposure of rats to 11 mg/L (250 times the normal exposure) for 4 hours was required before dichlorvos was detectable in the rats [2]. Even then, it was detected only in the kidneys. Following exposure to 50 mg/L, the half-life for dichlorvos in the rat kidney was 13.5 minutes [2]. The reason for this rapid disappearance of dichlorvos is the presence of degrading enzymes in both tissues and blood plasma. When dichlorvos is absorbed after ingestion, it is moved rapidly to the liver where it is rapidly detoxified. Thus poisoning by nonlethal doses of dichlorvos is usually followed by rapid detoxification in the liver and recovery [2]. Rats given oral or dermal doses at the LD50 level either died within 1 hour of dosing or recovered completely [2]. Dichlorvos does not accumulate in body tissues and has not been detected in the milk of cows or rats, even when the animals were given doses high enough to produce symptoms of severe poisoning [2].

• Effects on birds: Dichlorvos is highly toxic to birds, including ducks and pheasants [13]; the LD50 in wild birds fed dichlorvos is 12 mg/kg.
• Effects on aquatic organisms: UV light makes dichlorvos 5 to 150 times more toxic to aquatic life [8]. Grass shrimp are more sensitive to dichlorvos than the sand shrimp, hermit crab, and mummichog. The LC50 (96-hour) for dichlorvos is 11.6 mg/L in fathead minnow, 0.9 mg/L in bluegill, 5.3 mg/L in mosquito fish, 0.004 mg/L in sand shrimp, 3.7 mg/L in mummichogs, and 1.8 mg/L in American eels. The LC50 (24-hour) for dichlorvos in bluegill sunfish is 1.0 mg/L [10]. Dichlorvos does not significantly bioaccumulate in fish [12].
• Effects on other organisms: Dichlorvos is toxic to bees [13].

• Breakdown in soil and groundwater: Dichlorvos has low persistence in soil. Half-lives of 7 days were measured on clay, sandy clay, and loose sandy soil [12,20]. In soil, dichlorvos is subject to hydrolysis and biodegradation. Volatilization from moist soils is expected to be slow. The pH of the media determines the rate of breakdown [12]. Breakdown is rapid in alkaline soils and water, but it is slow in acidic media. For instance, at pH 9.1 the half-life of dichlorvos is about 4.5 hours. At pH 1 (very acidic), the half-life is 50 hours [12]. Dichlorvos does not adsorb to soil particles and it is likely to contaminate groundwater [12,20]. When spilled on soil, dichlorvos leached into the ground with 18 to 20% penetrating to a depth of 12 inches within 5 days [12].
• Breakdown in water: In water, dichlorvos remains in solution and does not adsorb to sediments. It degrades primarily by hydrolysis, with a half-life of approximately 4 days in lakes and rivers. This half-life will vary from 20 to 80 hours between pH 4 and pH 9. Hydrolysis is slow at pH 4 and rapid at pH 9 [8,12]. Biodegradation may occur under acidic conditions, which slow hydrolysis, or where populations of acclimated microorganisms exist, as in polluted waters. Volatilization from water is slow. It has been estimated at 57 days from river water and over 400 days from ponds [12].
• Breakdown in vegetation: Except for cucumbers, roses, and some chrysanthemums, plants tolerate dichlorvos very well [8].

• Appearance: Dichlorvos is a colorless to amber liquid with a mild chemical odor [13].
• Chemical Name: 2,2-dichlorovinyl dimethyl phosphate [13]
• CAS Number: 62-73-7
• Molecular Weight: 220.98
• Water Solubility: 10,000 mg/L (estimated) [13]
• Solubility in Other Solvents: dichloromethane, v.s.; 2-propanol, v.s.; toluene v.s.; ethanol s.; chloroform s.; acetone s.; kerosene s. [13]
• Melting Point: Not Available
• Vapor Pressure: 290 mPa @ 20 C [13]
• Partition Coefficient: Not Available
• Adsorption Coefficient: 30 (estimated) [20]

• ADI: 0.004 mg/kg/day [38]
• MCL: Not Available
• RfD: 0.0005 mg/kg/day [53]
• PEL: 1.0 mg/m3 (8-hour) (skin) [39]
• HA: Not Available
• TLV: Not Available

• Phone: 213-264-3910
• Emergency: 800-228-5635, ext. 169

Αρχική Δημοσίευση από Toeman:

Dichlorvos​

Trade and Other Names: Dichlorvos is also called DDVP. Trade names include Apavap, Benfos, Cekusan, Cypona, Derriban, Derribante, Devikol, Didivane, Duo-Kill, Duravos, Elastrel, Fly-Bate, Fly-Die, Fly-Fighter, Herkol, Marvex, No-Pest, Prentox, Vaponite, Vapona, Verdican, Verdipor, and Verdisol. Trade names used outside of the U.S. include Doom, Nogos, and Nuvan.
RegulatoryStatus: The EPA has classified it as toxicity class I - highly toxic, because it may cause cancer and there is only a small margin of safety for other effects. Products containing dichlorvos must bear the Signal Words DANGER - POISON. Dichlorvos is a Restricted Use Pesticide (RUP) and may be purchased and used only by certified applicators.
Chemical Class: organophosphate
Introduction: Dichlorvos is an organophosphate compound used to control household, public health, and stored product insects. It is effective against mushroom flies, aphids, spider mites, caterpillars, thrips, and white flies in greenhouse, outdoor fruit, and vegetable crops. Dichlorvos is used to treat a variety of parasitic worm infections in dogs, livestock, and humans. Dichlorvos can be fed to livestock to control botfly larvae in the manure. It acts against insects as both a contact and a stomach poison. It is used as a fumigant and has been used to make pet collars and pest strips. It is available as an aerosol and soluble concentrate.
Toxicological Effects:

• Acute toxicity: Dichlorvos is highly toxic by inhalation, dermal absorption, and ingestion [2,8]. Because dichlorvos is volatile, inhalation is the most common route of exposure. As with all organophosphates, dichlorvos is readily absorbed through the skin. Acute illness from dichlorvos is limited to the effects of cholinesterase inhibition. Compared to poisoning by other organophosphates, dichlorvos causes a more rapid onset of symptoms, which is often followed by a similarly rapid recovery [2,8]. This occurs because dichlorvos is rapidly metabolized and eliminated from the body. Persons with reduced lung function, convulsive disorders, liver disorders, or recent exposure to cholinesterase inhibitors will be at increased risk from exposure to dichlorvos. Alcoholic beverages may enhance the toxic effects of dichlorvos. High environmental temperatures or exposure of dichlorvos to light may enhance its toxicity [2,8]. Dichlorvos is mildly irritating to skin [8]. Concentrates of dichlorvos may cause burning sensations, or actual burns [2]. Application of 1.67 mg/kg dichlorvos in rabbits' eyes produced mild redness and swelling, but no injury to the cornea [8]. Symptoms of acute exposure to organophosphate or cholinesterase-inhibiting compounds may include the following: numbness, tingling sensations, incoordination, headache, dizziness, tremor, nausea, abdominal cramps, sweating, blurred vision, difficulty breathing or respiratory depression, slow heartbeat. Very high doses may result in unconsciousness, incontinence, and convulsions or fatality. Some organophosphates may cause delayed symptoms beginning 1 to 4 weeks after an acute exposure that may or may not have produced immediate symptoms. In such cases, numbness, tingling, weakness, and cramping may appear in the lower limbs and progress to incoordination and paralysis. Improvement may occur over months or years, but some residual impairment may remain [8]. The oral LD50 for dichlorvos is 61 to 175 mg/kg in mice, 100 to 1090 mg/kg in dogs, 15 mg/kg in chickens, 25 to 80 mg/kg in rats, 157 mg/kg in pigs, and 11 to 12.5 mg/kg in rabbits [2,8,13]. The dermal LD50 for dichlorvos is 70.4 to 250 mg/kg in rats, 206 mg/kg in mice, and 107 mg/kg in rabbits [2,8,13]. The 4-hour LC50 for dichlorvos is greater than 0.2 mg/L in rats [8].
• Chronic toxicity: Repeated or prolonged exposure to organophosphates may result in the same effects as acute exposure, including the delayed symptoms. Other effects reported in workers repeatedly exposed include impaired memory and concentration, disorientation, severe depressions, irritability, confusion, headache, speech difficulties, delayed reaction times, nightmares, sleepwalking, and drowsiness or insomnia. An influenza like condition with headache, nausea, weakness, loss of appetite, and malaise has also been reported [8]. Repeated, small doses generally have no effect on treated animals. Doses of up to 4 mg/kg of a slow release formulation, given to cows to reduce flies in their feces, had no visibly adverse effects on the cows; but blood tests of these cows indicated cholinesterase inhibition [2]. Feeding studies indicate that a dosage of dichlorvos very much larger than doses which inhibit cholinesterase are needed to produce illness. Rats tolerated dietary doses as high as 62.5 mg/kg/day for 90 days with no visible signs of illness, while a dietary level of 0.25 mg/kg/day for only 4 days produced a reduction in cholinesterase levels [2]. Rats exposed to air concentrations of 0.5 mg/L of dichlorvos over a 5-week period exhibited significantly decreased cholinesterase activity in the plasma, red blood cells, and brain. Dogs fed dietary doses of 1.6 or 12.5 mg/kg/day for 2 years showed decreased red blood cell cholinesterase activity, increased liver weights, and increased liver cell size occurred [10]. Chronic exposure to dichlorvos will cause fluid to build up in the lungs (pulmonary edema). Liver enlargement has occurred in pigs maintained for long periods of time on high doses [2]. Dichlorvos caused adverse liver effects, and lung hemorrhages may occur at high doses in dogs [8]. In male rats, repeated high doses caused abnormalities in the tissues of the lungs, heart, thyroid, liver, and kidneys [8].
• Reproductive effects: There is no evidence that dichlorvos affects reproduction. When male and female rats were given a diet containing 5 mg/kg/day dichlorvos just before mating, and through pregnancy and lactation for females, there were no effects on reproduction or on the survival or growth of the offspring, even though severe cholinesterase inhibition occurred in the mothers and significant inhibition occurred in the offspring. The same results were observed in a three-generation study with rats fed dietary levels up to 25 mg/kg/day [2]. Once in the bloodstream, dichlorvos may cross the placenta [8].
• Teratogenic effects: There is no evidence that dichlorvos is teratogenic. A dose of 12 mg/kg/day was not teratogenic in rabbits and did not interfere with reproduction in any way. There was no evidence of teratogenicity when rats and rabbits were exposed to air concentrations of up to 6.25 mg/L throughout pregnancy. Dichlorvos was not teratogenic when given orally to rats [2].
• Mutagenic effects: Dichlorvos can bind to molecules such as DNA. For this reason, there has been extensive testing of dichlorvos for mutagenicity. Several studies have shown dichlorvos to be a mutagen [10]; for example, dichlorvos is reported positive in the Ames mutagenicity assay and in other tests involving bacterial or animal cell cultures. However, no evidence of mutagenicity has been found in tests performed on live animals. Its lack of mutagenicity in live animals may be due to rapid metabolism and excretion [2].
• Carcinogenic effects: Dichlorvos has been classified as a possible human carcinogen because it caused tumors in rats and mice in some studies but not others [11]. When dichlorvos was administered by gavage (stomach tube) to mice for 5 days per week for 103 weeks at doses of 20 mg/kg/day in males and 40 mg/kg/day in females, there was an increased incidence of benign tumors in the lining of the stomach in both sexes. When rats were given doses of 4 or 8 mg/kg/day for 5 days per week for 103 weeks, there was an increased incidence of benign tumors of the pancreas and of leukemia in male rats at both doses. At the highest dose, there was also an increased incidence of benign lung tumors in males. In female rats, there was an increase in the incidence of benign tumors of the mammary gland [10]. However, no tumors caused by dichlorvos were found in rats fed up to 25 mg/kg/day for 2 years, or in dogs fed up to 11 mg/kg/day for 2 years. No evidence of carcinogenicity was found when rats were exposed to air containing up to 5 mg/L for 23 hours/day for 2 years [11]. A few tumors were found in the esophagus of mice given dichlorvos orally, even though tumors of this kind are normally rare [8]. In sum, current evidence about the carcinogenicity of dichlorvos is inconclusive.
• Organ toxicity: Dichlorvos primarily affects the nervous system through cholinesterase inhibition, the blockage of an enzyme required for proper nerve functioning.

• Fate in humans and animals: Among the organophosphates, dichlorvos is remarkable for its rapid metabolism and excretion by mammals. Exposure of rats to 11 mg/L (250 times the normal exposure) for 4 hours was required before dichlorvos was detectable in the rats [2]. Even then, it was detected only in the kidneys. Following exposure to 50 mg/L, the half-life for dichlorvos in the rat kidney was 13.5 minutes [2]. The reason for this rapid disappearance of dichlorvos is the presence of degrading enzymes in both tissues and blood plasma. When dichlorvos is absorbed after ingestion, it is moved rapidly to the liver where it is rapidly detoxified. Thus poisoning by nonlethal doses of dichlorvos is usually followed by rapid detoxification in the liver and recovery [2]. Rats given oral or dermal doses at the LD50 level either died within 1 hour of dosing or recovered completely [2]. Dichlorvos does not accumulate in body tissues and has not been detected in the milk of cows or rats, even when the animals were given doses high enough to produce symptoms of severe poisoning [2].

Ecological Effects:

• Effects on birds: Dichlorvos is highly toxic to birds, including ducks and pheasants [13]; the LD50 in wild birds fed dichlorvos is 12 mg/kg.
• Effects on aquatic organisms: UV light makes dichlorvos 5 to 150 times more toxic to aquatic life [8]. Grass shrimp are more sensitive to dichlorvos than the sand shrimp, hermit crab, and mummichog. The LC50 (96-hour) for dichlorvos is 11.6 mg/L in fathead minnow, 0.9 mg/L in bluegill, 5.3 mg/L in mosquito fish, 0.004 mg/L in sand shrimp, 3.7 mg/L in mummichogs, and 1.8 mg/L in American eels. The LC50 (24-hour) for dichlorvos in bluegill sunfish is 1.0 mg/L [10]. Dichlorvos does not significantly bioaccumulate in fish [12].
• Effects on other organisms: Dichlorvos is toxic to bees [13].

Environmental Fate:

• Breakdown in soil and groundwater: Dichlorvos has low persistence in soil. Half-lives of 7 days were measured on clay, sandy clay, and loose sandy soil [12,20]. In soil, dichlorvos is subject to hydrolysis and biodegradation. Volatilization from moist soils is expected to be slow. The pH of the media determines the rate of breakdown [12]. Breakdown is rapid in alkaline soils and water, but it is slow in acidic media. For instance, at pH 9.1 the half-life of dichlorvos is about 4.5 hours. At pH 1 (very acidic), the half-life is 50 hours [12]. Dichlorvos does not adsorb to soil particles and it is likely to contaminate groundwater [12,20]. When spilled on soil, dichlorvos leached into the ground with 18 to 20% penetrating to a depth of 12 inches within 5 days [12].
• Breakdown in water: In water, dichlorvos remains in solution and does not adsorb to sediments. It degrades primarily by hydrolysis, with a half-life of approximately 4 days in lakes and rivers. This half-life will vary from 20 to 80 hours between pH 4 and pH 9. Hydrolysis is slow at pH 4 and rapid at pH 9 [8,12]. Biodegradation may occur under acidic conditions, which slow hydrolysis, or where populations of acclimated microorganisms exist, as in polluted waters. Volatilization from water is slow. It has been estimated at 57 days from river water and over 400 days from ponds [12].
• Breakdown in vegetation: Except for cucumbers, roses, and some chrysanthemums, plants tolerate dichlorvos very well [8].

Physical Properties:

• Appearance: Dichlorvos is a colorless to amber liquid with a mild chemical odor [13].
• Chemical Name: 2,2-dichlorovinyl dimethyl phosphate [13]
• CAS Number: 62-73-7
• Molecular Weight: 220.98
• Water Solubility: 10,000 mg/L (estimated) [13]
• Solubility in Other Solvents: dichloromethane, v.s.; 2-propanol, v.s.; toluene v.s.; ethanol s.; chloroform s.; acetone s.; kerosene s. [13]
• Melting Point: Not Available
• Vapor Pressure: 290 mPa @ 20 C [13]
• Partition Coefficient: Not Available
• Adsorption Coefficient: 30 (estimated) [20]

Exposure Guidelines:

• ADI: 0.004 mg/kg/day [38]
• MCL: Not Available
• RfD: 0.0005 mg/kg/day [53]
• PEL: 1.0 mg/m3 (8-hour) (skin) [39]
• HA: Not Available
• TLV: Not Available

Basic Manufacturer:
Amvac Chemical Corp.
4100 E. Washington Blvd.
Los Angeles, CA 90023

• Phone: 213-264-3910
• Emergency: 800-228-5635, ext. 169

Τα 0,032 ppm τα σκέφτηκες μόνος σου σαν δοσολογία ή ρώτησες γεωπόνο;
Δεν γνωρίζω πράμα για διχλωρβό αλλά τσέκαρε με προσοχή τα παραπάνω (σου έχω κοκκινήσει τα βασικά) και κυρίως για την ADI (Acceptable Daily Income ή Induce) που καθορίζει μέχρι ποια ποσότητα ημερησίως μπορείς άφοβα να εκτεθείς σε αυτήν.

Ρώτα Γεωπόνο α-π-α-ρ-α-ι-τ-ή-τ-ω-ς ...

Υ.γ Από όσο είδα κάνει για χρήση υπαίθριων φρούτων (σαν τα νεκταρίνια) αλλά είναι εξαιρετικά επικίνδυνο φάρμακο. Είναι στη λίστα των καρκινογόνων Χ.Ο.

Υ.γ.2 Η USA Enviromental Protection Agency "τράβηξε" απαγόρευση στο DDVP από το 1981. Από τότε πλησίασε πολλές φορές στο να απαγορευτεί σε παγκόσμια κλίμακα (όπως π.χ. το βρωμιούχο μεθύλιο που είναι απολυμαντικό εδάφους βέβαια αλλά ακόμα το βρίσκεις σε αποθήκες και κυρίως στην Ελλάδα, δυστυχώς) όμως συνεχίζει να διατίθεται κανονικότατα. Δεν υπάρχει κάποια επβεβαιωμένη (και καλά) καρκινογεννετική επίδραση του εώς σήμερα με βάση κάποια πιστοποιημένη επιδημιολογική μελέτη.

...και μην ξεχνάς. η Φυσιολογία σήμερα έχει φτάσει στο επίπεδο να θεωρεί τη δόση τοξική, όχι την ουσία.

Πχ αν καταναλώσεις 3 κιλά ζάχαρη να σε σκοτώσουν και με 1 ppm HCN να τη βγάλεις καθαρός.
Πάντως μιας και πρόκειται για πυρηνοκαρπο θα συνιστούσα να μη ψέκαζες με το συγκεκριμένο παρασιτοκτόνο.Εκτός και έχεις μεγάλη προσβολή.

Αυτά.

Click για ανάπτυξη...