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FUNGICIDE RESIDUE AND HEALTH
HAZARDS
Submitted by,
Ranapratap A. Raut
Ph. D. (1st Year)
Department of Plant Pathology,
N. M. College of Agriculture,
NAU, Navsari (Gujrat)
 Pesticides have consistently revealed their worth through increased agriculture productivity,
reduced insect- borne, endemic diseases and protection as well as restoration of plantations,
forests, harvested wood products, homes and fiber.
 Currently, pesticides are very valuable in developing nations, particularly those in tropical are as
looking for an entry in the global economy by providing off-season fresh vegetables and fruits to
nations in more temperate weathers.
 However, these goals cannot be achieved without the increased use of pesticides, mainly
insecticides, herbicides and fungicides.
 The increased use of chemical pesticides has resulted in contamination of the environment and
also caused many associated long-term effects on human health.
 Pesticides have been associated with a wide spectrum of human health hazards, ranging from
short-term impacts such as headaches and nausea to chronic impacts like cancer, reproductive
harm and endocrine disruption
Fungicide
 A fungicide is a specific type of pesticide that controls fungal disease by specifically
inhibiting or killing the fungus causing the disease.
Fungicide residue
 Fungicide residue refers to the fungicide or metabolic products of the fungicide that may
remain in food grains, vegetables and fruits after they are applied to crops.
The amount of initially laid down pesticide after application on the surface or substrate is
termed as deposit while the amount of pesticide left over after a lapse of time may be
referred as residue.
It is expressed as parts per million (ppm).
 Persistence – Period for which the pesticide remain
unaltered.
 Deposit –Amount of initially laid down chemical after
application on the surface.
 Surface residue – Amount of insecticide that remain
on treated surface after a lapse of time.
 Cuticular residue - Residue found in the cuticular
region of plant.
 Harvest time residue - Residue found in the substrate
at the time of harvest
Related Terms
 Contamination of crop or animals
exposed to chemical in the environment
 Intentional use of pesticide for protection
of growing crops and stored products
 Unintentional exposure to pesticides
such as would occur in crops, grown in
soil treated previously or contaminated
by foliar treatment of other crops grown
earlier in the rotation.
How pesticide residue occur in agriculture commodities
REGULATION
 Each country adopts their own agricultural policies and Maximum Residue Limits (MRL)
and Acceptable Daily Intake (ADI).
 Some countries use the International Maximum Residue Limits - Codex Alimentarius to
define the residue limits; this was established by Food and Agriculture Organization of
the United Nations (FAO) and World Health Organization (WHO) in 1963 to develop
international food standards, guidelines codes of practices, and recommendation for food
safety.
 Currently the CODEX has 185 member countries.
Maximum Residue Limits (MRL)
 Maximum concentration of a residue that is legally permitted or recognized as acceptable
in or on, a food, agricultural commodity or animal feedstuff as set by codex or national
regulatory authority (mg/kg).
Acceptable Daily Intake (ADI)
 Estimate of the amount of pesticide in food and drinking water which can be ingested
daily over a life time by humans without appreciable health risk(mg/kg body weight/day).
Maximum Residue Limits (MRL) in India
Central Codex committee of Food Standards
(The Prevention of Food Adulteration Act, 1954)
Sr. No. Pesticides Food MRL (mg/kg)
1 Dithiocarbamates Tomatoes 3.0
2
Benomyl
Mango 2.0
Other fruits 1.0
Vegetables 0.50
3 Captafol Tomato 5.0
4 Copper oxychloride Fruits and vegetables 20
5
Carbendazim
Mango 2.0
Banana 1.0
Other fruits 5.0
Dry Fruits 0.01
Vegetables 0.50
6 Hexaconazole Apple 0.1
7 Dodine Apple 5.0
Maximum Residue Limits (MRL) in India
Central Codex committee of Food Standards
(The Prevention of Food Adulteration Act, 1954)
Sr. No. Pesticides Food MRL (mg/kg)
8 Penconazole Grapes 0.2
9 Myclobutanil Grapes 1.0
10 Chlorothalonil Potato 0.1
11 Propiconazole Wheat 0.05
12 Captan Fruits and vegetables 15.0
13 Mancozeb Chillies 1.0
14 Tricyclazole Rice 0.02
Toxic effects of pesticide residues on human health
 Toxic effects of pesticides depend upon their toxicological properties, the level of residues and
degree of exposure of human beings to residues.
 The presence of pesticide residues in grains does not necessarily mean that it is hazardous.
 To be toxic, the residues have to be present in quantities large enough to be considered unsafe.
 The organophosphate, organochlorine and related pesticides act by binding to the enzyme
acetylcholinesterase, disrupting nerve function, resulting in paralysis and may cause death.
 They may produce acute effects manifesting as meiosis, urination, diarrhea, diaphoresis,
lacrimation, excitation of central nervous system and salivation
 Specific effects of pesticides can include damage to the central and peripheral nervous systems,
cancer, allergies and hypersensitivities, reproductive disorders and disruption of the immune
system
1. Neuronal damage due to cholinergic neuronal excitotoxicity and dysfunction
 Following exposure to organophosphates,
accumulation of acetylcholine at synapses
results in rapid and profound excitotoxicity
and dysfunction of cholinergic neurons in
the brain.
 Overstimulation of muscarinic
acetylcholine receptors may also disrupt
the balance of excitatory and inhibitory
mechanisms to cause neuronal excitotoxic
lesions leading to seizures and respiratory
depression.
 Secondary neuronal damage is an indirect consequence of the initial lesion and a major
contributor to the ultimate neuronal cell death and neural loss in the injured brain
leading to serious neuropsychiatric impairments, including memory loss, inability to
concentrate, speech problems, motor and sensory deficits, and behavioural problems
2. Long-term neuropsychiatric and neurological disorders
 Exposure to organophosphates involve
damage to cholinergic neurons of basal
forebrain and the limbic system, which may
cause memory, cognitive, mental, emotional,
motor and sensory deficits by disrupting this
putative sensory-limbic gating mechanism.
 In 1991, US soldiers were exposed to sarin
and cyclosarin when two large chemical
ammunition caches were destroyed at
Khamisiyah, Iraq during the Gulf War. The
Gulf War-deployed veterans exposed to sarin
 Memory and cognitive deficits are one of the most
common and persistent behavioral sequelae in
victims exposed to organophosphates.
 Exposure to organophosphatessarin and cyclosarin
at Khamisiyah resulted in long-term cognitive and
memory impairments in the Gulf War-deployed
veterans in 1991. Chronic memory and cognitive
impairments were also observed in the victims of
the Tokyo subway sarin attack.
 Loss of cholinergic neurons in the basal forebrain
with aging results in a decline in cognitive capacity
3. Persistent memory and cognitive deficits
Clinical study has demonstrated that the Gulf War-
deployed veterans exposed to sarin and cyclosarin at
Khamisiyah suffered impaired fine psychomotor
dexterity, reduced visuospatial abilities and deficits in
motor function and coordination.
After the Tokyo subway sarin attack, a chronic decline
of psychomotor function existed in 23 subway workers
exposed to sarin for 7 years.
The high-exposure subway workers had a significantly
slower performance of the finger tapping tests of both
the dominant and non-dominant hands than control
group.
4. Psychomotor performance deficits and somatic complaints
 In another clinical study, most of the victims of the Tokyo subway sarin attack were
found to have long-lasting somatic complaints (such as gastrointestinal problems,
constipation, heartburn, nausea, vomiting, colitis, migraines, headaches, backaches,
and skin disorders) at 5 - 6 years after poisoning.
 The long lasting somatic complaints and decreased psychomotor function of the
victims exposed to organophosphates may be associated with neuronal damage in the
cortex and thalamus
5. Oxidative stress
 In sub chronic or chronic
organophosphate exposition
induction of oxidative stress has
been reported as the main
mechanism of organophosphate
toxicity.
 Oxidative stress is induced in
both acute and chronic
intoxication with
organophosphate compounds in
humans and experimental
animals.
 Hyperglycaemia is one of the mechanism of oxidative
stress in organophosphate intoxication. Studies on chronic
exposure to carbamate insecticides and case reports of
long-term exposure give equivocal results.
 An extensive survey of the toxicology of the common
insecticide, carbaryl, reports a variety of reversible
neurobehavioral and neurotoxic effects in vertebrates, all
associated with acute poisoning symptoms.
 The carbamate, carbofuran, has been observed to
accentuate oxidative stress in rat brain by inducing lipid
peroxidation and diminishing the antioxidant defense.
 The studies on cancer analyze the risks associated with the
consumption of specific products which have some pesticide
residues.
 These consumption products include fish, water, seafood, and
milk or other dairy products. In general, these studies find a
small but statistically significant association between cancer
risks and some specific pesticide residues, such as
dichlorodiphenyltrichloroethane and
dichlorodiphenyltrichloroethane.
 Specifically polychlorinated biphenyls present a higher risk for
consumers.
 Organochlorine pesticide residue levels were reported
significantly higher in the cancer patients.
6. Development of cancer
7. Reproductive disorders
Results indicated that increase of insecticides in blood level in vertebrates causes
reproductive dysfunction and suggested that for human beings food like fish, chick and goat
containing beyond permissible limit of insecticides must be avoided.
Consumption of high pesticide residue fruits and vegetables was associated with lower total
sperm count, ejaculate volume and percentage of morphologically normal sperm among
men attending a fertility clinic.
Pesticides exposure may lead to reduced fertility, early and late pregnancy loss, prolonged
time-to-pregnancy, spontaneous abortion, and premature birth in female and genetic
alterations in sperm, reduced sperm count, damage to germinal epithelium and altered
hormone function in male.
Thank You…….

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FUNGICIDE RESIDUE AND HEALTH HAZARDS.pptx

  • 1. FUNGICIDE RESIDUE AND HEALTH HAZARDS Submitted by, Ranapratap A. Raut Ph. D. (1st Year) Department of Plant Pathology, N. M. College of Agriculture, NAU, Navsari (Gujrat)
  • 2.  Pesticides have consistently revealed their worth through increased agriculture productivity, reduced insect- borne, endemic diseases and protection as well as restoration of plantations, forests, harvested wood products, homes and fiber.  Currently, pesticides are very valuable in developing nations, particularly those in tropical are as looking for an entry in the global economy by providing off-season fresh vegetables and fruits to nations in more temperate weathers.  However, these goals cannot be achieved without the increased use of pesticides, mainly insecticides, herbicides and fungicides.  The increased use of chemical pesticides has resulted in contamination of the environment and also caused many associated long-term effects on human health.  Pesticides have been associated with a wide spectrum of human health hazards, ranging from short-term impacts such as headaches and nausea to chronic impacts like cancer, reproductive harm and endocrine disruption
  • 3. Fungicide  A fungicide is a specific type of pesticide that controls fungal disease by specifically inhibiting or killing the fungus causing the disease. Fungicide residue  Fungicide residue refers to the fungicide or metabolic products of the fungicide that may remain in food grains, vegetables and fruits after they are applied to crops. The amount of initially laid down pesticide after application on the surface or substrate is termed as deposit while the amount of pesticide left over after a lapse of time may be referred as residue. It is expressed as parts per million (ppm).
  • 4.  Persistence – Period for which the pesticide remain unaltered.  Deposit –Amount of initially laid down chemical after application on the surface.  Surface residue – Amount of insecticide that remain on treated surface after a lapse of time.  Cuticular residue - Residue found in the cuticular region of plant.  Harvest time residue - Residue found in the substrate at the time of harvest Related Terms
  • 5.  Contamination of crop or animals exposed to chemical in the environment  Intentional use of pesticide for protection of growing crops and stored products  Unintentional exposure to pesticides such as would occur in crops, grown in soil treated previously or contaminated by foliar treatment of other crops grown earlier in the rotation. How pesticide residue occur in agriculture commodities
  • 6. REGULATION  Each country adopts their own agricultural policies and Maximum Residue Limits (MRL) and Acceptable Daily Intake (ADI).  Some countries use the International Maximum Residue Limits - Codex Alimentarius to define the residue limits; this was established by Food and Agriculture Organization of the United Nations (FAO) and World Health Organization (WHO) in 1963 to develop international food standards, guidelines codes of practices, and recommendation for food safety.  Currently the CODEX has 185 member countries.
  • 7. Maximum Residue Limits (MRL)  Maximum concentration of a residue that is legally permitted or recognized as acceptable in or on, a food, agricultural commodity or animal feedstuff as set by codex or national regulatory authority (mg/kg). Acceptable Daily Intake (ADI)  Estimate of the amount of pesticide in food and drinking water which can be ingested daily over a life time by humans without appreciable health risk(mg/kg body weight/day).
  • 8. Maximum Residue Limits (MRL) in India Central Codex committee of Food Standards (The Prevention of Food Adulteration Act, 1954) Sr. No. Pesticides Food MRL (mg/kg) 1 Dithiocarbamates Tomatoes 3.0 2 Benomyl Mango 2.0 Other fruits 1.0 Vegetables 0.50 3 Captafol Tomato 5.0 4 Copper oxychloride Fruits and vegetables 20 5 Carbendazim Mango 2.0 Banana 1.0 Other fruits 5.0 Dry Fruits 0.01 Vegetables 0.50 6 Hexaconazole Apple 0.1 7 Dodine Apple 5.0
  • 9. Maximum Residue Limits (MRL) in India Central Codex committee of Food Standards (The Prevention of Food Adulteration Act, 1954) Sr. No. Pesticides Food MRL (mg/kg) 8 Penconazole Grapes 0.2 9 Myclobutanil Grapes 1.0 10 Chlorothalonil Potato 0.1 11 Propiconazole Wheat 0.05 12 Captan Fruits and vegetables 15.0 13 Mancozeb Chillies 1.0 14 Tricyclazole Rice 0.02
  • 10. Toxic effects of pesticide residues on human health  Toxic effects of pesticides depend upon their toxicological properties, the level of residues and degree of exposure of human beings to residues.  The presence of pesticide residues in grains does not necessarily mean that it is hazardous.  To be toxic, the residues have to be present in quantities large enough to be considered unsafe.  The organophosphate, organochlorine and related pesticides act by binding to the enzyme acetylcholinesterase, disrupting nerve function, resulting in paralysis and may cause death.  They may produce acute effects manifesting as meiosis, urination, diarrhea, diaphoresis, lacrimation, excitation of central nervous system and salivation  Specific effects of pesticides can include damage to the central and peripheral nervous systems, cancer, allergies and hypersensitivities, reproductive disorders and disruption of the immune system
  • 11. 1. Neuronal damage due to cholinergic neuronal excitotoxicity and dysfunction  Following exposure to organophosphates, accumulation of acetylcholine at synapses results in rapid and profound excitotoxicity and dysfunction of cholinergic neurons in the brain.  Overstimulation of muscarinic acetylcholine receptors may also disrupt the balance of excitatory and inhibitory mechanisms to cause neuronal excitotoxic lesions leading to seizures and respiratory depression.
  • 12.  Secondary neuronal damage is an indirect consequence of the initial lesion and a major contributor to the ultimate neuronal cell death and neural loss in the injured brain leading to serious neuropsychiatric impairments, including memory loss, inability to concentrate, speech problems, motor and sensory deficits, and behavioural problems
  • 13. 2. Long-term neuropsychiatric and neurological disorders  Exposure to organophosphates involve damage to cholinergic neurons of basal forebrain and the limbic system, which may cause memory, cognitive, mental, emotional, motor and sensory deficits by disrupting this putative sensory-limbic gating mechanism.  In 1991, US soldiers were exposed to sarin and cyclosarin when two large chemical ammunition caches were destroyed at Khamisiyah, Iraq during the Gulf War. The Gulf War-deployed veterans exposed to sarin
  • 14.  Memory and cognitive deficits are one of the most common and persistent behavioral sequelae in victims exposed to organophosphates.  Exposure to organophosphatessarin and cyclosarin at Khamisiyah resulted in long-term cognitive and memory impairments in the Gulf War-deployed veterans in 1991. Chronic memory and cognitive impairments were also observed in the victims of the Tokyo subway sarin attack.  Loss of cholinergic neurons in the basal forebrain with aging results in a decline in cognitive capacity 3. Persistent memory and cognitive deficits
  • 15. Clinical study has demonstrated that the Gulf War- deployed veterans exposed to sarin and cyclosarin at Khamisiyah suffered impaired fine psychomotor dexterity, reduced visuospatial abilities and deficits in motor function and coordination. After the Tokyo subway sarin attack, a chronic decline of psychomotor function existed in 23 subway workers exposed to sarin for 7 years. The high-exposure subway workers had a significantly slower performance of the finger tapping tests of both the dominant and non-dominant hands than control group. 4. Psychomotor performance deficits and somatic complaints
  • 16.  In another clinical study, most of the victims of the Tokyo subway sarin attack were found to have long-lasting somatic complaints (such as gastrointestinal problems, constipation, heartburn, nausea, vomiting, colitis, migraines, headaches, backaches, and skin disorders) at 5 - 6 years after poisoning.  The long lasting somatic complaints and decreased psychomotor function of the victims exposed to organophosphates may be associated with neuronal damage in the cortex and thalamus
  • 17. 5. Oxidative stress  In sub chronic or chronic organophosphate exposition induction of oxidative stress has been reported as the main mechanism of organophosphate toxicity.  Oxidative stress is induced in both acute and chronic intoxication with organophosphate compounds in humans and experimental animals.
  • 18.  Hyperglycaemia is one of the mechanism of oxidative stress in organophosphate intoxication. Studies on chronic exposure to carbamate insecticides and case reports of long-term exposure give equivocal results.  An extensive survey of the toxicology of the common insecticide, carbaryl, reports a variety of reversible neurobehavioral and neurotoxic effects in vertebrates, all associated with acute poisoning symptoms.  The carbamate, carbofuran, has been observed to accentuate oxidative stress in rat brain by inducing lipid peroxidation and diminishing the antioxidant defense.
  • 19.  The studies on cancer analyze the risks associated with the consumption of specific products which have some pesticide residues.  These consumption products include fish, water, seafood, and milk or other dairy products. In general, these studies find a small but statistically significant association between cancer risks and some specific pesticide residues, such as dichlorodiphenyltrichloroethane and dichlorodiphenyltrichloroethane.  Specifically polychlorinated biphenyls present a higher risk for consumers.  Organochlorine pesticide residue levels were reported significantly higher in the cancer patients. 6. Development of cancer
  • 20. 7. Reproductive disorders Results indicated that increase of insecticides in blood level in vertebrates causes reproductive dysfunction and suggested that for human beings food like fish, chick and goat containing beyond permissible limit of insecticides must be avoided. Consumption of high pesticide residue fruits and vegetables was associated with lower total sperm count, ejaculate volume and percentage of morphologically normal sperm among men attending a fertility clinic. Pesticides exposure may lead to reduced fertility, early and late pregnancy loss, prolonged time-to-pregnancy, spontaneous abortion, and premature birth in female and genetic alterations in sperm, reduced sperm count, damage to germinal epithelium and altered hormone function in male.