**6. Pesticide residues in food, water and air**

#### **6.1 Pesticide residues**

'Pesticide residue' means any specified substance in food, agricultural commodities, or animal feed resulting from the use of pesticides. The term also includes any derivatives of a pesticide, such as conversion products, metabolites, reaction products, and impurities considered to be toxic. Application of pesticides during the production or storage of agricultural commodities result in pesticide residues in food (fruits, vegetables, grain, meat, etc). Pesticide residues are also found in the drinking water. Pesticide residues can build up to harmful levels through bioaccumulation and bio-magnification within the food chain.

WHO, in collaboration with FAO performs pesticide risk assessment to humans, both through direct exposure and through residues in food. The WHO core assessment group on pesticide residues review toxicological data and establish the acceptable daily intakes (ADIs) and acute reference doses (ARfDs) of pesticide residues for different commodities through a lifetime of food consumption. The ADIs are amount of pesticide residues which will not result in adverse health effects. Codex

**63**

WHO [8].

included in the EPA list [11].

*Pesticides and Human Health*

*DOI: http://dx.doi.org/10.5772/intechopen.93806*

agricultural purpose, e.g. DDT, Aldrin, etc.

**6.2 Pesticide residues in food, water and air**

pounds can be independent, additive or synergistic.

**7. Impacts of pesticide use on human health**

**7.1 Acute health effects of pesticide exposure**

Alimentarius Commission (the intergovernmental standards-setting body for food) establishes maximum residue limits (MRLs) for pesticides in food based on ADIs. The MRL depends on the crop it is used on, and the same pesticide active ingredient may have different MRL values when used on different crops. Extraneous maximum residue limit (EMRL) refers to the maximum permitted limit of residues of mostly POP pesticides, which were previously used as pesticides but not registered any more, and residues arising from environmental contamination (including previous agricultural use) or residues from uses of these pesticides other than for

There are several reports of pesticide residues detected on food exceeding the MRL values. For example, in India, vegetable samples were tested for the presence of OC, OP and pyrethroid insecticides, and 15.3% samples exceeded the MRL. In two Brazilian pesticide residue monitoring programs less than 3% of the samples had residue levels above the MRL. Pesticide residues were detected in 34% of samples of cereal grains collected throughout Poland and 3% samples contained residues over the maximum limit. A study from Maule Region (Talca, Chile) found pesticide residues on the fruits and vegetables schoolchildren brought as snack [5]. The pesticide residues detected in fruits and vegetables from Lithuania had multiple pesticides; 9 residues in grapes and tea, 5-9 residues in orange, mandarins, lemons, peaches, pears and 3-5 residues in pomegranates, plums, cucumbers, tomatoes and strawberries, and found that 2.6% samples exceeded the MRL values [6]. In a European Union study 14–23% of the samples had detectable residues of more than one active ingredient where 3.0–5.5% samples had residues levels above the MRL [7]. Exposure to multiple pesticide residues could be due to intake from a single food item containing multiple residues or from several food items each containing one or more residues. The combined toxic effects of two or more com-

Both recreational and medicinal cannabis samples contained high levels of residual pesticides and pesticides not legally allowed to be used on cannabis products in Oregon. Medicinal cannabis products were found to have mean levels of residual pesticides that were 3-12 times higher than recreational products, and 9 of the 50 pesticides identified were classified highly or extremely hazardous by the

Pesticide residues have been found in surface, groundwater and potable water samples from India [9]. Pesticide residues levels in river water and in drinking water samples in Turkey were significantly high compared with guideline values set by Turkey, EU and WHO as hazardous to human health [10]. Higher concentrations of pesticides in ambient air were recorded from potato farm sites in Prince Edward Island, Canada, Taihu Lake region of China and Kaweah Reservoir, CA, USA. A total of 87 pesticides were identified in the household dust samples from the rural Yakima Valley of Washington state, 47 of these have evidence of neurotoxicity

The short-term acute adverse effects pesticide exposure on human health are stinging eyes, rashes, blisters, skin irritations, blindness, nausea, dizziness, diarrhea

#### *Pesticides and Human Health DOI: http://dx.doi.org/10.5772/intechopen.93806*

*Emerging Contaminants*

Fungicides inhibit fungal growth by interfering with critical cellular processes. Fungicide resistance action committee (FRAC) classify fungicides and bactericides into 50 groups based on the site of action. Within each group, there are target sites, which are the specific enzymes to which the fungicides bind. The different known target sites include nucleic acids metabolism, cytoskeleton and motor protein, respiration, amino acids and protein synthesis, signal transduction, lipid synthesis or transport/membrane integrity or function, sterol biosynthesis in membranes, cell wall biosynthesis, melanin synthesis in cell wall and host plant defense induction. Some fungicides and herbicides are considered endocrine disrupting pesticides.

Herbicides are pesticides that inhibit or interrupt normal plant growth and development. Herbicides are widely used in agriculture, landscape industry, and non-crop areas for weed management. Herbicides resistance action committee (HRAC) has classified herbicides into 27 groups. These include: growth regulators (synthetic auxins; auxin transport inhibitors), seedling growth inhibitors, photosynthetic inhibitors, amino acid synthesis inhibitors, lipid synthesis inhibitors, cell

Growth regulator herbicides consist of the synthetic auxin and auxin transport

inhibitory compounds and the most commonly used synthetic auxins include 2,4-*Dichlorophenoxyacetic acid* (2,4-D)*,* fluroxypyr, dicamba, quinclorac, dichlorprop, MCPA (2-methyl-4-chlorophenoxyacetic acid), mecoprop and picloram. These are commonly used systemic herbicides which mimic the plant growth hormone auxin (indole acetic acid) [4]. Some of these synthetic auxin herbicides disrupt human hormonal system. Atrazine is also a commonly used photosynthetic inhibitor herbicide. Glyphosate (Roundup) is an amino acid derivative and inhibits synthase of EPSPS enzyme, which is involved in the synthesis of the aromatic amino acids (tyrosine, tryptophan, and phenylalanine). Paraquat (gramoxone) is an electron diverter, and as a respiratory inhibitor can be a significant risk to

'Pesticide residue' means any specified substance in food, agricultural commodities, or animal feed resulting from the use of pesticides. The term also includes any derivatives of a pesticide, such as conversion products, metabolites, reaction products, and impurities considered to be toxic. Application of pesticides during the production or storage of agricultural commodities result in pesticide residues in food (fruits, vegetables, grain, meat, etc). Pesticide residues are also found in the drinking water. Pesticide residues can build up to harmful levels through bio-

WHO, in collaboration with FAO performs pesticide risk assessment to humans, both through direct exposure and through residues in food. The WHO core assessment group on pesticide residues review toxicological data and establish the acceptable daily intakes (ADIs) and acute reference doses (ARfDs) of pesticide residues for different commodities through a lifetime of food consumption. The ADIs are amount of pesticide residues which will not result in adverse health effects. Codex

**5.2 Fungicides**

**5.3 Herbicides**

membrane disrupters, pigment inhibitors.

humans if inhaled or ingested.

**6.1 Pesticide residues**

**6. Pesticide residues in food, water and air**

accumulation and bio-magnification within the food chain.

**62**

Alimentarius Commission (the intergovernmental standards-setting body for food) establishes maximum residue limits (MRLs) for pesticides in food based on ADIs.

The MRL depends on the crop it is used on, and the same pesticide active ingredient may have different MRL values when used on different crops. Extraneous maximum residue limit (EMRL) refers to the maximum permitted limit of residues of mostly POP pesticides, which were previously used as pesticides but not registered any more, and residues arising from environmental contamination (including previous agricultural use) or residues from uses of these pesticides other than for agricultural purpose, e.g. DDT, Aldrin, etc.

#### **6.2 Pesticide residues in food, water and air**

There are several reports of pesticide residues detected on food exceeding the MRL values. For example, in India, vegetable samples were tested for the presence of OC, OP and pyrethroid insecticides, and 15.3% samples exceeded the MRL. In two Brazilian pesticide residue monitoring programs less than 3% of the samples had residue levels above the MRL. Pesticide residues were detected in 34% of samples of cereal grains collected throughout Poland and 3% samples contained residues over the maximum limit. A study from Maule Region (Talca, Chile) found pesticide residues on the fruits and vegetables schoolchildren brought as snack [5].

The pesticide residues detected in fruits and vegetables from Lithuania had multiple pesticides; 9 residues in grapes and tea, 5-9 residues in orange, mandarins, lemons, peaches, pears and 3-5 residues in pomegranates, plums, cucumbers, tomatoes and strawberries, and found that 2.6% samples exceeded the MRL values [6]. In a European Union study 14–23% of the samples had detectable residues of more than one active ingredient where 3.0–5.5% samples had residues levels above the MRL [7]. Exposure to multiple pesticide residues could be due to intake from a single food item containing multiple residues or from several food items each containing one or more residues. The combined toxic effects of two or more compounds can be independent, additive or synergistic.

Both recreational and medicinal cannabis samples contained high levels of residual pesticides and pesticides not legally allowed to be used on cannabis products in Oregon. Medicinal cannabis products were found to have mean levels of residual pesticides that were 3-12 times higher than recreational products, and 9 of the 50 pesticides identified were classified highly or extremely hazardous by the WHO [8].

Pesticide residues have been found in surface, groundwater and potable water samples from India [9]. Pesticide residues levels in river water and in drinking water samples in Turkey were significantly high compared with guideline values set by Turkey, EU and WHO as hazardous to human health [10]. Higher concentrations of pesticides in ambient air were recorded from potato farm sites in Prince Edward Island, Canada, Taihu Lake region of China and Kaweah Reservoir, CA, USA. A total of 87 pesticides were identified in the household dust samples from the rural Yakima Valley of Washington state, 47 of these have evidence of neurotoxicity included in the EPA list [11].

### **7. Impacts of pesticide use on human health**

#### **7.1 Acute health effects of pesticide exposure**

The short-term acute adverse effects pesticide exposure on human health are stinging eyes, rashes, blisters, skin irritations, blindness, nausea, dizziness, diarrhea and death. Exposure to pesticides in agricultural work can cause serious risks to the respiratory system causing chronic cough, dyspnea, wheezing and expectoration, decreased lung capacity, asthma, and bronchitis. These respiratory problems were found in workers in flower crops in Ethiopia, coffee plantations in Brazil and banana plantations in Costa Rica. In banana farming in Rio Grande do Norte (Brazil), the use of pesticides was related to the symptoms of burning in the throat and lungs, airway congestion, cramps, skin peeling, diarrhea, headache, chest pain, weakness, cough and skin irritation.

In banana production region of the Ribeira Valley (Brazil), workers (majority males, low schooling, mean age 39.6 years and 13.8 years of working time) had moderate obstructive disorder (10.0%) and mild obstructive disorder (13.3%) with decreased FEV1 (forced expiratory volume in 1 second) and FEV1/FVC (the ratio between forced expiratory volume in the first second and forced vital capacity and is very important for the detection of obstructive disorders). Similarly, exposures to mixtures (pollutants and pesticides) in children with asthma in California were also associated with reduced lung function measures FEV1 and FVC [12].

Many studies have found positive associations with pesticide exposure and children's respiratory and allergic effects such as asthma, wheezing, coughs, acute respiratory infections, hay fever, rhinitis, eczema, chronic phlegm, and lung function impairments. A study of school-age children with asthma in the agricultural community of Yakima Valley (Washington State) found that increase in exposures to OP insecticides was related with increase in LTE4 levels which was associated with a higher risk of asthma morbidity [13]. The neonicotinoid insecticides (e.g. imidacloprid, nitenpyram) are nicotinic receptors agonists and their exposure cause nausea, vomiting, muscle weakness, respiratory effects, headache, lethargy, and tachycardia.

#### **7.2 Chronic effects of pesticide exposure**

The long-term chronic adverse effects of pesticides exposure are cancers, birth defects, reproductive harm, neurological and developmental toxicity, immunotoxicity, and disruption of the endocrine system. The chronic effects of pesticides on human can be categorized into three major groups; neurotoxic effects, genotoxic and carcinogenic effects, and reproductive effects.

#### *7.2.1 Neurotoxic effects*

Neurotoxicity can be defined as any adverse effect on the central or peripheral nervous system caused by chemical, biological or physical agents. A developing nervous system in children (during replication, migration, differentiation, myelination of neurons, and synapse formation) is more susceptible to neurotoxic chemicals including pesticides. Chemicals (pesticides) can cause neuronal cell death by disruption of the cytoskeleton, induction of oxidative stress, calcium overload, or by damaging mitochondria. Most of the synthetic insecticides, some fungicides and herbicides, currently in use are neurotoxicants.

Pesticide molecules are small and lipophilic in nature, and can enter from blood to brain and then in neurons, glial cells and brain micro vessels. Pesticides can disrupt blood-brain barrier receptors in the central nervous system which enhance chronic toxicity and affect the receptor-mediated transcytosis. Neuronal cells are more susceptible to oxidative stress due to their high polyunsaturated fat content in the myelin sheaths, low anti-oxidative capabilities, enzymatic systems with transient metals that aid in the production of free radicals, and demand for high oxygen and glucose metabolism rate.

**65**

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impairment.

psychomotricity.

cause cognitive impairment.

*DOI: http://dx.doi.org/10.5772/intechopen.93806*

OPs and carbamates bind to and phosphorylate/carbamalate the AChE which causes accumulation of acetylcholine at cholinergic synapses causing overstimulation of muscarinic and nicotinic cholinergic receptors. Neuropsychiatric disorders, such as anxiety and depression, are observed in patients with acute and long-term poisoning from OPs. OPs may also cause an intermediate syndrome and OP-induced delayed polyneuropathy (OPIDP) 1-3 weeks after a single exposure. In carbamates, the AChE inhibition is reversible and acute intoxication is generally resolved within a few hours. The OP insecticides can disturb the function of mitochondria by inducing oxidative stress in central nervous system through critical depletion of mitochondrial energy, the activation of proteolytic enzymes, and DNA fragmentation leading to apoptosis. The dysfunction of mitochondria and oxidative stress is responsible for several neurological diseases, including Parkinson's disease, seizure, cognitive dysfunction, attention and memory deficits, dementia, depression, and Alzheimer's disease. OP triggered induction of a xanthine oxidase may play a role in cognitive

In a study, increased inhibition of cholinesterase enzyme with increased exposure to OP insecticides was confirmed in both occupationally exposed (OE) and environmentally exposed (EE) groups of people. The OP exposure, mainly in the EE group, was associated with a diminished neuropsychological performance; general mental status, language, memory, attention, executive function, praxis and

Acute poisoning due to exposure to OP (particularly chlorpyrifos) was reported with higher prevalence of peripheral polyneuropathy, and deterioration of cognitive functions (verbal fluency, and visual and auditory memory) was observed in agricultural workers and in inhabitants of rural agricultural areas. Exposure to OP insecticides in rural schoolchildren was associated with a lower processing speed in

Exposure to type I pyrethroids cause tremor syndrome (behavioral arousal, aggressive sparring, increased startle response, and fine body tremor progressing to whole-body tremor, and prostration) while type II pyrethroids exposure cause salivation syndrome (profuse salivation, coarse tremor progressing to choreoatetosis, and clonic seizure). The poisoned cerebral cortex affect learning, memory, emotions, and movement. Pyrethroids exposure has been positively associated with hearing loss in U.S. adolescents. Pyrethroids exposure induced Tau protein malfunction which may be the mechanism underlying cognitive impairment. Paraquat, triazine and pyrazole (herbicides) through oxidative stress, raised influx of calcium and the stimulation of nitrogen oxide species, and aggravated Aβ amyloidogenesis

Exposure to endocrine disrupting chemicals (EDCs) including many pesticides can disrupt maternal thyroid imbalance which can result in permanent and lifelong neurodevelopmental consequences for their children, including attention-deficit disorder, autism spectrum disorder, and cognitive and behavioral dysfunction. Workers of fruit and seed export companies in a rural area of Santiago exposed to methyl bromide (CH3Br, a fumigant) had increased concentration of CH3Br in blood after application which resulted in a higher frequency of insomnia, headaches, paresthesias, mood swings, memory loss, and decreased concentration [14]. Parkinson's disease (PD) is characterized by progressive degeneration of dopaminergic neurons of the nigrostriatal pathway and the formation of alpha-synuclein (α-syn)-containing Lewy bodies. Dieldrin (OC) is selectively toxic to dopaminergic cells, disrupts striatal dopamine activity, and may promote α-syn aggregation while ziram (dithiocarbamate fungicide) increases the probability of synaptic vesicle release by dysregulation of the ubiquitin signaling system and increases excitability

children and an IQ lower than expected for their age.

in both aminergic and glutamatergic neurons leading to PD.

#### *Pesticides and Human Health DOI: http://dx.doi.org/10.5772/intechopen.93806*

*Emerging Contaminants*

tachycardia.

*7.2.1 Neurotoxic effects*

and glucose metabolism rate.

weakness, cough and skin irritation.

**7.2 Chronic effects of pesticide exposure**

and carcinogenic effects, and reproductive effects.

herbicides, currently in use are neurotoxicants.

and death. Exposure to pesticides in agricultural work can cause serious risks to the respiratory system causing chronic cough, dyspnea, wheezing and expectoration, decreased lung capacity, asthma, and bronchitis. These respiratory problems were found in workers in flower crops in Ethiopia, coffee plantations in Brazil and banana plantations in Costa Rica. In banana farming in Rio Grande do Norte (Brazil), the use of pesticides was related to the symptoms of burning in the throat and lungs, airway congestion, cramps, skin peeling, diarrhea, headache, chest pain,

In banana production region of the Ribeira Valley (Brazil), workers (majority males, low schooling, mean age 39.6 years and 13.8 years of working time) had moderate obstructive disorder (10.0%) and mild obstructive disorder (13.3%) with decreased FEV1 (forced expiratory volume in 1 second) and FEV1/FVC (the ratio between forced expiratory volume in the first second and forced vital capacity and is very important for the detection of obstructive disorders). Similarly, exposures to mixtures (pollutants and pesticides) in children with asthma in California were also

Many studies have found positive associations with pesticide exposure and children's respiratory and allergic effects such as asthma, wheezing, coughs, acute respiratory infections, hay fever, rhinitis, eczema, chronic phlegm, and lung function impairments. A study of school-age children with asthma in the agricultural community of Yakima Valley (Washington State) found that increase in exposures to OP insecticides was related with increase in LTE4 levels which was associated with a higher risk of asthma morbidity [13]. The neonicotinoid insecticides (e.g. imidacloprid, nitenpyram) are nicotinic receptors agonists and their exposure cause nausea, vomiting, muscle weakness, respiratory effects, headache, lethargy, and

The long-term chronic adverse effects of pesticides exposure are cancers, birth defects, reproductive harm, neurological and developmental toxicity, immunotoxicity, and disruption of the endocrine system. The chronic effects of pesticides on human can be categorized into three major groups; neurotoxic effects, genotoxic

Neurotoxicity can be defined as any adverse effect on the central or peripheral nervous system caused by chemical, biological or physical agents. A developing nervous system in children (during replication, migration, differentiation, myelination of neurons, and synapse formation) is more susceptible to neurotoxic chemicals including pesticides. Chemicals (pesticides) can cause neuronal cell death by disruption of the cytoskeleton, induction of oxidative stress, calcium overload, or by damaging mitochondria. Most of the synthetic insecticides, some fungicides and

Pesticide molecules are small and lipophilic in nature, and can enter from blood

to brain and then in neurons, glial cells and brain micro vessels. Pesticides can disrupt blood-brain barrier receptors in the central nervous system which enhance chronic toxicity and affect the receptor-mediated transcytosis. Neuronal cells are more susceptible to oxidative stress due to their high polyunsaturated fat content in the myelin sheaths, low anti-oxidative capabilities, enzymatic systems with transient metals that aid in the production of free radicals, and demand for high oxygen

associated with reduced lung function measures FEV1 and FVC [12].

**64**

OPs and carbamates bind to and phosphorylate/carbamalate the AChE which causes accumulation of acetylcholine at cholinergic synapses causing overstimulation of muscarinic and nicotinic cholinergic receptors. Neuropsychiatric disorders, such as anxiety and depression, are observed in patients with acute and long-term poisoning from OPs. OPs may also cause an intermediate syndrome and OP-induced delayed polyneuropathy (OPIDP) 1-3 weeks after a single exposure. In carbamates, the AChE inhibition is reversible and acute intoxication is generally resolved within a few hours.

The OP insecticides can disturb the function of mitochondria by inducing oxidative stress in central nervous system through critical depletion of mitochondrial energy, the activation of proteolytic enzymes, and DNA fragmentation leading to apoptosis. The dysfunction of mitochondria and oxidative stress is responsible for several neurological diseases, including Parkinson's disease, seizure, cognitive dysfunction, attention and memory deficits, dementia, depression, and Alzheimer's disease. OP triggered induction of a xanthine oxidase may play a role in cognitive impairment.

In a study, increased inhibition of cholinesterase enzyme with increased exposure to OP insecticides was confirmed in both occupationally exposed (OE) and environmentally exposed (EE) groups of people. The OP exposure, mainly in the EE group, was associated with a diminished neuropsychological performance; general mental status, language, memory, attention, executive function, praxis and psychomotricity.

Acute poisoning due to exposure to OP (particularly chlorpyrifos) was reported with higher prevalence of peripheral polyneuropathy, and deterioration of cognitive functions (verbal fluency, and visual and auditory memory) was observed in agricultural workers and in inhabitants of rural agricultural areas. Exposure to OP insecticides in rural schoolchildren was associated with a lower processing speed in children and an IQ lower than expected for their age.

Exposure to type I pyrethroids cause tremor syndrome (behavioral arousal, aggressive sparring, increased startle response, and fine body tremor progressing to whole-body tremor, and prostration) while type II pyrethroids exposure cause salivation syndrome (profuse salivation, coarse tremor progressing to choreoatetosis, and clonic seizure). The poisoned cerebral cortex affect learning, memory, emotions, and movement. Pyrethroids exposure has been positively associated with hearing loss in U.S. adolescents. Pyrethroids exposure induced Tau protein malfunction which may be the mechanism underlying cognitive impairment. Paraquat, triazine and pyrazole (herbicides) through oxidative stress, raised influx of calcium and the stimulation of nitrogen oxide species, and aggravated Aβ amyloidogenesis cause cognitive impairment.

Exposure to endocrine disrupting chemicals (EDCs) including many pesticides can disrupt maternal thyroid imbalance which can result in permanent and lifelong neurodevelopmental consequences for their children, including attention-deficit disorder, autism spectrum disorder, and cognitive and behavioral dysfunction. Workers of fruit and seed export companies in a rural area of Santiago exposed to methyl bromide (CH3Br, a fumigant) had increased concentration of CH3Br in blood after application which resulted in a higher frequency of insomnia, headaches, paresthesias, mood swings, memory loss, and decreased concentration [14].

Parkinson's disease (PD) is characterized by progressive degeneration of dopaminergic neurons of the nigrostriatal pathway and the formation of alpha-synuclein (α-syn)-containing Lewy bodies. Dieldrin (OC) is selectively toxic to dopaminergic cells, disrupts striatal dopamine activity, and may promote α-syn aggregation while ziram (dithiocarbamate fungicide) increases the probability of synaptic vesicle release by dysregulation of the ubiquitin signaling system and increases excitability in both aminergic and glutamatergic neurons leading to PD.

#### *7.2.2 Genotoxic and carcinogenic effects*

A genotoxic agent can be a physical, chemical or biological agent that can interact with the genetic material (DNA) causing alterations, damage or ruptures, and those that interfere with enzymatic processes of repair, genesis or polymerization of proteins involved in chromosome segregation. These alterations could lead to impaired embryonic development or be the initial steps in the development of cancer. Pesticides exposure can cause genomic damage. Genetic damage caused by pesticides is broadly classified into three classes; (i) Pre-mutagenic damage like DNA strand breaks and DNA adducts (ii) gene mutations like insertion, deletion, inversion and translocation (iii) chromosomal aberrations, including loss or gain of whole chromosome (aneuploidy), deletion or breaks (clastogenicity), and chromosomal rearrangements.

Farmers exposed to pesticide mixtures in Greece had possible clastogenic (chromosome breakage cause mutation) and aneugenic (abnormal number of chromosomes) effect of pesticides on the genetic material. DNA methylation changes in the placenta were significantly associated with the maternal plasma concentrations of OCs in early pregnancy causing prenatal toxicity. OPs affect DNA methylation, induce the AChE gene expression and activate the NMDA glutamate receptors resulting in calcium influx in the post-synaptic neurons leading to degeneration.

Genetic damage has been reported from exposure to malathion (OP), carbofuran (carbamate), triflumuron (Insect growth regulator), imidacloprid, acetamiprid and thiamethoxam (neonicotinoid insecticides), pentachlorophenol (OC), Emamectin benzoate (used in agriculture, household, and veterinary medicine), and tembotrione (novel post-emergence herbicide) (**Table 2**).

Cancer is characterized by an uncontrolled cell growth with limitless replication, resistance to apoptosis, alteration of growth factors (GFs), resistance to chemotherapy, metastasis and angiogenesis. Cancer develops as a result of multifactorial complex interactions of genetic and lifestyle factors including, diet, stress, physical and biological agents, infections, and exposure to the hazardous chemical substances. Pesticides exposure acts as a stimulant to cancer and chronic low-dose is considered one of the important risk factors for the increasing cancer incidence. **Table 3** presents a list of pesticides suggesting carcinogenicity in different types of studies.


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Non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL)

*DOI: http://dx.doi.org/10.5772/intechopen.93806*

MoC Nonachlor/

trans-nonachlor hexachlorobenzene

Diazinon

P,p′-DDE

Heptachlor

Malathion

Diazinon Dimethoate

Fluvalinate Bifenthrin Cyhalothrin Cypermethrin

Hexachlorobenzene

OC Mirex Case control

Breast OC Pp'-DDT Histopathology [22]

OP Chlorpyrifos MCF-7 breast cancer

Terbufos Case control/MCF-7/

PYR Flucythrinate AutoDock Vina 1.1.1 [27]

NEO Thiacloprid imidacloprid Hs578t cells [28] PTH Captan Agricultural health [29] GLY Glyphosate Case control [30]

**Type of cancer ToP Name of pesticide Type of study Reference**

OC P,p'-DDT Case control [15]

HCH Case control

Chlordane Case control Lindane Case control OP Malathion Case control [17]

P,p'-DDE Agricultural health [16]

Blood

Terbufos Case control [18] Dimethoate chlorpyrifos Agricultural health [15]

Mecoprop Epidemiological [20]

Pp'-DDD Histopathology [23]

β-HCH Histopathology [24]

cells

MCF-10F

[25]

[26]

PYR Permethrin Case control [16] NPYR Pyrethrum Agricultural health [17] PHE 2,4-D Case control [19]

CHL Dichlorprop Case control [21] BNZ Dicamba Case control [20] GLY Glyphosate Case control [16]

Agricultural health

#### **Table 2.** *Pesticides hazard classification by FAO.*

