On Human-beings

34 1.3.4. Based on their hazzard

At 2009, Classification the WHO (World Health Organization) Hazard Classes have been aligned in an appropriate way with the GHS (Globally Harmonized System of Classification and Labelling of Chemicals) Acute Toxicity Hazard Categories for acute oral or dermal toxicity as the starting point for allocating pesticides to a WHO Hazard Class. , the classification of some pesticides has been adjusted to take account of severe hazards to health other than acute toxicity [13].

Table 1.3 : GHS Classification of Pesticides by Hazard

GHS Category

Classification criteria

Oral Dermal

LD₅₀ (mg/kg bw)

Hazard Statement

LD₅₀ (mg/kg bw)

Hazard Statement

Category 1 < 5 Fatal if

swallowed < 50 Fatal in contact

with skin

Category 2 5 - 50 Fatal if

swallowed 50 - 200 Fatal in contact with skin

Category 3 50 - 300 Toxic if

swallowed 200 - 1000 Toxic in contact with skin Category 4 300 - 2000 Harmful if

swallowed 1000 - 2000 Harmful in contact with skin Category 5 2000 - 5000 May be harmful

if swallowed 2000 - 5000 May be harmful in contact with skin

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extermination of household pests, removal of lice, and garden and lawn treatments [29].

There are three main routes of exposure: oral, dermal, and inhalation.

Ingestion of food or water containing pesticides is oral exposure. Inhalation exposure can occur by breathing air containing pesticides as vapor, aerosol, or small particles. Dermal exposure occurs when the skin comes in contact with pesticides [29].

1.4.1.1 Acute toxicity

Most pesticide poisoning cases involve either organophosphate or carbamate insecticides. Both chemical groups affect humans by inhibiting acetyl cholinesterase, an enzyme essential to proper functioning of the nervous system.

Fungicides as a class are probably responsible for a disproportionate number of irritant injuries to skin and mucous membranes, as well as dermal sensitization, rather than frequent or severe systemic poisonings because many of them have low toxicity in mammals and are formulated as suspensions of wettable powders or granules and are inefficiently absorbed [29].

A large number of organochlorine insecticides (not more authorized in developed countries, but some of them still used in developing countries) are the active ingredients of various home and garden products and some agricultural and environmental pest control products. Other most hazardous compounds, such as DDT, aldrin, dieldrin, or heptachlor, are still environmental contaminants due to their high environmental persistence. The main target of acute toxic action of organochlorine pesticides is the nervous system, where these compounds induce a hyperexcitable state. Severe intoxication by these compounds causes myoclonic jerking movements, and then generalized tonic-clonic convulsions followed by coma and respiratory depression [29].

36 1.4.1.2 Long-Term Health Effects

1.4.1.2.1 Neurological effects

Findings from many epidemiological studies have provided support to the hypothesis that pesticide exposure may increase risk of Parkinson’s disease, a late onset progressive neurological disorder associated with selective degeneration of nigrostriatal dopaminergic neurons. Organochlorines, organophosphorus compounds, chlorophenoxy acids/esters, and botanicals have been identified as specific classes of pesticides posing a risk for the occurrence of Parkinson’s disease [29].

1.4.1.2.2 Carcinogenicity

Pesticides are currently classified by international agencies and committees for their potential carcinogenic properties on the basis of the available evidence from human (epidemiological) and experimental studies. Several agrochemical ingredients have been classified as potentially carcinogenic to humans. Some pesticides with sufficient or limited evidence of carcinogenicity such as chlordecone, DDT, pentachlorophenol, captafol, and aldicarb have been banned or their use has been restricted in some countries. These compounds are widespread environmental pollutants due to their bioaccumulation and persistence in nature. Residues of these pesticides have been detected in the food chain and in different biological media in humans. A large number of organophosphate pesticides are not classifiable as to their carcinogenicity to humans. Few pesticides belonging to the chemical families of carbamates or dithiocarbamates have been demonstrated as animal carcinogens. The principal hazard of these compounds is the presence of impurities and the metabolic and degradation products of thiocarbamates: the production of carcinogenic N-nitroso compounds by the reaction of many thio- and alkyl-carbamates, such as molinate, triallate, and butylate, with nitrite. As an example, N-nitrosocarbaryl, a derivative of carbaryl, is a potent carcinogen

37

in rats. Ethylene thiourea, a degradation product of ethylene bisdithiocarbamate fungicides, such as mancozeb, maneb, metiram, zineb, and others, is a potent thyroid carcinogen in rats, although it is not considered a human carcinogen. Captafol, a chloroalkyl compound widely used as fungicide, demonstrates a carcinogenic effect with sufficient evidence on multiple target organs in two rodent species [14].

1.4.1.2.3 Allergies

Allergic effects are harmful effects that some people develop in reaction to substances that do not cause the same reaction in the most other people.

Allergic reactions are not through to occur during a person’s first exposure to a substance. Later exposures result in the allergic response. This process is called sensitization, and substances that cause people to become allergic to them are known as sensitizers. Some people become allergic to pesticides.

Allergic effects to pesticides include: systemic effects, such as asthma or even life threatening shock, skin irritation, such as rush, blisters, or open sores, and eye and nose irritation, such as itchy, watery eyes and sneezing [15].

1.4.1.2.4 Endocrine System

Many chemicals that have been identified as endocrine disruptors are pesticides.

EDCs act mainly by interfering with natural hormones because of their strong potential to bind to estrogen or androgen receptors. In particular, EDCs can bind to and activate various hormone receptors and then mimic the natural hormone’s action (agonist action). EDCs may also bind to these receptors without activating them. This antagonist action blocks the receptors and inhibits their action. Finally, EDCs may also interfere with the synthesis, transport, metabolism and elimination of hormones, thereby decreasing the

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concentration of natural hormones. For example, thyroid hormone production can be inhibited by some ten endocrine disruptor pesticides (amitrole, cyhalothrin, fipronil, ioxynil, maneb, mancozeb, pentachloronitrobenzene, prodiamine, pyrimethanil, thiazopyr, ziram, zineb) [16].

1.4.1.2.5 Reproductive System

The presence of pesticides in the body for a longer time also affects reproductive capabilities by altering the levels of male and female reproductive hormones. Consequently, it results in stillbirth, birth defects, spontaneous abortion and infertility [32].

1.6.1.2.6 Other Organs

Lon-term exposure to pesticide also damages liver, lungs, kidneys and may cause blood diseases [17].