Ecology: the biology of interaction. 6.06. The problem of pesticides
Overall, it can be said that the use of pesticides initially leads to a surge in yields, which is then followed by a decline. One of the dangerous features of pesticides (as with many other pollutants) is their ability to concentrate as they are transferred through trophic chains.
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6.05. Food security
D. Shabanov, M. Kravchenko. Ecology: Biology of Interaction Chapter 6. Human Ecology and Conservation
6.07. The Problem of Energy Supply
6.06. Pesticide issue The development of agriculture in recent decades is closely linked to the increasing use of pesticides (“chemical poisons”). “The use of broad‑spectrum pesticides is prone to the ‘re‑emergence’ of pests, i.e., their appearance after treatment in greater numbers than before. This is because the preparation kills not only the pests but also their predators that used to control them. A good example of this is the use of DDT to combat the cabbage white butterfly larvae, or simply the cabbage white (Pieris rapae), which parasitizes Brussels sprouts. Initially, DDT applications gave a noticeable effect, but gradually the abundance of pests became even higher than on control (unsprayed) plots. The difference was even more pronounced with repeated DDT applications to ‘suppress’ new pest outbreaks. Analysis of the agro‑ecosystem showed that the concentration of pesticide in the leaves eaten by the larvae quickly declines due to overall growth of the green parts of the cabbage. However, the level of the chemical poison in the soil remains high, especially if post‑harvest plant residues are incorporated into it. As a result, larvae hatching from eggs laid on leaves after treatment suffer only slightly, whereas the numbers of their main enemies—ground beetles (Harpalus rufipes) and harvestmen (Phalangium opilio)—decrease. With fewer predators, pests substantially increase their chances of survival, which is not compensated even by the poison. Further use only worsens the situation” (Material from Wikipedia—free encyclopedia, 2007). It should be added that, since the “pests” become fast‑reproducing animal species, many of them develop resistance to the used pesticides, followed by widespread dissemination of resistant forms. This problem is addressed by shifting to new, more effective pesticides. Overall, pesticide use initially leads to a yield jump, which is then followed by a decline. One dangerous feature of pesticides (as with many other pollutants) is their ability to concentrate through trophic transfer. This effect has been especially well studied using DDT (dichlorodiphenyltrichloroethane), the first pesticide to achieve widespread use. The insecticidal properties of DDT were discovered in 1938 (the discovery earned a Nobel Prize). After World War II, DDT became almost a panacea for all insect‑related problems. Near‑complete eradication of lice in developed countries was a result of its use. Unfortunately, over time adverse consequences of its use began to appear. DDT and its breakdown products can accumulate in fatty tissues. For example, a study of one water body registered the following DDT concentrations (in ppm—weight parts per million): water — 0.00005; plankton — 0.04; fish — 0.2–2 (predatory); heron — 3.5; gull egg — 6; cormorant — 26 (Odum, 1975). As can be seen, moving to higher trophic levels leads to concentration (bioaccumulation) of the contaminant in biomass. Accumulation of DDT in the eggs of large birds disrupts calcium metabolism and increases shell fragility. The spread of DDT through trophic chains has contaminated the entire biosphere; for instance, it caused damage to penguin egg shells in Antarctica, where it was never applied. “Breast milk of nursing mothers in the USA contains four times more DDT than sanitary standards allow for cow’s milk. In the USA this is commented as follows: ‘If mother’s milk were in a different package, it would not be allowed on the market at all’” (V. Eykhler, 1993). As the pathways of DDT transfer and its accumulation in organisms became clear, production and use of this substance were banned. Specialists point out that DDT is not more dangerous than other pesticides that continue to be used. DDT simply had bad luck—it was the first pesticide whose harm was well studied. Overall, pesticide use leads to the following adverse consequences: — development of resistance in pests; — resurgence of pests and secondary outbreaks of their populations; — increased costs of food production; — destruction of natural regulators of pest populations; — detrimental effects on the environment and human health. A partial solution to the pesticide problem is the use of unstable, rapidly degrading pesticides in the natural environment. A complete solution involves biological control measures against “pests,” including: — use of natural enemies; — use of crop varieties resistant to phytophagous insects; — release of artificially sterilized males (such males mate with “wild” females, which then produce no offspring); — agrotechnical control methods (altering environmental parameters: sanitary‑hygienic measures, changes in agronomy, crop rotation, polyculture, customs control, etc.); — use of natural compounds affecting “pests”—hormones, attractants, etc. Pesticide is a fairly broad term denoting any substance used to destroy pests or weeds. Pesticides include insecticides, bactericides, fungicides, acaricides, zoocides (targeting rodents), nemacides (targeting mollusks), herbicides (weed‑killing agents). Some of the most common pesticide categories are: — Organophosphorus compounds (OPs): chlorpyrifos, carbofuran, methyl‑nitrophos, avin, methyl‑acetophos, etc. Neurotoxic poisons. Mild poisoning—headache, sweating, lethargy, insomnia. Later—fear, depression, damage to digestive and respiratory organs. Chronic poisoning—toxic neurasthenia, vegetovascular dystonia. Frequent mental effects—irritability, memory impairment, reduced intelligence. — Chlorinated compounds: DDT, HCH (hexachlorocyclohexane), heptachlor, chlorindane‑polychloropinen, polychlorocamphene, chlorobenzene. Highly stable, lipophilic, capable of accumulating in organisms (in lipid media, from which they do not transfer to water). Powerful excretion (and contamination) route—through breast milk. Nervous tissue and cardiac muscle are most sensitive. Chronic poisoning—headache, dizziness, tingling in extremities, liver pain, digestive disturbances. — Organomercury compounds: granosan, mercuric, mercurhexane. Intended for seed treatment. Poisoning possible during grain theft. With grain‑eating birds and fish from water bodies receiving runoff, mercury in the form of methylmercury spreads through ecosystems. Causes various metabolic disorders. Chronic poisoning: emotional instability, headache, dizziness, memory decline, insomnia, fatigue, sweating, hand tremor. — Carbamates: carbaryl, thiuram, carbofuran, carbendazim—products of carbamic acid and its derivatives. Not highly toxic, similar in action to OPs, carcinogenic, with very broad activity. — Nitrophenolic compounds: nitrophen, dinitrophen—products of coal‑tar phenols processing. Acute poisoning—heat‑stroke‑like syndrome; chronic—euphoria, drowsiness, headache, sweating, dermatoses. — Copper‑containing preparations: copper sulfate, copper sulfate, Bordeaux mixture, copper oxychloride, copper trichlorophenolate. Fungicides and seed treatments. Gastrointestinal, respiratory organ damage, dermatitis. Some other toxicants, although not classified as pesticides, are ecologically similar to them. These include: — Nitrates (nitrites)—most often the result of excessive or improper soil fertilization. Nitrites bind to oxyhemoglobin, forming methemoglobin. Lethal dose—about 3.5 g sodium nitrate. Chronic poisoning manifests as lethargy and depression; in large doses nitrites damage kidneys, liver, CNS, gastrointestinal tract. — Lead. Main source—tetraethyllead, used to raise gasoline octane, in printing equipment, radiation shielding (large amounts of lead were dispersed after the Chernobyl accident). Easily inhaled as dust. Deposits in tissues, especially bones. Protoplasmic toxin. Increases brain excitability. Early symptoms—dark lines on the front teeth. Late—lead encephalopathy. — Other heavy metals: mercury, zinc, manganese, chromium, nickel, cadmium, etc.
6.06. Pesticide issue The development of agriculture in recent decades is closely linked to the increasing use of pesticides (“chemical poisons”). “The use of broad‑spectrum pesticides is prone to the ‘re‑emergence’ of pests, i.e., their appearance after treatment in greater numbers than before. This is because the preparation kills not only the pests but also their predators that used to control them. A good example of this is the use of DDT to combat the cabbage white butterfly larvae, or simply the cabbage white (Pieris rapae), which parasitizes Brussels sprouts. Initially, DDT applications gave a noticeable effect, but gradually the abundance of pests became even higher than on control (unsprayed) plots. The difference was even more pronounced with repeated DDT applications to ‘suppress’ new pest outbreaks. Analysis of the agro‑ecosystem showed that the concentration of pesticide in the leaves eaten by the larvae quickly declines due to overall growth of the green parts of the cabbage. However, the level of the chemical poison in the soil remains high, especially if post‑harvest plant residues are incorporated into it. As a result, larvae hatching from eggs laid on leaves after treatment suffer only slightly, whereas the numbers of their main enemies—ground beetles (Harpalus rufipes) and harvestmen (Phalangium opilio)—decrease. With fewer predators, pests substantially increase their chances of survival, which is not compensated even by the poison. Further use only worsens the situation” (Material from Wikipedia—free encyclopedia, 2007). It should be added that, since the “pests” become fast‑reproducing animal species, many of them develop resistance to the used pesticides, followed by widespread dissemination of resistant forms. This problem is addressed by shifting to new, more effective pesticides. Overall, pesticide use initially leads to a yield jump, which is then followed by a decline. One dangerous feature of pesticides (as with many other pollutants) is their ability to concentrate through trophic transfer. This effect has been especially well studied using DDT (dichlorodiphenyltrichloroethane), the first pesticide to achieve widespread use. The insecticidal properties of DDT were discovered in 1938 (the discovery earned a Nobel Prize). After World War II, DDT became almost a panacea for all insect‑related problems. Near‑complete eradication of lice in developed countries was a result of its use. Unfortunately, over time adverse consequences of its use began to appear. DDT and its breakdown products can accumulate in fatty tissues. For example, a study of one water body registered the following DDT concentrations (in ppm—weight parts per million): water — 0.00005; plankton — 0.04; fish — 0.2–2 (predatory); heron — 3.5; gull egg — 6; cormorant — 26 (Odum, 1975). As can be seen, moving to higher trophic levels leads to concentration (bioaccumulation) of the contaminant in biomass. Accumulation of DDT in the eggs of large birds disrupts calcium metabolism and increases shell fragility. The spread of DDT through trophic chains has contaminated the entire biosphere; for instance, it caused damage to penguin egg shells in Antarctica, where it was never applied. “Breast milk of nursing mothers in the USA contains four times more DDT than sanitary standards allow for cow’s milk. In the USA this is commented as follows: ‘If mother’s milk were in a different package, it would not be allowed on the market at all’” (V. Eykhler, 1993). As the pathways of DDT transfer and its accumulation in organisms became clear, production and use of this substance were banned. Specialists point out that DDT is not more dangerous than other pesticides that continue to be used. DDT simply had bad luck—it was the first pesticide whose harm was well studied. Overall, pesticide use leads to the following adverse consequences: — development of resistance in pests; — resurgence of pests and secondary outbreaks of their populations; — increased costs of food production; — destruction of natural regulators of pest populations; — detrimental effects on the environment and human health. A partial solution to the pesticide problem is the use of unstable, rapidly degrading pesticides in the natural environment. A complete solution involves biological control measures against “pests,” including: — use of natural enemies; — use of crop varieties resistant to phytophagous insects; — release of artificially sterilized males (such males mate with “wild” females, which then produce no offspring); — agrotechnical control methods (altering environmental parameters: sanitary‑hygienic measures, changes in agronomy, crop rotation, polyculture, customs control, etc.); — use of natural compounds affecting “pests”—hormones, attractants, etc. Pesticide is a fairly broad term denoting any substance used to destroy pests or weeds. Pesticides include insecticides, bactericides, fungicides, acaricides, zoocides (targeting rodents), nemacides (targeting mollusks), herbicides (weed‑killing agents). Some of the most common pesticide categories are: — Organophosphorus compounds (OPs): chlorpyrifos, carbofuran, methyl‑nitrophos, avin, methyl‑acetophos, etc. Neurotoxic poisons. Mild poisoning—headache, sweating, lethargy, insomnia. Later—fear, depression, damage to digestive and respiratory organs. Chronic poisoning—toxic neurasthenia, vegetovascular dystonia. Frequent mental effects—irritability, memory impairment, reduced intelligence. — Chlorinated compounds: DDT, HCH (hexachlorocyclohexane), heptachlor, chlorindane‑polychloropinen, polychlorocamphene, chlorobenzene. Highly stable, lipophilic, capable of accumulating in organisms (in lipid media, from which they do not transfer to water). Powerful excretion (and contamination) route—through breast milk. Nervous tissue and cardiac muscle are most sensitive. Chronic poisoning—headache, dizziness, tingling in extremities, liver pain, digestive disturbances. — Organomercury compounds: granosan, mercuric, mercurhexane. Intended for seed treatment. Poisoning possible during grain theft. With grain‑eating birds and fish from water bodies receiving runoff, mercury in the form of methylmercury spreads through ecosystems. Causes various metabolic disorders. Chronic poisoning: emotional instability, headache, dizziness, memory decline, insomnia, fatigue, sweating, hand tremor. — Carbamates: carbaryl, thiuram, carbofuran, carbendazim—products of carbamic acid and its derivatives. Not highly toxic, similar in action to OPs, carcinogenic, with very broad activity. — Nitrophenolic compounds: nitrophen, dinitrophen—products of coal‑tar phenols processing. Acute poisoning—heat‑stroke‑like syndrome; chronic—euphoria, drowsiness, headache, sweating, dermatoses. — Copper‑containing preparations: copper sulfate, copper sulfate, Bordeaux mixture, copper oxychloride, copper trichlorophenolate. Fungicides and seed treatments. Gastrointestinal, respiratory organ damage, dermatitis. Some other toxicants, although not classified as pesticides, are ecologically similar to them. These include: — Nitrates (nitrites)—most often the result of excessive or improper soil fertilization. Nitrites bind to oxyhemoglobin, forming methemoglobin. Lethal dose—about 3.5 g sodium nitrate. Chronic poisoning manifests as lethargy and depression; in large doses nitrites damage kidneys, liver, CNS, gastrointestinal tract. — Lead. Main source—tetraethyllead, used to raise gasoline octane, in printing equipment, radiation shielding (large amounts of lead were dispersed after the Chernobyl accident). Easily inhaled as dust. Deposits in tissues, especially bones. Protoplasmic toxin. Increases brain excitability. Early symptoms—dark lines on the front teeth. Late—lead encephalopathy. — Other heavy metals: mercury, zinc, manganese, chromium, nickel, cadmium, etc.
6.06. Pesticide issue The development of agriculture in recent decades is closely linked to the increasing use of pesticides (“chemical poisons”). “The use of broad‑spectrum pesticides is prone to the ‘re‑emergence’ of pests, i.e., their appearance after treatment in greater numbers than before. This is because the preparation kills not only the pests but also their predators that used to control them. A good example of this is the use of DDT to combat the cabbage white butterfly larvae, or simply the cabbage white (Pieris rapae), which parasitizes Brussels sprouts. Initially, DDT applications gave a noticeable effect, but gradually the abundance of pests became even higher than on control (unsprayed) plots. The difference was even more pronounced with repeated DDT applications to ‘suppress’ new pest outbreaks. Analysis of the agro‑ecosystem showed that the concentration of pesticide in the leaves eaten by the larvae quickly declines due to overall growth of the green parts of the cabbage. However, the level of the chemical poison in the soil remains high, especially if post‑harvest plant residues are incorporated into it. As a result, larvae hatching from eggs laid on leaves after treatment suffer only slightly, whereas the numbers of their main enemies—ground beetles (Harpalus rufipes) and harvestmen (Phalangium opilio)—decrease. With fewer predators, pests substantially increase their chances of survival, which is not compensated even by the poison. Further use only worsens the situation” (Material from Wikipedia—free encyclopedia, 2007). It should be added that, since the “pests” become fast‑reproducing animal species, many of them develop resistance to the used pesticides, followed by widespread dissemination of resistant forms. This problem is addressed by shifting to new, more effective pesticides. Overall, pesticide use initially leads to a yield jump, which is then followed by a decline. One dangerous feature of pesticides (as with many other pollutants) is their ability to concentrate through trophic transfer. This effect has been especially well studied using DDT (dichlorodiphenyltrichloroethane), the first pesticide to achieve widespread use. The insecticidal properties of DDT were discovered in 1938 (the discovery earned a Nobel Prize). After World War II, DDT became almost a panacea for all insect‑related problems. Near‑complete eradication of lice in developed countries was a result of its use. Unfortunately, over time adverse consequences of its use began to appear. DDT and its breakdown products can accumulate in fatty tissues. For example, a study of one water body registered the following DDT concentrations (in ppm—weight parts per million): water — 0.00005; plankton — 0.04; fish — 0.2–2 (predatory); heron — 3.5; gull egg — 6; cormorant — 26 (Odum, 1975). As can be seen, moving to higher trophic levels leads to concentration (bioaccumulation) of the contaminant in biomass. Accumulation of DDT in the eggs of large birds disrupts calcium metabolism and increases shell fragility. The spread of DDT through trophic chains has contaminated the entire biosphere; for instance, it caused damage to penguin egg shells in Antarctica, where it was never applied. “Breast milk of nursing mothers in the USA contains four times more DDT than sanitary standards allow for cow’s milk. In the USA this is commented as follows: ‘If mother’s milk were in a different package, it would not be allowed on the market at all’” (V. Eykhler, 1993). As the pathways of DDT transfer and its accumulation in organisms became clear, production and use of this substance were banned. Specialists point out that DDT is not more dangerous than other pesticides that continue to be used. DDT simply had bad luck—it was the first pesticide whose harm was well studied. Overall, pesticide use leads to the following adverse consequences: — development of resistance in pests; — resurgence of pests and secondary outbreaks of their populations; — increased costs of food production; — destruction of natural regulators of pest populations; — detrimental effects on the environment and human health. A partial solution to the pesticide problem is the use of unstable, rapidly degrading pesticides in the natural environment. A complete solution involves biological control measures against “pests,” including: — use of natural enemies; — use of crop varieties resistant to phytophagous insects; — release of artificially sterilized males (such males mate with “wild” females, which then produce no offspring); — agrotechnical control methods (altering environmental parameters: sanitary‑hygienic measures, changes in agronomy, crop rotation, polyculture, customs control, etc.); — use of natural compounds affecting “pests”—hormones, attractants, etc. Pesticide is a fairly broad term denoting any substance used to destroy pests or weeds. Pesticides include insecticides, bactericides, fungicides, acaricides, zoocides (targeting rodents), nemacides (targeting mollusks), herbicides (weed‑killing agents). Some of the most common pesticide categories are: — Organophosphorus compounds (OPs): chlorpyrifos, carbofuran, methyl‑nitrophos, avin, methyl‑acetophos, etc. Neurotoxic poisons. Mild poisoning—headache, sweating, lethargy, insomnia. Later—fear, depression, damage to digestive and respiratory organs. Chronic poisoning—toxic neurasthenia, vegetovascular dystonia. Frequent mental effects—irritability, memory impairment, reduced intelligence. — Chlorinated compounds: DDT, HCH (hexachlorocyclohexane), heptachlor, chlorindane‑polychloropinen, polychlorocamphene, chlorobenzene. Highly stable, lipophilic, capable of accumulating in organisms (in lipid media, from which they do not transfer to water). Powerful excretion (and contamination) route—through breast milk. Nervous tissue and cardiac muscle are most sensitive. Chronic poisoning—headache, dizziness, tingling in extremities, liver pain, digestive disturbances. — Organomercury compounds: granosan, mercuric, mercurhexane. Intended for seed treatment. Poisoning possible during grain theft. With grain‑eating birds and fish from water bodies receiving runoff, mercury in the form of methylmercury spreads through ecosystems. Causes various metabolic disorders. Chronic poisoning: emotional instability, headache, dizziness, memory decline, insomnia, fatigue, sweating, hand tremor. — Carbamates: carbaryl, thiuram, carbofuran, carbendazim—products of carbamic acid and its derivatives. Not highly toxic, similar in action to OPs, carcinogenic, with very broad activity. — Nitrophenolic compounds: nitrophen, dinitrophen—products of coal‑tar phenols processing. Acute poisoning—heat‑stroke‑like syndrome; chronic—euphoria, drowsiness, headache, sweating, dermatoses. — Copper‑containing preparations: copper sulfate, copper sulfate, Bordeaux mixture, copper oxychloride, copper trichlorophenolate. Fungicides and seed treatments. Gastrointestinal, respiratory organ damage, dermatitis. Some other toxicants, although not classified as pesticides, are ecologically similar to them. These include: — Nitrates (nitrites)—most often the result of excessive or improper soil fertilization. Nitrites bind to oxyhemoglobin, forming methemoglobin. Lethal dose—about 3.5 g sodium nitrate. Chronic poisoning manifests as lethargy and depression; in large doses nitrites damage kidneys, liver, CNS, gastrointestinal tract. — Lead. Main source—tetraethyllead, used to raise gasoline octane, in printing equipment, radiation shielding (large amounts of lead were dispersed after the Chernobyl accident). Easily inhaled as dust. Deposits in tissues, especially bones. Protoplasmic toxin. Increases brain excitability. Early symptoms—dark lines on the front teeth. Late—lead encephalopathy. — Other heavy metals: mercury, zinc, manganese, chromium, nickel, cadmium, etc.
As a result of clarifying the pathways of DDT transmission and its accumulation in organisms, the production and consumption of this substance were banned. Experts point out that DDT is no more dangerous than other pesticides that continue to be used. DDT simply didn't 'get caught red-handed' – it was the first pesticide whose harmfulness was well studied.
In general, it can be said that the use of pesticides leads to the following adverse consequences: - development of pest resistance; - resurgence of pests and secondary outbreaks of their populations; - increased costs of food production; - destruction of natural pest population regulators; - adverse effects on the environment and human health.
A partial solution to the pesticide problem is the use of unstable pesticides that decompose quickly in the natural environment. A complete solution is the application of biological pest control measures, including: — the use of natural enemies; — the use of varieties resistant to plant-eating insects; — the release of artificially sterilized males (such males mate with "wild" females, which as a result do not produce offspring); — agrotechnical control measures (changing environmental parameters: sanitary and hygienic measures, changes in agricultural techniques, crop rotation, polyculture, customs control, etc.); — the use of natural compounds that act on pests, such as hormones, attractants, etc.
A pesticide is a fairly broad term that denotes any substance used to destroy pests or weeds. Pesticides include insecticides, bactericides, fungicides, acaricides, rodenticides (aimed at rodents), nematicides (aimed against mollusks), and herbicides (weed control agents). Some of the most common categories of pesticides are as follows.
— Organophosphorus compounds (OPC): chlorophos, carbophos, methylnitrophos, avenin, methylacetophos, etc. Neurotoxic poisons. Mild poisoning - headache, sweating, weakness, insomnia. Further - fear, depression, damage to the digestive and respiratory organs. Chronic poisoning - toxic neurasthenia, vegetative-vascular dystonia. Frequent mental disorders - irritability, memory impairment, decreased intelligence.
Organochlorine compounds: DDT, HCH (hexachlorocyclohexane), heptachlor, chlordane-polychloropinene, polychlorocamphene, chlorobenzene. Highly persistent, fat-soluble, capable of accumulating in organisms (in lipid environments, from which they do not pass into water). A powerful route of excretion (and infection) is through breast milk. The most sensitive tissues are nervous tissue and cardiac muscle. Chronic poisoning symptoms include headache, dizziness, tingling in the limbs, liver pain, and digestive disorders.
— Organomercury compounds: granosan, merkuram, merkgexan. Purpose — seed treatment. Poisoning is possible when stealing grain. With grain-eating birds and fish from water bodies, where water flows from fields, mercury in the form of methylmercury spreads through ecosystems. Cause various metabolic disorders. Chronic poisoning: emotional instability, headache, dizziness, memory impairment, insomnia, fatigue, sweating, trembling of the fingers.
— Carbamates: sevin, tiuram, ziram, zineb — products of carbamic acid and its derivatives. Low toxicity, similar in action to organophosphorus compounds, carcinogenic, have a very wide spectrum of action.
— Nitrophenolic compounds: nitrophenol, dinitrophenol — products of coal tar phenol processing. Acute poisoning — "heatstroke" syndrome, chronic — euphoria, drowsiness, headache, sweating, dermatoses.
— Copper-containing preparations: copper sulfate, copper(II) sulfate, Bordeaux mixture, copper oxychloride, copper trichlorophenolate. Fungicides and seed treatments. Gastrointestinal tract damage, respiratory organs, dermatitis.
Some other poisons, although not belonging to pesticides, are ecologically quite similar to them. These include the following substances.
— Nitrates (nitrites) are most often the result of excessive or improper fertilization of soils. Nitrites bind with oxyhemoglobin, forming methemoglobin. The lethal dose is from 3.5 g of sodium nitrate. Chronic poisoning manifests as lethargy and depression; in large doses, nitrites affect the kidneys, liver, central nervous system, and gastrointestinal tract.
— Lead. The main source is tetraethyl lead, used to increase the octane number of gasoline, printing equipment, radiation shielding (a lot of lead was dispersed after the Chernobyl accident). Easily absorbed in the form of dust. Deposited in tissues, especially bones. A protoplasmic poison. Increases brain excitability. Early symptoms include dark bands on the front teeth. Later symptoms include lead encephalopathy.
— Other heavy metals: mercury, zinc, manganese, chromium, nickel, cadmium, etc.
6.05. Food security
D. Shabanov, M. Kravchenko. Ecology: Biology of Interaction Chapter 6. Human Ecology and Conservation
6.07. The Problem of Energy Supply