Poisons and Toxins
Poisons and Toxins
Poisons and toxins
A chemical is said to be a poison if it causes some degree of metabolic disfunction in organisms. Strictly speaking, a toxin is a poisonous chemical of biological origin, being produced by a microorganism, plant , or animal . In common usage, however, the words poison and toxin are often used interchangeably, and in this essay they are also treated as synonyms.
It is important to understand that potentially, all chemicals are toxic. All that is required for a chemical to cause toxicity, is a dose (or exposure) that is large enough to affect the physiology of an organism . This fact was first recognized by a Swiss physician and alchemist known as Paracelsus (1493-1541), who is commonly acknowledged as the parent of the modern science of toxicology . Paracelsus wrote that: "Dosage alone determines poisoning." In other words, if an exposure to a chemical is to cause poisoning, it must result in a dose that exceeds a threshold of physiological tolerance. Smaller exposures to the same chemical do not cause poisoning, at least not on the short term. (The differences between short-term and longer-term toxicities are discussed in the next section.) Species of plants, animals, and microorganisms differ enormously in their tolerance of exposures to potentially toxic chemicals. Even within populations of the same species, there can be substantial differences in sensitivity to chemical exposures. Some individuals, for example, may be extremely sensitive to poisoning by particular chemicals, a phenomenon known as hypersensitivity.
Because chemicals are present everywhere, all organisms are continuously exposed to potentially toxic substances. In particular, the environments of modern humans involve especially complex mixtures of chemicals, many of which are synthesized through manufacturing and are then deliberately or accidentally released into the environment. People are routinely exposed to potentially toxic chemicals through their food, medicine, water , and the atmosphere.
Toxicity can be expressed in many ways. Some measures of toxicity examine biochemical responses to exposures to chemicals. These responses may be detectable at doses that do not result in more directly observed effects, such as tissue damage, or death of the organism. This sort of small-dose, biochemical toxicity might be referred to as a type of "hidden injury," because of the lack of overt, visible symptoms and damages. Other measures of toxicity may rely on the demonstration of a loss of productivity, or tissue damage, or ultimately, death of the organism. In extreme cases, it is possible to demonstrate toxicity to entire ecosystems.
The demonstration of obvious tissue damage, illness, or death after a short-term exposure to a large dose of some chemical is known as acute toxicity. There are many kinds of toxicological assessments of the acute toxicity of chemicals. These can be used to bioassay the relative toxicity of chemicals in the laboratory. They can also assess damages caused to people in their workplace, or to ecosystems in the vicinity of chemical emission sources ambient environment. One example of a commonly used index of acute toxicity is known as the LD50, which is based on the dose of chemical that is required to kill one-half of a laboratory population of organisms during a short-term, controlled exposure. Consider, for example, the following LD50's for laboratory rats (measured in mg of chemical per kg of body weight): sucrose (table sugar) 30,000 mg/kg; ethanol (drinking alcohol ) 13,700; glyphosate (a herbicide) 4,300; sodium chloride (table salt ) 3,750; malathion (an insecticide) 2,000; acetylsalicylic acid (aspirin) 1,700; mirex (an insecticide) 740; 2,4-D (a herbicide) 370; DDT (an insecticide) 200; caffeine (a natural alkaloid ) 200; nicotine (a natural alkaloid) 50; phosphamidon (an insecticide) 24; carbofuran (an insecticide) 10; saxitoxin (paralytic shellfish poison) 0.8; tetrodotoxin (globe-fish poison) 0.01; TCDD (a dioxin isomer ) 0.01.
Clearly, chemicals vary enormously in their acute toxicity. Even routinely encountered chemicals can, however, be toxic, as is illustrated by the data for table sugar.
Toxic effects of chemicals may also develop after a longer period of exposure to smaller concentrations than are required to cause acute poisoning. These long-term effects are known as chronic toxicity. In humans and other animals, long-term, chronic toxicity can occur in the form of increased rates of birth defects , cancers, organ damages, and reproductive dysfunctions, such as spontaneous abortions. In plants, chronic toxicity is often assayed as decreased productivity, in comparison with plants that are not chronically exposed to the toxic chemicals in question. Because of their relatively indeterminate nature and long-term lags in development, chronic toxicities are much more difficult to demonstrate than acute toxicities.
It is important to understand that there appear to be thresholds of tolerance to exposures to most potentially toxic chemicals. These thresholds of tolerance must be exceeded by larger doses before poisoning is caused. Smaller, sub-toxic exposures to chemicals might be referred to as contamination , while larger exposures are considered to represent poisoning, or pollution in the ecological context.
The notion of contamination is supported by several physiological mechanisms that are capable of dealing with the effects of relatively small exposures to chemicals. For example, cells have some capability for repairing damages caused to DNA (deoxyribonucleic acid) and other nuclear materials. Minor damages caused by toxic chemicals might be mended, and therefore tolerated. Organisms also have mechanisms for detoxifying some types of poisonous chemicals. The mixed-function oxidases, for example, are enzymes that can detoxify certain chemicals, such as chlorinated hydrocarbons , by metabolizing them into simpler, less-toxic substances. Organisms can also partition certain chemicals into tissues that are less vulnerable to their poisonous influence. For example, chlorinated hydrocarbons are most often deposited in the fatty tissues of animals.
All of these physiological mechanisms of dealing with small exposures to potentially toxic chemicals can, however, be overwhelmed by exposures that exceed the limits of tolerance. These larger exposures cause poisoning of people and other organisms and ecological damages.
Some naturally occurring poisons
Many poisonous chemicals are present naturally in the environment. For example, all of metals and other elements are widespread in the environment, but under some circumstances they may occur naturally in concentrations that are large enough to be poisonous to at least some organisms.
Examples of natural "pollution" can involve surface exposure of minerals containing large concentrations of toxic elements, such as copper , lead, selenium, or arsenic. For example, soils influenced by a mineral known as serpentine can have large concentrations of toxic nickel and cobalt, and can be poisonous to most plants.
In other cases, certain plants may selectively take up elements from their environment, to the degree that their foliage becomes acutely toxic to herbivorous animals. For example, soils in semi-arid regions of the western United States often contain selenium. This element can be bioaccumulated by certain species of legumes known as locoweeds (Astragalus spp.), to the degree that the plants become extremely poisonous to cattle and to other large animals that might eat their toxic foliage.
In some circumstances, the local environment can become naturally polluted by gases at toxic concentrations, poisoning plants and animals. This can happen in the vicinity of volcanoes, where vents known as fumaroles frequently emit toxic sulfur dioxide , which can poison and kill nearby plants. The sulfur dioxide can also dry-deposit to the nearby ground and surface water, causing a severe acidification, which results in soluble aluminum ions becoming toxic.
Other naturally occurring toxins are biochemicals that are synthesized by plants and animals, often as a deterrent to herbivores and predators, respectively. In fact, some of the most toxic chemicals known to science are biochemicals synthesized by organisms. One such example is tetrodotoxin, synthesized by the Japanese globe fish (Spheroides rubripes), and extremely toxic even if ingested in tiny amounts. Only slightly less toxic is saxitoxin, synthesized by species of marine phytoplankton , but accumulated by shellfish. When people eat these shellfish, a deadly syndrome known as paralytic shellfish poisoning results. There are numerous other examples of deadly biochemicals, such as snake and bee venoms, toxins produced by pathogenic microorganisms, and mushroom poisons.
Poisons produced by human technology
Of course, in the modern world, humans are responsible for many of the toxic chemicals that are now being dispersed into the environment. In some cases, humans are causing toxic damages to organisms and ecosystems by emitting large quantities of chemicals that also occur naturally, such as sulfur dioxide, hydrocarbons, and metals. Pollution or poisoning by these chemicals represents an intensification of damages that may already be present naturally, although not to nearly the same degree or extent that results from additional human emissions.
Humans are also, however, synthesizing large quantities of novel chemicals that do not occur naturally, and these are also being dispersed widely into the environment. These synthetic chemicals include thousands of different pesticidal chemicals, medicines, and diverse types of industrial chemicals, all of them occurring in complex mixtures of various forms. Many of these chemicals are directly toxic to humans and to other organisms that are exposed to them, as is the case with many pesticides . Others result in toxicity indirectly, as may occur when chlorofluorocarbons (CFCs) , which are normally quite inert chemicals, find their way to the upper atmospheric layer called the stratosphere. There the CFCs degrade into simpler chemicals that consume ozone , resulting in less shielding of Earth's surface from the harmful effects of solar ultraviolet radiation , with subsequent toxic effects such as skin cancers, cataracts, and immune disorders.
As an example of toxicity caused to humans, consider the case of the accidental release in 1984 at Bhopal, India, of about 40 tonnes of poisonous methyl isocyanate vapor, an intermediate chemical in the manufacturing of an agricultural insecticide. This emission caused the death of almost 3,000 people and more than 20,000 others were seriously injured.
As an example of toxicity caused to other animals, consider the effects of the use of carbofuran, an insecticide used in agriculture in North America . Carbofuran exerts its toxic effect by poisoning a specific enzyme , known as acetylcholine esterase, which is essential for maintaining the functioning of the nervous system . This enzyme is critical to the healthy functioning of insects , but it also occurs in vertebrates such as birds and mammals . As a result, the normal use of carbofuran in agriculture results in toxic exposures to numerous birds, mammals, and other animals that are not the intended targets of the insecticide application. Many of these non-target animals are killed by their exposure to carbofuran, a chemical that is well-known as causing substantial ecological damages during the course of its normal, legal usage in agriculture.
It is critical to understand that while any chemical can cause poisoning, a threshold of tolerable dose must be exceeded for this to actually happen. The great challenge of toxicology is to provide society with a clearer understanding of the exposures to potentially toxic chemicals that can be tolerated by humans, other species, and ecosystems before unacceptable damages are caused. Many naturally occurring and synthetic chemicals can be used for diverse, useful purposes, but it is important that we understand the potentially toxic consequences of increasing exposures to these substances.
See also Bioaccumulation.
Freedman, B. Environmental Ecology. 2nd ed. San Diego: Academic Press, 1995.
Klaassen, Curtis D. Casarett and Doull's Toxicology. 6th ed. Columbus: McGraw-Hill, Inc., 2001.
Smith, R.P. A Primer of Environmental Toxicology. Philadelphia: Lea & Febiger, 1992.
"Better Killing Through Chemistry." Scientific American (December 2001).
KEY TERMS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
- Acute toxicity
—A poisonous effect produced by a single, short-term exposure to a toxic chemical, resulting in obvious tissue damage, and even death of the organism.
—This is an estimate of the concentration or effect of a potentially toxic chemical, measured using a biological response under standardized conditions.
- Chronic toxicity
—This is a poisonous effect that is produced by a long period of exposure to a moderate, sub-acute dose of some toxic chemical. Chronic toxicity may result in anatomical damages or disease, but it is not generally the direct cause of death of the organism.
—In toxicology, exposure refers to the concentration of a chemical in the environment, or to the accumulated dose that an organism encounters.
- Hidden injury
—This refers to physiological damages, such as changes in enzyme or other biochemical functions, that occur after exposure to a dose of a poison that is not sufficient to cause acute injuries.
—In toxicology, response refers to effects on physiology or organisms that are caused by exposure to one or more poisons.