Poisons and Toxins
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.