Biodegradation is the disintegration of materials by bacteria, fungi, or other biological means.

The term is often used in relation to: biomedicine, waste management, ecology, and the bioremediation of the natural environment. It is now commonly associated with environmentally-friendly products, capable of decomposing back into natural elements.

Although often conflated, "biodegradable" is distinct in meaning from: "compostable". While biodegradable simply means "can be consumed by microorganisms", "compostable" makes the further specific demand that the object break down under composting conditions.

Organic material can be degraded aerobically (with oxygen) or anaerobically (without oxygen). Decomposition of biodegradable substances may include both biological and abiotic steps.

Biodegradable matter is generally organic material that provides a nutrient for microorganisms. These are so numerous and diverse that a huge range of compounds can be biodegraded, including hydrocarbons (oils), polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs) and pharmaceutical substances.

Microorganisms secrete biosurfactant, an extracellular surfactant, to enhance this process.

In practice, almost all chemical compounds and materials are subject to biodegradation processes. The significance, however, is in the relative rates of such processes, such as days, weeks, years or centuries. A number of factors determine the rate at which this degradation of organic compounds occurs. Salient factors include light, water and oxygen. Temperature is also important because chemical reactions proceed more quickly at higher temperatures. The degradation rate of many organic compounds is limited by their bioavailability. Compounds must be released into solution before organisms can degrade them.

Biodegradability can be measured in a number of ways. Respirometry tests can be used for aerobic microbes. First one places a solid waste sample in a container with microorganisms and soil, and then aerates the mixture. Over the course of several days, microorganisms digest the sample bit by bit and produce carbon dioxide – the resulting amount of CO serves as an indicator of degradation. Biodegradability can also be measured by anaerobic microbes and the amount of methane or alloy that they are able to produce. In formal scientific literature, the process is termed bioremediation.

Decomposition is the process by which organic substances are broken down into simpler matter. The process is a part of nutrient cycle and is essential for recycling the finite matter that occupies physical space in the biosphere. Bodies of living organisms begin to decompose shortly after death. Animals, such as worms, also help decompose the organic materials. Organisms that do this are known as decomposers. Although no two organisms decompose in the same way, they all undergo the same sequential stages of decomposition. The science which studies decomposition is generally referred to as "taphonomy" from the Greek word "taphos", meaning tomb.

One can differentiate abiotic from biotic decomposition (biodegradation). The former means "degradation of a substance by chemical or physical processes, e.g., hydrolysis. The latter means "the metabolic breakdown of materials into simpler components by living organisms", typically by microorganisms.

Once kidney failure has developed in dogs and cats, the outcome is poor.

Ethylene glycol poisoning is a relatively common occurrence worldwide. Human poisoning often occurs in isolated cases, but may also occur in epidemics. Many cases of poisoning are the result of using ethylene glycol as a cheap substitute for alcohol or intentional ingestions in suicide attempts. Less commonly it has been used as a means of homicide. Children or animals may be exposed by accidental ingestion; children and animals often consume large amounts due to ethylene glycol having a sweet taste. In the United States there were 5816 cases reported to poison centers in 2002. Additionally, ethylene glycol was the most common chemical responsible for deaths reported by US poison centers in 2003. In Australia there were 17 cases reported to the Victorian poison center and 30 cases reported to the New South Wales poison center in 2007. However, these numbers may underestimate actual numbers because not all cases attributable to ethylene glycol are reported to poison control centers. Most deaths from ethylene glycol are intentional suicides; deaths in children due to unintentional ingestion are extremely rare.

In an effort to prevent poisoning, often a bittering agent called denatonium benzoate, known by the trade name Bitrex, is added to ethylene glycol preparations as an adversant to prevent accidental or intentional ingestion. The bittering agent is thought to stop ingestion as part of the human defense against ingestion of harmful substances is rejection of bitter tasting substances. In the United States, eight states (Oregon, California, New Mexico, Virginia, Arizona, Maine, Tennessee, Washington) have made the addition of bittering agents to antifreeze compulsory. Three follow up studies targeting limited populations or suicidal persons to assess the efficacy of bittering agents in preventing toxicity or death have, however, shown limited benefit of bittering ethylene glycol preparations in these two populations. Specifically, Mullins finds that bittering of antifreeze does not reduce reported cases of poisoning of preschoolers in the US state of Oregon. Similarly, White found that adding bittering agents did not decrease the frequency or severity of antifreeze poisonings in children under the age of 5. Additionally, another study by White found that suicidal persons are not deterred by the bittered taste of antifreeze in their attempts to kill themselves. These studies did not focus on poisoning of domestic pets or livestock, for example, or inadvertent exposure to bittered antifreeze among a large population (of non-preschool age children).

Poisoning of a raccoon was diagnosed in 2002 in Prince Edward Island, Canada. An online veterinary manual provides information on lethal doses of ethylene glycol for chicken, cattle, as well as cats and dogs, adding that younger animals may be more susceptible.

A body buried in a sufficiently dry environment may be well preserved for decades. This was observed in the case for murdered civil rights activist Medgar Evers, who was found to be almost perfectly preserved over 30 years after his death, permitting an accurate autopsy when the case of his murder was re-opened in the 1990s.

Bodies submerged in a peat bog may become naturally "embalmed", arresting decomposition and resulting in a preserved specimen known as a bog body. The time for an embalmed body to be reduced to a skeleton varies greatly. Even when a body is decomposed, embalming treatment can still be achieved (the arterial system decays more slowly) but would not restore a natural appearance without extensive reconstruction and cosmetic work, and is largely used to control the foul odors due to decomposition.

An animal can be preserved almost perfectly, for millions of years in a resin such as amber.

There are some examples where bodies have been inexplicably preserved (with no human intervention) for decades or centuries and appear almost the same as when they died. In some religious groups, this is known as incorruptibility. It is not known whether or for how long a body can stay free of decay without artificial preservation.

The GM2 gangliosidoses are a group of three related genetic disorders that result from a deficiency of the enzyme beta-hexosaminidase. This enzyme catalyzes the biodegradation of fatty acid derivatives known as gangliosides. The diseases are better known by their individual names.

Beta-hexosaminidase is a vital hydrolytic enzyme, found in the lysosomes, that breaks down lipids. When beta-hexosaminidase is no longer functioning properly, the lipids accumulate in the nervous tissue of the brain and cause problems. Gangliosides are made and biodegraded rapidly in early life as the brain develops. Except in some rare, late-onset forms, the GM2 gangliosidoses are fatal.

All three disorders are rare in the general population. Tay-Sachs disease has become famous as a public health model because an enzyme assay test for TSD was discovered and developed in the late 1960s and early 1970s, providing one of the first "mass screening" tools in medical genetics. It became a research and public health model for understanding and preventing all autosomal genetic disorders.

Tay-Sachs disease, AB variant, and Sandhoff disease might easily have been defined together as a single disease, because the three disorders are associated with failure of the same metabolic pathway and have the same outcome. Classification and naming for many genetic disorders reflects history, because most diseases were first observed and classified based on biochemistry and pathophysiology before genetic diagnosis was available. However, the three GM2 gangliosidoses were discovered and named separately. Each represents a distinct molecular point of failure in a subunit that is required for activation of the enzyme.

Tay–Sachs disease is a rare autosomal recessive genetic disorder that causes a progressive deterioration of nerve cells and of mental and physical abilities that begins around six months of age and usually results in death by the age of four. It is the most common of the GM2 gangliosidoses. The disease occurs when harmful quantities of cell membrane gangliosides accumulate in the brain's nerve cells, eventually leading to the premature death of the cells.

As of 2010, even with the best care, children with infantile Tay–Sachs disease usually die by the age of 4.

Ashkenazi Jews have a high incidence of Tay–Sachs and other lipid storage diseases. In the United States, about 1 in 27 to 1 in 30 Ashkenazi Jews is a recessive carrier. The disease incidence is about 1 in every 3,500 newborn among Ashkenazi Jews. French Canadians and the Cajun community of Louisiana have an occurrence similar to the Ashkenazi Jews. Irish Americans have a 1 in 50 chance of being a carrier. In the general population, the incidence of carriers as heterozygotes is about 1 in 300. The incidence is approximately 1 in 320,000 newborns in the general population in United States.

Three general classes of theories have been proposed to explain the high frequency of Tay–Sachs carriers in the Ashkenazi Jewish population:

- Heterozygote advantage. When applied to a particular allele, this theory posits that mutation carriers have a selective advantage, perhaps in a particular environment.

- Reproductive compensation. Parents who lose a child because of disease tend to "compensate" by having additional children to replace them. This phenomenon may maintain and possibly even increase the incidence of autosomal recessive disease.

- Founder effect. This hypothesis states that the high incidence of the 1278insTATC chromosomes is the result of an elevated allele frequency that existed by chance in an early founder population.

Tay–Sachs disease was one of the first genetic disorders for which epidemiology was studied using molecular data. Studies of Tay–Sachs mutations using new molecular techniques such as linkage disequilibrium and coalescence analysis have brought an emerging consensus among researchers supporting the founder effect theory.