Common symptoms of mercury poisoning include peripheral neuropathy, presenting as paresthesia or itching, burning, pain, or even a sensation that resembles small insects crawling on or under the skin (formication); skin discoloration (pink cheeks, fingertips and toes); swelling; and desquamation (shedding or peeling of skin).

Mercury irreversibly inhibits selenium-dependent enzymes (see below) and may also inactivate "S"-adenosyl-methionine, which is necessary for catecholamine catabolism by catechol-"O"-methyl transferase. Due to the body's inability to degrade catecholamines (e.g. epinephrine), a person suffering from mercury poisoning may experience profuse sweating, tachycardia (persistently faster-than-normal heart beat), increased salivation, and hypertension (high blood pressure).

Affected children may show red cheeks, nose and lips, loss of hair, teeth, and nails, transient rashes, hypotonia (muscle weakness), and increased sensitivity to light. Other symptoms may include kidney dysfunction (e.g. Fanconi syndrome) or neuropsychiatric symptoms such as emotional lability, memory impairment, or insomnia.

Thus, the clinical presentation may resemble pheochromocytoma or Kawasaki disease. Desquamation (skin peeling) can occur with severe mercury poisoning acquired by handling elemental mercury.

Mercury poisoning is a type of metal poisoning due to mercury exposure. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia (pink's disease) in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury is unclear.

Forms of mercury exposure include metal, vapor, salt, and organic compound. Most exposure is from eating fish, amalgam based dental fillings, or exposure at work. In fish, those higher up in the food chain generally have higher levels of mercury. Less commonly poisoning may occur as an attempt to end one's life. Human activities that release mercury into the environment include the burning of coal and mining of gold. Tests of the blood, urine, and hair for mercury are available but do not relate well to the amount in the body.

Prevention includes eating a diet low in mercury, removing mercury from medical and other devices, proper disposal of mercury, and not mining further mercury. In those with acute poisoning from inorganic mercury salts, chelation with either dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) appears to improve outcomes if given within a few hours of exposure. Chelation for those with long-term exposure is of unclear benefit. In certain communities that survive on fishing, rates of mercury poisoning among children have been as high as 1.7 per 100.

If cyanide is inhaled it can cause a coma with seizures, apnea, and cardiac arrest, with death following in a matter of seconds. At lower doses, loss of consciousness may be preceded by general weakness, giddiness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the person progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. A cherry red skin color that changes to dark may be present as the result of increased venous hemoglobin oxygen saturation. Cyanide does not directly cause cyanosis. A fatal dose for humans can be as low as 1.5 mg/kg body weight.

Symptoms of arsenic poisoning begin with headaches, confusion, severe diarrhea, and drowsiness. As the poisoning develops, convulsions and changes in fingernail pigmentation called leukonychia striata (Mees's lines, or Aldrich-Mees's lines) may occur. When the poisoning becomes acute, symptoms may include diarrhea, vomiting, vomiting blood, blood in the urine, cramping muscles, hair loss, stomach pain, and more convulsions. The organs of the body that are usually affected by arsenic poisoning are the lungs, skin, kidneys, and liver. The final result of arsenic poisoning is coma and death.

Arsenic is related to heart disease (hypertension-related cardiovascular disease), cancer, stroke (cerebrovascular diseases), chronic lower respiratory diseases, and diabetes.

Chronic exposure to arsenic is related to vitamin A deficiency, which is related to heart disease and night blindness.

Inorganic arsenites (arsenic(III)) in drinking water have a much higher acute toxicity than organic arsenates (arsenic(V)). The acute minimal lethal dose of arsenic in adults is estimated to be 70 to 200 mg or 1 mg/kg/day.

Exposure to lower levels of cyanide over a long period (e.g., after use of improperly processed cassava roots as a primary food source in tropical Africa) results in increased blood cyanide levels, which can result in weakness and a variety of symptoms, including permanent paralysis, nervous lesions, hypothyroidism, and miscarriages. Other effects include mild liver and kidney damage.

Metal toxicity or metal poisoning is the toxic effect of certain metals in certain forms and doses on life. Some metals are toxic when they form poisonous soluble compounds. Certain metals have no biological role, i.e. are not essential minerals, or are toxic when in a certain form. In the case of lead, any measurable amount may have negative health effects. Often heavy metals are thought as synonymous, but lighter metals may also be toxic in certain circumstances, such as beryllium and lithium. Not all heavy metals are particularly toxic, and some are essential, such as iron. The definition may also include trace elements when in abnormally high doses may be toxic. An option for treatment of metal poisoning may be chelation therapy, which is a technique which involves the administration of chelation agents to remove metals from the body.

Toxic metals sometimes imitate the action of an essential element in the body, interfering with the metabolic process resulting in illness. Many metals, particularly heavy metals are toxic, but some heavy metals are essential, and some, such as bismuth, have a low toxicity. Most often the definition of toxic metals includes at least cadmium, manganese, lead, mercury and the radioactive metals. Metalloids (arsenic, polonium) may be included in the definition. Radioactive metals have both radiological toxicity and chemical toxicity. Metals in an oxidation state abnormal to the body may also become toxic: chromium(III) is an essential trace element, but chromium(VI) is a carcinogen.

Toxicity is a function of solubility. Insoluble compounds as well as the metallic forms often exhibit negligible toxicity. The toxicity of any metal depends on its ligands. In some cases, organometallic forms, such as methylmercury and tetraethyl lead, can be extremely toxic. In other cases, organometallic derivatives are less toxic such as the cobaltocenium cation.

Decontamination for toxic metals is different from organic toxins: because toxic metals are elements, they cannot be destroyed. Toxic metals may be made insoluble or collected, possibly by the aid of chelating agents, or through bioremediation. Alternatively, they can be diluted into a sufficiently large reservoir, such as the sea, because immediate toxicity is a function of concentration rather than amount.

Toxic metals can bioaccumulate in the body and in the food chain. Therefore, a common characteristic of toxic metals is the chronic nature of their toxicity. This is particularly notable with radioactive heavy metals such as radium, which imitates calcium to the point of being incorporated into human bone, although similar health implications are found in lead or mercury poisoning. The exceptions to this are barium and aluminium, which can be removed efficiently by the kidneys.

Poisoning is a condition or a process in which an organism becomes chemically harmed (poisoned) by a toxic substance or venom of an animal.

Acute poisoning is exposure to a poison on one occasion or during a short period of time. Symptoms develop in close relation to the degree of exposure. Absorption of a poison is necessary for systemic poisoning (that is, in the blood throughout the body). In contrast, substances that destroy tissue but do not absorb, such as lye, are classified as corrosives rather than poisons. Furthermore, many common household medications are not labeled with skull and crossbones, although they can cause severe illness or even death. In the medical sense, toxicity and poisoning can be caused by less dangerous substances than those legally classified as a poison. Toxicology is the study and practice of the symptoms, mechanisms, diagnosis, and treatment of poisoning.

Chronic poisoning is long-term repeated or continuous exposure to a poison where symptoms do not occur immediately or after each exposure. The patient gradually becomes ill, or becomes ill after a long latent period. Chronic poisoning most commonly occurs following exposure to poisons that bioaccumulate, or are biomagnified, such as mercury, gadolinium, and lead.

Contact or absorption of poisons can cause rapid death or impairment. Agents that act on the nervous system can paralyze in seconds or less, and include both biologically derived neurotoxins and so-called nerve gases, which may be synthesized for warfare or industry.

Inhaled or ingested cyanide, used as a method of execution in gas chambers, almost instantly starves the body of energy by inhibiting the enzymes in mitochondria that make ATP. Intravenous injection of an unnaturally high concentration of potassium chloride, such as in the execution of prisoners in parts of the United States, quickly stops the heart by eliminating the cell potential necessary for muscle contraction.

Most biocides, including pesticides, are created to act as poisons to target organisms, although acute or less observable chronic poisoning can also occur in non-target organisms (secondary poisoning), including the humans who apply the biocides and other beneficial organisms. For example, the herbicide 2,4-D imitates the action of a plant hormone, which makes its lethal toxicity specific to plants. Indeed, 2,4-D is not a poison, but classified as "harmful" (EU).

Many substances regarded as poisons are toxic only indirectly, by toxication. An example is "wood alcohol" or methanol, which is not poisonous itself, but is chemically converted to toxic formaldehyde and formic acid in the liver. Many drug molecules are made toxic in the liver, and the genetic variability of certain liver enzymes makes the toxicity of many compounds differ between individuals.

Exposure to radioactive substances can produce radiation poisoning, an unrelated phenomenon.

Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If exposure occurs over a brief period of time symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.

The most common reason for long-term exposure is contaminated drinking water. Groundwater most often becomes contaminated naturally; however, contamination may also occur from mining or agriculture. Recommended levels in water are less than 10–50 µg/l (10–50 parts per billion). Other routes of exposure include toxic waste sites and traditional medicines. Most cases of poisoning are accidental. Arsenic acts by changing the functioning of around 200 enzymes. Diagnosis is by testing the urine, blood, or hair.

Prevention is by using water that does not contain high levels of arsenic. This may be achieved by the use of special filters or using rainwater. There is not good evidence to support specific treatments for long-term poisoning. For acute poisonings treating dehydration is important. Dimercaptosuccinic acid (DMSA) or dimercaptopropane sulfonate (DMPS) may be used while dimercaprol (BAL) is not recommended. Hemodialysis may also be used.

Through drinking water, more than 200 million people globally are exposed to higher than safe levels of arsenic. The areas most affected are Bangladesh and West Bengal. Acute poisoning is uncommon. The toxicity of arsenic has been described as far back as 1500 BC in the Ebers papyrus.

Cadmium is a naturally occurring toxic heavy metal with common exposure in industrial workplaces, plant soils, and from smoking. Due to its low permissible exposure to humans, overexposure may occur even in situations where trace quantities of cadmium are found. Cadmium is used extensively in electroplating, although the nature of the operation does not generally lead to overexposure. Cadmium is also found in some industrial paints and may represent a hazard when sprayed. Operations involving removal of cadmium paints by scraping or blasting may pose a significant hazard. Cadmium is also present in the manufacturing of some types of batteries. Exposures to cadmium are addressed in specific standards for the general industry, shipyard employment, construction industry, and the agricultural industry.

Tin poisoning refers to the toxic effects of tin and its compounds. Cases of poisoning from tin metal, its oxides, and its salts are "almost unknown"; on the other hand certain organotin compounds are almost as toxic as cyanide.

Argyria or argyrosis is a condition caused by inappropriate exposure to chemical compounds of the element silver, or to silver dust. The most dramatic symptom of argyria is that the skin turns blue or bluish-grey. It may take the form of "generalized argyria" or "local argyria". Generalized argyria affects large areas over much of the visible surface of the body. Local argyria shows in limited regions of the body, such as patches of skin, parts of the mucous membrane or the conjunctiva.

Tin has no known natural biological role in living organisms. It is not easily absorbed by animals and humans. The low toxicity is relevant to the widespread use of tin in dinnerware and canned food. Nausea, vomiting and diarrhea have been reported after ingesting canned food containing 200 mg/kg of tin. This observation led, for example, the Food Standards Agency in the UK to propose upper limits of 200 mg/kg. A study showed that 99.5% of the controlled food cans contain tin in an amount below that level. However un-lacquered tin cans with food of a low pH for example fruits and pickled vegetables can contain elevated concentrations of tin.

The toxic effects of tin compounds is based on the interference with the iron and copper metabolism. For example, it affects heme and cytochrome P450, and decreases their effectiveness.

Organotin compounds can be very toxic. "Tri-"n"-alkyltins" are phytotoxic and, depending on the organic groups, can be powerful bactericides and fungicides. Other triorganotins are used as miticides and acaricides.

Tributyltin (TBT) was extensively used in marine antifouling paints, until discontinued for leisure craft due to concerns over longer term marine toxicity in high traffic areas such as marinas with large numbers of static boats.

Acute mercury exposure has given rise to psychotic reactions such as delirium, hallucinations, and suicidal tendency. Occupational exposure has resulted in erethism, with irritability, excitability, excessive shyness, and insomnia as the principal features of a broad-ranging functional disturbance. With continuing exposure, a fine tremor develops, initially involving the hands and later spreading to the eyelids, lips, and tongue, causing violent muscular spasms in the most severe cases. The tremor is reflected in the handwriting which has a characteristic appearance. In milder cases, erethism and tremor regress slowly over a period of years following removal from exposure. Decreased nerve conduction velocity in mercury-exposed workers has been demonstrated. Long-term, low-level exposure has been found to be associated with less pronounced symptoms of erethism, characterized by fatigue, irritability, loss of memory, vivid dreams, and depression (WHO, 1976).

Effects of chronic occupational exposure to mercury, such as that commonly experienced by affected hatters, include mental confusion, emotional disturbances, and muscular weakness. Severe neurological damage and kidney damage can also occur. Neurological effects include Korsakoff's dementia and erethism (the set of neurological symptoms characteristically associated with mercury poisoning). Signs and symptoms can include red fingers, red toes, red cheeks, sweating, loss of hearing, bleeding from the ears and mouth, loss of appendages such as teeth, hair, and nails, lack of coordination, poor memory, shyness, insomnia, nervousness, tremors, and dizziness. A survey of exposed U.S. hatters revealed predominantly neurological symptomatology, including intention tremor. After chronic exposure to the mercury vapours, hatters tended to develop characteristic psychological traits, such as pathological shyness and marked irritability (box). Such manifestations among hatters prompted several popular names for erethism, including "mad hatter disease", "mad hatter syndrome", "hatter's shakes" and "Danbury shakes".

Erethism or erethism mercurialis is a neurological disorder which affects the whole central nervous system, as well as a symptom complex derived from mercury poisoning. This is also sometimes known as the mad hatter disease. Historically, this was common among old England felt-hatmakers who used mercury to stabilize the wool in a process called felting, where hair was cut from a pelt of an animal such as a rabbit. The industrial workers were exposed to the mercury vapors, giving rise to the expression “mad as a hatter.” Some believe that the character the Mad Hatter in Lewis Carroll's Alice in Wonderland is an example of someone suffering from erethism, but the origin of this account is unclear. The character was almost certainly based on Theophilus Carter, an eccentric furniture dealer who was well known to Carroll.

Mad hatter disease, or mad hatter syndrome, was an occupational disease among hatmakers, caused by chronic mercury poisoning. It affected those whose felting work involved prolonged exposure to mercury vapors. The neurotoxic effects included tremor and the pathological shyness and irritability characteristic of erethism.

Erethism is due to mercury poisoning. Mercury is an element that is found all over the earth in soil, rocks, and water. People who get erethism are usually exposed to jobs that have something to do with these elements, such as construction. People who work in factory jobs tend to have a higher chance of getting erethism. The problem with mercury is that if humans are exposed to any of the forms of mercury, depending on the amount (dose), route (ingestion, skin contact, inhalation), duration (time) of exposure, it can be toxic. Some elemental and chemical forms of mercury (vapor, methylmercury, inorganic mercury) are more toxic than other forms. The human fetus and medically compromised people (for example, patients with lung or kidney problems) are the most susceptible to the toxic effects of mercury.

It is commonly characterized through behavioral changes such as irritability, low self-confidence, depression, apathy, shyness and timidity, and in some extreme cases with prolonged exposure to mercury vapors, delirium, personality changes and memory loss occur as a result. People with erethism find it difficult to interact socially with others, with behaviors similar to that of a social phobia. Although most of the effects of erethism are neurological, some physical problems arise as well, including a decrease in physical strength, “headaches, general pain, and tremors after exposure to metallic mercury” as well as irregular heartbeat. It has been documented that “the tremor in the hands can be so severe that the victim is unable to hold a glass of water without spilling its contents.”

The primary risk factor for erethism is long-term exposure to mercury vapors and gasses at high levels. One group at risk for mercury poisoning is industrial workers and those exposed to high levels of mercury residing naturally in the environment. Erethism is not as serious an issue as it was back before acceptable working condition regulations were enforced. Preventing mercury levels from getting too high limits the amount available for inhalation.

There is a risk of mercury poisoning in the home in some cases. Exposure to mercury vapor may stem from cultural and religious reasons where mercury is sprinkled on the floor of a home or car, burned in a candle, or mixed with perfume. Due to widespread use and popular concern, the risk of toxicity from dental amalgam has been exhaustively investigated. Many studies have not revealed convincing evidence of toxicity . However, in 2015 research showed that an increased mercury release from dental amalgam restorations after exposure to electromagnetic fields is a potential hazard for hypersensitive people and pregnant women.

A chemical burn occurs when living tissue is exposed to a corrosive substance such as a strong acid or base. Chemical burns follow standard burn classification and may cause extensive tissue damage. The main types of irritant and/or corrosive products are: acids, bases, oxidizers / reducing agents, solvents, and alkylants. Additionally, chemical burns can be caused by some types of chemical weapons, e.g., vesicants such as mustard gas and Lewisite, or urticants such as phosgene oxime.

Chemical burns may:

- need no source of heat,

- occur immediately on contact,

- not be immediately evident or noticeable,

- be extremely painful,

- diffuse into tissue and damage structures under skin without immediately apparent damage to skin surface.

The exact symptoms of a chemical burn depend on the chemical involved. Symptoms include itching, bleaching or darkening of skin, burning sensations, trouble breathing, coughing blood and/or tissue necrosis. Common sources of chemical burns include sulfuric acid (HSO), hydrochloric acid (HCl), sodium hydroxide (NaOH), lime (CaO), silver nitrate (AgNO), and hydrogen peroxide (HO). Effects depend on the substance; hydrogen peroxide removes a bleached layer of skin, while nitric acid causes a characteristic color change to yellow in the skin, and silver nitrate produces noticeable black stains. Chemical burns may occur through direct contact on body surfaces, including skin and eyes, via inhalation, and/or by ingestion. Lipophilic substances that diffuse efficiently in human tissue, e.g., hydrofluoric acid, sulfur mustard, and dimethyl sulfate, may not react immediately, but instead produce the burns and inflammation hours after the contact. Chemical fabrication, mining, medicine, and related professional fields are examples of occupations where chemical burns may occur. Hydrofluoric acid leaches into the bloodstream and reacts with calcium and magnesium, and the resulting salts can cause cardiac arrest after eating through skin.

Cadmium (Cd) is an extremely toxic industrial and environmental pollutant classified as a human carcinogen [Group 1 – according to International Agency for Research on Cancer; Group 2a – according to Environmental Protection Agency (EPA); and 1B carcinogen classified by European Chemical Agency

Acute exposure to cadmium fumes may cause flu-like symptoms including chills, fever, and muscle ache sometimes referred to as "the cadmium blues." Symptoms may resolve after a week if there is no respiratory damage. More severe exposures can cause tracheo-bronchitis, pneumonitis, and pulmonary edema. Symptoms of inflammation may start hours after the exposure and include cough, dryness and irritation of the nose and throat, headache, dizziness, weakness, fever, chills, and chest pain.

Inhaling cadmium-laden dust quickly leads to respiratory tract and kidney problems which can be fatal (often from renal failure). Ingestion of any significant amount of cadmium causes immediate poisoning and damage to the liver and the kidneys. Compounds containing cadmium are also carcinogenic.

The bones become soft ("osteomalacia"), lose bone mineral density ("osteoporosis") and become weaker. This causes the pain in the joints and the back, and also increases the risk of fractures. In extreme cases of cadmium poisoning, mere body weight causes a fracture.

The kidneys lose their function to remove acids from the blood in "proximal renal tubular dysfunction". The kidney damage inflicted by cadmium poisoning is irreversible. The "proximal renal tubular dysfunction" creates low phosphate levels in the blood ("hypophosphatemia"), causing muscle weakness and sometimes coma. The dysfunction also causes gout, a form of arthritis due to the accumulation of uric acid crystals in the joints because of high acidity of the blood ("hyperuricemia"). Another side effect is increased levels of chloride in the blood ("hyperchloremia"). The kidneys can also shrink up to 30%. Cadmium exposure is also associated with the development of kidney stones.

Similar to zinc, long term exposure to cadmium fumes can cause irreversible total loss of smell.

Inside cells, cadmium ions act as a hydrogen peroxide generator. This sudden surge of cytosolic hydrogen peroxide causes increased lipid peroxidation and additionally depletes ascorbate and glutathione stores. Hydrogen peroxide can also convert thiol groups on proteins into nonfunctional sulfones and is also capable of directly attacking nuclear DNA. This oxidative stress causes the afflicted cell to manufacture large amounts of inflammatory cytokines.

Carbon monoxide is not toxic to all forms of life. Its harmful effects are due to binding with hemoglobin so its danger to organisms that do not use this compound is doubtful. It thus has no effect on photosynthesising plants. It is easily absorbed through the lungs. Inhaling the gas can lead to hypoxic injury, nervous system damage, and even death. Different people and populations may have different carbon monoxide tolerance levels. On average, exposures at 100 ppm or greater is dangerous to human health. In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period; in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached. Carbon monoxide exposure may lead to a significantly shorter life span due to heart damage. The carbon monoxide tolerance level for any person is altered by several factors, including activity level, rate of ventilation, a pre-existing cerebral or cardiovascular disease, cardiac output, anemia, sickle cell disease and other hematological disorders, barometric pressure, and metabolic rate.

Acute inhalation injury may result from frequent and widespread use of household cleaning agents and industrial gases (including chlorine and ammonia). The airways and lungs receive continuous first-pass exposure to non-toxic and irritant or toxic gases via inhalation. Irritant gases are those that, on inhalation, dissolve in the water of the respiratory tract mucosa and provoke an inflammatory response, usually from the release of acidic or alkaline radicals. Smoke, chlorine, phosgene, sulfur dioxide, hydrogen chloride, hydrogen sulfide, nitrogen dioxide, ozone, and ammonia are common irritants.

Depending on the type and amount of irritant gas inhaled, victims can experience symptoms ranging from minor respiratory discomfort to acute airway and lung injury and even death. A common response cascade to a variety of irritant gases includes inflammation, edema and epithelial sloughing, which if left untreated can result in scar formation and pulmonary and airway remodeling. Currently, mechanical ventilation remains the therapeutic mainstay for pulmonary dysfunction following acute inhalation injury.

The main manifestations of carbon monoxide poisoning develop in the organ systems most dependent on oxygen use, the central nervous system and the heart. The initial symptoms of acute carbon monoxide poisoning include headache, nausea, malaise, and fatigue. These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis. Headache is the most common symptom of acute carbon monoxide poisoning; it is often described as dull, frontal, and continuous. Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia; central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and death. Less common symptoms of acute carbon monoxide poisoning include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney failure, skin lesions, and visual and auditory problems.

One of the major concerns following acute carbon monoxide poisoning is the severe delayed neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like syndromes, cortical blindness, and a depressed mood. Depression may occur in those who did not have pre-existing depression. These delayed neurological sequelae may occur in up to 50% of poisoned people after 2 to 40 days. It is difficult to predict who will develop delayed sequelae; however, advanced age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms.

One classic sign of carbon monoxide poisoning is more often seen in the dead rather than the living – people have been described as looking red-cheeked and healthy (see below). However, since this "cherry-red" appearance is common only in the deceased, and is unusual in living people, it is not considered a useful diagnostic sign in clinical medicine. In pathological (autopsy) examination the ruddy appearance of carbon monoxide poisoning is notable because unembalmed dead persons are normally bluish and pale, whereas dead carbon-monoxide poisoned persons may simply appear unusually lifelike in coloration. The colorant effect of carbon monoxide in such postmortem circumstances is thus analogous to its use as a red colorant in the commercial meat-packing industry.

In epidemiology, environmental diseases are diseases that can be directly attributed to environmental factors (as distinct from genetic factors or infection). Apart from the true monogenic genetic disorders, environmental diseases may determine the development of disease in those genetically predisposed to a particular condition. Stress, physical and mental abuse, diet, exposure to toxins, pathogens, radiation, and chemicals found in almost all personal care products and household cleaners are possible causes of a large segment of non-hereditary disease. If a disease process is concluded to be the result of a combination of genetic and "environmental factor" influences, its etiological origin can be referred to as having a multifactorial pattern.

There are many different types of environmental disease including:

- Lifestyle disease such as cardiovascular disease, diseases caused by substance abuse such as alcoholism, and smoking-related disease

- Disease caused by physical factors in the environment, such as skin cancer caused by excessive exposure to ultraviolet radiation in sunlight

- Disease caused by exposure to toxic or irritant chemicals in the environment such as toxic metals

==Environmental Diseases vs. Pollution-

Related Diseases==

Environmental diseases are a direct result from the environment. This includes diseases caused by substance abuse, exposure to toxic chemicals, and physical factors in the environment, like UV radiation from the sun, as well as genetic predisposition. Meanwhile, pollution-related diseases are attributed to exposure to toxins in the air, water, and soil. Therefore all pollution-related disease are environmental diseases, but not all environmental diseases are pollution-related diseases.

Epidemic dropsy is a form of edema of extremities due to poisoning by "Argemone mexicana" (Mexican prickly poppy).

Epidemic dropsy is a clinical state resulting from use of edible oils adulterated with "Argemone mexicana" seed oil.

Sanguinarine and dihydrosanguinarine are two major toxic alkaloids of argemone oil, which cause widespread capillary dilatation, proliferation and increased capillary permeability. When mustard oil is adulterated deliberately (as in most cases) or accidentally with argemone oil, proteinuria (specifically loss of albumin) occurs, with a resultant edema as would occur in nephrotic syndrome.

Other major symptoms are pitting edema of extremities, headache, nausea, loose bowels, erythema, glaucoma and breathlessness.

Leakage of the protein-rich plasma component into the extracellular compartment leads to the formation of edema. The haemodynamic consequences of this vascular dilatation and permeability lead to a state of relative hypovolemia with a constant stimulus for fluid and salt conservation by the kidneys. Illness begins with gastroenteric symptoms followed by cutaneous erythema and pigmentation. Respiratory symptoms such as cough, shortness of breath and orthopnoea, progressing to frank right-sided congestive cardiac failure, are seen.

Mild to moderate anaemia, hypoproteinaemia, mild to moderate renal azotemia, retinal haemorrhages, and glaucoma are common manifestations. There is no specific therapy. Removal of the adulterated oil and symptomatic treatment of congestive cardiac failure and respiratory symptoms, along with administration of antioxidants and multivitamins, remain the mainstay of treatment.

Epidemic dropsy occurs as an epidemic in places where use of mustard oil, (from the seeds of Brassica "juncea" commonly known as Indian mustard ) as cooking medium is common.

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.

Hydrogen narcosis (also known as the hydrogen effect) is the psychotropic state induced by breathing hydrogen at high pressures. Hydrogen narcosis produces symptoms such as hallucinations, disorientation, and confusion, which are similar to hallucinogenic drugs. It can be experienced by deep-sea divers who dive to below sea level breathing hydrogen mixtures. However, hydrogen has far less narcotic effect than nitrogen (which causes the better known nitrogen narcosis) and is very rarely used in diving. In tests of the effect of hydrogen narcosis, where divers dived to with a hydrogen–helium–oxygen (Hydreliox) mixture containing 49% hydrogen, it was found that while the narcotic effect of hydrogen was detectable, the neurological symptoms of high-pressure nervous syndrome were only moderate.

Smoke inhalation injury, either by itself but more so in the presence of body surface burn, can result in severe lung-induced morbidity and mortality. The most common cause of death in burn centers is now respiratory failure. The September 11 attacks in 2001 and forest fires in U.S. states such as California and Nevada are examples of incidents that have caused smoke inhalation injury. Injury to the lungs and airways is not only due to deposition of fine particulate soot but also due to the gaseous components of smoke, which include phosgene, carbon monoxide, and sulfur dioxide.