The signs and symptoms are generally flu-like. They include fever, chills, nausea, headache, fatigue, muscle aches, joint pains, lack of appetite, shortness of breath, pneumonia, chest pain, change in blood pressure, and coughing. A sweet or metallic taste in the mouth may also be reported, along with a dry or irritated throat which may lead to hoarseness. Symptoms of a more severe metal toxicity may also include a burning sensation in the body, shock, no urine output, collapse, convulsions, shortness of breath, yellow eyes or yellow skin, rash, vomiting, watery or bloody diarrhea or low or high blood pressure, which require prompt medical attention. Flu-like symptoms normally disappear within 24 to 48 hours. Full recovery often requires one to three weeks.

Chronic exposure to excessive manganese levels can lead to a variety of psychiatric and motor disturbances, termed manganism. Generally, exposure to ambient manganese air concentrations in excess of 5 micrograms Mn/m can lead to Mn-induced symptoms.

In initial stages of manganism, neurological symptoms consist of reduced response speed, irritability, mood changes, and compulsive behaviors. Upon protracted exposure symptoms are more prominent and resemble those of idiopathic Parkinson's disease, as which it is often misdiagnosed, although there are particular differences in both the symptoms (nature of tremors, for example), response to drugs such as levodopa, and affected portion of the basal ganglia. Symptoms are also similar to Lou Gehrig's disease and multiple sclerosis.

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.

The symptoms of organophosphate poisoning include muscle weakness, fatigue, muscle cramps, fasciculation, and paralysis. Other symptoms include hypertension, and hypoglycemia.

Overstimulation of nicotinic acetylcholine receptors in the central nervous system, due to accumulation of ACh, results in anxiety, headache, convulsions, ataxia, depression of respiration and circulation, tremor, general weakness, and potentially coma. When there is expression of muscarinic overstimulation due to excess acetylcholine at muscarinic acetylcholine receptors symptoms of visual disturbances, tightness in chest, wheezing due to bronchoconstriction, increased bronchial secretions, increased salivation, lacrimation, sweating, peristalsis, and urination can occur.

The effects of organophosphate poisoning on muscarinic receptors are recalled using the mnemonic SLUDGEM (salivation, lacrimation, urination, defecation, gastrointestinal motility, emesis, miosis) An additional mnemonic is MUDDLES: miosis, urination, diarrhea, diaphoresis, lacrimation, excitation, and salivation.

The onset and severity of symptoms, whether acute or chronic, depends upon the specific chemical, the route of exposure (skin, lungs, or GI tract), the dose, and the individuals ability to degrade the compound, which the PON1 enzyme level will affect.

Neurotoxic effects have also been linked to poisoning with OP pesticides causing four neurotoxic effects in humans: cholinergic syndrome, intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP), and chronic organophosphate-induced neuropsychiatric disorder (COPIND). These syndromes result after acute and chronic exposure to OP pesticides.

Cholinergic syndrome occurs in acute poisonings with OP pesticides and is directly related to levels of AChE activity. Symptoms include miosis, sweating, lacrimation, gastrointestinal symptoms, respiratory difficulties, shortness of breath, slowed heart rate, cyanosis, vomiting, diarrhea, trouble sleeping, as well as other symptoms. Along with these central effects can be seen and finally seizures, convulsions, coma, respiratory failure. If the person survives the first day of poisoning personality changes can occur, aggressive events, psychotic episodes, disturbances and deficits in memory and attention, as well as other delayed effects. When death occurs, it is most commonly due to respiratory failure from the combination of central and peripheral effects, paralysis of respiratory muscles and depression of the brain respiratory center. For people afflicted with cholinergic syndrome, atropine sulfate combined with an oxime is used to combat the effects of the acute OP poisoning. Diazepam is sometimes also administered in combination with the atropine and oximes.

The intermediate syndrome (IMS) appears in the interval between the end of the cholinergic crisis and the onset of OPIDP. Symptoms associated with IMS manifest within 24–96 hours after exposure. The exact etiology, incidence, and risk factors associated with IMS are not clearly understood, but IMS is recognized as a disorder of neuromuscular junctions. IMS occurs when a person has a prolonged and severe inhibition of AChE and has been linked to specific OP pesticides such as methylparathion, dichlorvos, and parathion. Patients present with increasing weakness of facial, neck flexor and respiratory muscles.

OPIDP occurs in a small percentage of cases, roughly two weeks after exposure, where temporary paralysis occurs. This loss of function and ataxia of peripheral nerves and spinal cord is the phenomenon of OPIDP. Once the symptoms begin with shooting pains in both legs, the symptoms continue to worsen for 3–6 months. In the most severe cases quadriplegia has been observed. Treatment only affects sensory nerves, not motor neurons which may permanently lose function. The aging and phosphorylation of more than 70% of functional NTE in peripheral nerves is one of the processes involved in OPIDP. Standard treatments for OP poisoning are ineffective for OPIDP.

COPIND occurs without cholinergic symptoms and is not dependent on AChE inhibition. COPIND appears with a delay and is long lasting. Symptoms associated with COPIND include cognitive deficit, mood change, autonomic dysfunction, peripheral neuropathy, and extrapyramidal symptoms. The underlying mechanisms of COPIND have not been determined, but it is hypothesized that withdrawal of OP pesticides after chronic exposure or acute exposure could be a factor.

Metal fume fever, also known as brass founders' ague, brass shakes, zinc shakes, galvie flu, metal dust fever, Welding Shivers, or Monday morning fever, is an illness primarily caused by exposure to chemicals such as zinc oxide (ZnO), aluminum oxide (AlO), or magnesium oxide (MgO) which are produced as byproducts in the fumes that result when certain metals are heated. Other common sources are fuming silver, gold, platinum, chromium (from stainless steel), nickel, arsenic, manganese, beryllium, cadmium, cobalt, lead, selenium, and zinc.

Welders are commonly exposed to the substances that cause metal fume fever from the base metal, plating, or filler. Brazing and soldering can also cause metal poisoning due to exposure to lead, zinc, copper, or cadmium. In extreme cases, cadmium (present in some older silver solder alloys) can cause loss of consciousness.

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.

Lead poisoning can cause a variety of symptoms and signs which vary depending on the individual and the duration of lead exposure. Symptoms are nonspecific and may be subtle, and someone with elevated lead levels may have no symptoms. Symptoms usually develop over weeks to months as lead builds up in the body during a chronic exposure, but acute symptoms from brief, intense exposures also occur.

Symptoms from exposure to organic lead, which is probably more toxic than inorganic lead due to its lipid solubility, occur rapidly. Poisoning by organic lead compounds has symptoms predominantly in the central nervous system, such as insomnia, delirium, cognitive deficits, tremor, hallucinations, and convulsions.

Symptoms may be different in adults and children; the main symptoms in adults are headache, abdominal pain, memory loss, kidney failure, male reproductive problems, and weakness, pain, or tingling in the extremities.

Early symptoms of lead poisoning in adults are commonly nonspecific and include depression, loss of appetite, intermittent abdominal pain, nausea, diarrhea, constipation, and muscle pain. Other early signs in adults include malaise, fatigue, decreased libido, and problems with sleep. An unusual taste in the mouth and personality changes are also early signs.

In adults, symptoms can occur at levels above 40 μg/dL, but are more likely to occur only above 50–60 μg/dL. Symptoms begin to appear in children generally at around 60 μg/dL. However, the lead levels at which symptoms appear vary widely depending on unknown characteristics of each individual. At blood lead levels between 25 and 60 μg/dL, neuropsychiatric effects such as delayed reaction times, irritability, and difficulty concentrating, as well as slowed motor nerve conduction and headache can occur. Anemia may appear at blood lead levels higher than 50 μg/dL. In adults, abdominal colic, involving paroxysms of pain, may appear at blood lead levels greater than 80 μg/dL. Signs that occur in adults at blood lead levels exceeding 100 μg/dL include wrist drop and foot drop, and signs of encephalopathy (a condition characterized by brain swelling), such as those that accompany increased pressure within the skull, delirium, coma, seizures, and headache. In children, signs of encephalopathy such as bizarre behavior, discoordination, and apathy occur at lead levels exceeding 70 μg/dL. For both adults and children, it is rare to be asymptomatic if blood lead levels exceed 100 μg/dL.

ICD-9-CM code 985.8 "Toxic effect of other specified metals" includes acute & chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc.

- In addition, it includes poisoning and toxic effects of other metals including tin, selenium nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc.

- Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium.

In acute poisoning, typical neurological signs are pain, muscle weakness, numbness and tingling, and, rarely, symptoms associated with inflammation of the brain. Abdominal pain, nausea, vomiting, diarrhea, and constipation are other acute symptoms. Lead's effects on the mouth include astringency and a metallic taste. Gastrointestinal problems, such as constipation, diarrhea, poor appetite, or weight loss, are common in acute poisoning. Absorption of large amounts of lead over a short time can cause shock (insufficient fluid in the circulatory system) due to loss of water from the gastrointestinal tract. Hemolysis (the rupture of red blood cells) due to acute poisoning can cause anemia and hemoglobin in the urine. Damage to kidneys can cause changes in urination such as decreased urine output. People who survive acute poisoning often go on to display symptoms of chronic poisoning.

A pesticide poisoning occurs when chemicals intended to control a pest affect non-target organisms such as humans, wildlife, or bees. There are three types of pesticide poisoning. The first of the three is a single and short-term very high level of exposure which can be experienced by individuals who commit suicide, as well as pesticide formulators. The second type of poisoning is long-term high-level exposure, which can occur in pesticide formulators and manufacturers. The third type of poisoning is a long-term low-level exposure, which individuals are exposed to from sources such as pesticide residues in food as well as contact with pesticide residues in the air, water, soil, sediment, food materials, plants and animals.

In developing countries, such as Sri Lanka, pesticide poisonings from short-term very high level of exposure (acute poisoning) is the most worrisome type of poisoning. However, in developed countries, such as Canada, it is the complete opposite: acute pesticide poisoning is controlled, thus making the main issue long-term low-level exposure of pesticides.

Manganism or manganese poisoning is a toxic condition resulting from chronic exposure to manganese. It was first identified in 1837 by James Couper.

Copper toxicity, also called copperiedus, refers to the consequences of an excess of copper in the body. Copperiedus can occur from eating acid foods cooked in uncoated copper cookware, or from exposure to excess copper in drinking water or other environmental sources.

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.

Health effects of pesticides may be acute or delayed in those who are exposed. A 2007 systematic review found that "most studies on non-Hodgkin lymphoma and leukemia showed positive associations with pesticide exposure" and thus concluded that cosmetic use of pesticides should be decreased. Strong evidence also exists for other negative outcomes from pesticide exposure including neurological problems, birth defects, fetal death, and neurodevelopmental disorder.

According to The Stockholm Convention on Persistent Organic Pollutants, 9 of the 12 most dangerous and persistent chemicals are pesticides.

A toxic heavy metal is any relatively dense metal or metalloid that is noted for its potential toxicity, especially in environmental contexts. The term has particular application to cadmium, mercury, lead and arsenic, all of which appear in the World Health Organisation's list of 10 chemicals of major public concern. Other examples include manganese, chromium, cobalt, nickel, copper, zinc, selenium, silver, antimony and thallium.

Heavy metals are found naturally in the earth. They become concentrated as a result of human caused activities and can enter plant, animal, and human tissues via inhalation, diet, and manual handling. Then, they can bind to and interfere with the functioning of vital cellular components. The toxic effects of arsenic, mercury, and lead were known to the ancients, but methodical studies of the toxicity of some heavy metals appear to date from only 1868. In humans, heavy metal poisoning is generally treated by the administration of chelating agents. Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health.

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.

Most pesticide-related illnesses have signs and symptoms that are similar to common medical conditions, so a complete and detailed environmental and occupational history is essential for correctly diagnosing a pesticide poisoning. A few additional screening questions about the patient's work and home environment, in addition to a typical health questionnaire, can indicate whether there was a potential pesticide poisoning.

If one is regularly using carbamate and organophosphate pesticides, it is important to obtain a baseline cholinesterase test. Cholinesterase is an important enzyme of the nervous system, and these chemical groups kill pests and potentially injure or kill humans by inhibiting cholinesterase. If one has had a baseline test and later suspects a poisoning, one can identify the extent of the problem by comparison of the current cholinesterase level with the baseline level.

Chloracne is very often seen in combination with hyperhidrosis (clammy, sweaty skin) and porphyria cutanea tarda (a skin condition of increased pigmentation, hair coarsening and blistering).

Acute health problems may occur in workers that handle pesticides, such as abdominal pain, dizziness, headaches, nausea, vomiting, as well as skin and eye problems. In China, an estimated half million people are poisoned by pesticides each year, 500 of whom die. Pyrethrins, insecticides commonly used in common bug killers, can cause a potentially deadly condition if breathed in.

Coal ash, also known as coal combustion residuals (CCRs), is the particulate residue that remains from burning coal. Depending on the chemical composition of the coal burned, this residue may contain toxic substances and pose a health risk to workers in coal-fired power plants.

Toluene toxicity refers to the harmful effects caused by toluene on the body

Kashin–Beck disease (KBD) is a chronic, endemic type of osteochondropathy (disease of the bone) that is mainly distributed from northeastern to southwestern China, involving 15 provinces. Tibet currently has the highest incidence rate of KBD in China. Southeast Siberia and North Korea are other affected areas. KBD usually involves children ages 5–15. To date, more than a million individuals have suffered from KBD. The symptoms of KBD include joint pain, morning stiffness in the joints, disturbances of flexion and extension in the elbows, enlarged inter-phalangeal joints and limited motion in many joints of the body. Death of cartilage cells in the growth plate and articular surface is the basic pathologic feature; this can result in growth retardation and secondary osteoarthrosis. Histological diagnosis of KBD is particularly difficult; clinical and radiological examinations have proved to be the best means for identifying KBD. Little is known about the early stages of KBD before the visible appearance of the disease becomes evident in the destruction of the joints.

This disease has been recognized for over 150 years but its cause has not yet been completely defined. Currently the accepted potential causes of KBD include mycotoxins present in grain, trace mineral deficiency in nutrition, and high levels of fulvic acid in drinking water. Selenium and iodine have been considered the most important deficiencies associated with KBD. Mycotoxins produced by fungi can contaminate grain, which may cause KBD because mycotoxins cause the production of free radicals. T-2 is the mycotoxin implicated with KBD, produced by members of several fungal genera. T-2 toxin can cause lesions in hematopoietic, lymphoid, gastrointestinal, and cartilage tissues, especially in physeal cartilage. Fulvic acid present in drinking water damages cartilage cells. Selenium supplementation in selenium deficient areas has been shown to prevent this disease. However, selenium supplementation in some areas showed no significant effect, proving that deficiency of selenium may not be the dominant cause in KBD. Recently a significant association between SNP rs6910140 of COL9A1 and Kashin–Beck disease was discovered genetically, suggesting a role of COL9A1 in the development of Kashin–Beck disease.

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.

Chloracne is an acne-like eruption of blackheads, cysts, and pustules associated with over-exposure to certain halogenated aromatic compounds, such as chlorinated dioxins and dibenzofurans. The lesions are most frequently found on the cheeks, behind the ears, in the armpits and groin region.

The condition was first described in German industrial workers in 1897 by Siegfried Bettmann, and was initially believed to be caused by exposure to chlorine (hence the name "chloracne"). It was only in the mid-1950s that chloracne was associated with aromatic hydrocarbons. The substances that may cause chloracne are now collectively known as chloracnegens.

Chloracne is particularly linked to toxic exposure to dioxins (byproducts of many chemical processes, including the manufacture of herbicides such as Agent Orange)—so much so that it is considered a clinical sign of dioxin exposure. The severity and onset of chloracne may follow a typical asymptotic dose-response relationship curve.