690 people from the Agano River basin have been certified as patients of Niigata Minamata disease.

Since the Niigata outbreak was the second recorded in Japan and occurred in the Lower Agano River Basin, it is sometimes called or . It is one of the Four Big Pollution Diseases of Japan.

, sometimes referred to as , is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, loss of peripheral vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect fetuses in the womb.

Minamata disease was first discovered in Minamata city in Kumamoto prefecture, Japan, in 1956. It was caused by the release of methylmercury in the industrial wastewater from the Chisso Corporation's chemical factory, which continued from 1932 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in Minamata Bay and the Shiranui Sea, which, when eaten by the local populace, resulted in mercury poisoning. While cat, dog, pig, and human deaths continued for 36 years, the government and company did little to prevent the pollution. The animal effects were severe enough in cats that they came to be named as having "dancing cat fever".

As of March 2001, 2,265 victims had been officially recognised as having Minamata disease (1,784 of whom had died) and over 10,000 had received financial compensation from Chisso. By 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination. On March 29, 2010, a settlement was reached to compensate as-yet uncertified victims.

A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. The original Minamata disease and Niigata Minamata disease are considered two of the four big pollution diseases of Japan.

Some of grain (73,201 tonnes of wheat grain and 22,262 tonnes of barley), coloured a pink-orange hue, were shipped to Iraq from the United States and Mexico. The wheat arrived in Basra on SS "Trade Carrier" between 16 September and 15 October, barley between 22 October and 24 November 1971. Iraq's government chose Mexipak, a high-yield wheat seed developed in Mexico by Norman Borlaug. The seeds contained an average of 7.9 μg/g of mercury, with some samples containing up to nearly twice that. The decision to use mercury-coated grain has been reported as made by the Iraqi government, rather than the supplier, Cargill. The three Northern governorates of Ninawa, Kirkuk and Erbil together received more than half the shipments. Contributing factors to the epidemic included the fact that distribution started late, and much grain arrived after the October–November planting season.

Farmers holding grain ingested it instead, since their own planting had been completed. Distribution was hurried and open, with grain being distributed free of charge or with payment in kind. Some farmers sold their own grain lest this new grain devalue what they had. This left them dependent on tainted grain for the winter. Many Iraqis were either unaware of the significant health risk posed, or chose to ignore the warnings. Initially, farmers were to certify with a thumbprint or signature that they understood the grain was poison, but according to some sources, distributors did not ask for such an indication. Warnings on the sacks were in Spanish and English, not at all understood, or included the black-and-white skull and crossbones design, which meant nothing to Iraqis. The long latent period may have granted farmers a false sense of security, when animals fed the grain appeared to be fine. The red dye washed off the grain; the mercury did not. Hence, washing may have given only the appearance of removing the poison.

Mercury was ingested through the consumption of homemade bread, meat and other animal products obtained from livestock given treated barley, vegetation grown from soil contaminated with mercury, game birds that had fed on the grain and fish caught in rivers, canals, and lakes into which treated grain had been dumped by the farmers. Ground seed dust inhalation was a contributing factor in farmers during sowing and grinding. Consumption of ground flour through homemade bread is thought to have been the major cause, since no cases were reported in urban areas, where government flour supplies were commercially regulated.

6,530 patients were admitted to hospitals with poisoning, and 459 deaths reported. Cases reached a peak of hundreds per day in January, and had largely subsided by the beginning of March. The last admittance was on 27 March; admissions represented every age and gender stratum, although those under the age of ten represented a third of admitted cases. This number is "certainly an underestimate", because of the availability of hospital treatment, hospital overcrowding and lack of faith in treatment. In the most severely affected areas, prevalence was 28% and mortality was 21% of the cases. Some Iraqi doctors believe both the number of cases and fatalities are at least ten times too low, with perhaps 100,000 cases of brain damage. One suggested reason for the vast discrepancy between reported and estimated numbers of deaths is the Iraqi custom, common to large parts of the Middle East, for a person to die at home when possible. Home deaths would not have been recorded.

A large number of patients with minor symptoms recovered completely; those with more serious symptoms improved. This was in contrast to expected outcomes, largely based on analysis of Minamata disease in Japan. In boys with mercury levels below clinical poisoning, a reduction in school performance was noted, although this correlation could not be confirmed. In infants, the mercury poisoning caused central nervous system damage. Relatively low doses caused slower development in children, and abnormal reflexes. Different treatments for mercury poisoning have since been developed, and "quiet baby syndrome", characterised by a baby who never cries, is now a recognised symptom of methylmercury-induced brain damage. Ongoing recommendations of the food regulation authorities have focused on consumption by pregnant women and infant children, noting the particular susceptibility of fetuses and infants to methylmercury poisoning. Data from Iraq have confirmed that methylmercury can pass to a child "in utero", and mercury levels were equal to or higher in the newborn child than in the mother.

In 1974, a joint Food and Agriculture Organization (FAO) and World Health Organisation (WHO) meeting made several recommendations to prevent a similar outbreak. These included stressing the importance of labelling bags in the local language and with locally understood warning symbols. The possibility of an additive creating a strong bitter taste was studied. The meeting urged governments to strictly regulate methyl- and ethylmercury use in their respective countries, including limiting use to where no other reasonable alternative was available. It also recommended the involvement of the FAO and WHO in assisting national governments in regulation and enforcement, and the setting up of national poison control centres. Over 9–13 November, a Conference on Intoxication due to Alkylmercury-Treated Seed was held in Baghdad. It supported the recommendations of the FAO/WHO report and further suggested that local and national media should publicise outbreaks, including size and symptoms; it considered the distribution of this information crucial. It also laid out a general plan as to the collection of relevant information from the field and potential analysis for further investigation. It called on national governments to make use of WHO involvement whenever feasible, and absolved world governments in clear terms, saying that "No country should ever feel that any blame will attach to it for allowing an outbreak to occur".

Iraq now has the highest incidence of Parkinson's in the world. Parkinson's symptoms are very similar to mercury poisoning symptoms. Mercury that enters the brain has a half-life of 27.5 years and chelators are not able to remove it.

Some elements otherwise regarded as toxic heavy metals are essential, in small quantities, for human health. These elements include vanadium, manganese, iron, cobalt, copper, zinc, selenium, strontium and molybdenum. A deficiency of these essential metals may increase susceptibility to heavy metal poisoning.

In humans, heavy metal poisoning is generally treated by the administration of chelating agents.

These are chemical compounds, such as (calcium disodium ethylenediaminetetraacetate) that convert heavy metals to chemically inert forms that can be excreted without further interaction with the body. Chelates are not without side effects and can also remove beneficial metals from the body. Vitamin and mineral supplements are sometimes co-administered for this reason.

Soils contaminated by heavy metals can be remediated by one or more of the following technologies: isolation; immobilization; toxicity reduction; physical separation; or extraction. "Isolation" involves the use of caps, membranes or below-ground barriers in an attempt to quarantine the contaminated soil. "Immobilization" aims to alter the properties of the soil so as to hinder the mobility of the heavy contaminants. "Toxicity reduction" attempts to oxidise or reduce the toxic heavy metal ions, via chemical or biological means into less toxic or mobile forms. "Physical separation" involves the removal of the contaminated soil and the separation of the metal contaminants by mechanical means. "Extraction" is an on or off-site process that uses chemicals, high-temperature volatization, or electrolysis to extract contaminants from soils. The process or processes used will vary according to contaminant and the characteristics of the site.

Methylmercury is the major source of organic mercury for all individuals. Due to bioaccumulation it works its way up through the food web and thus biomagnifies, resulting in high concentrations among populations of some species. Top predatory fish, such as tuna or swordfish, are usually of greater concern than smaller species. The US FDA and the EPA advise women of child-bearing age, nursing mothers, and young children to completely avoid swordfish, shark, king mackerel and tilefish from the Gulf of Mexico, and to limit consumption of albacore ("white") tuna to no more than per week, and of all other fish and shellfish to no more than per week. A 2006 review of the risks and benefits of fish consumption found, for adults, the benefits of one to two servings of fish per week outweigh the risks, even (except for a few fish species) for women of childbearing age, and that avoidance of fish consumption could result in significant excess coronary heart disease deaths and suboptimal neural development in children.

The period between exposure to methylmercury and the appearance of symptoms in adult poisoning cases is long. The longest recorded latent period is five months after a single exposure, in the Dartmouth case (see History); other latent periods in the range of weeks to months have also been reported. No explanation for this long latent period is known. When the first symptom appears, typically paresthesia (a tingling or numbness in the skin), it is followed rapidly by more severe effects, sometimes ending in coma and death. The toxic damage appears to be determined by the peak value of mercury, not the length of the exposure.

Methylmercury exposure during rodent gestation, a developmental period that approximately models human neural development during the first two trimesters of gestation, has long-lasting behavioral consequences that appear in adulthood and, in some cases, may not appear until aging. Prefrontal cortex or dopamine neurotransmission could be especially sensitive to even subtle gestational methylmercury exposure and suggests that public health assessments of methylmercury based on intellectual performance may underestimate the impact of methylmercury in public health.

Ethylmercury is a breakdown product of the antibacteriological agent ethylmercurithiosalicylate, which has been used as a topical antiseptic and a vaccine preservative (further discussed under Thiomersal below). Its characteristics have not been studied as extensively as those of methylmercury. It is cleared from the blood much more rapidly, with a half-life of seven to 10 days, and it is metabolized much more quickly than methylmercury. It is presumed not to have methylmercury's ability to cross the blood–brain barrier via a transporter, but instead relies on simple diffusion to enter the brain. Other exposure sources of organic mercury include phenylmercuric acetate and phenylmercuric nitrate. These compounds were used in indoor latex paints for their antimildew properties, but were removed in 1990 because of cases of toxicity.

Some of the toxic effects of mercury are partially or wholly reversible, either through specific therapy or through natural elimination of the metal after exposure has been discontinued. Autopsy findings point to a half-life of inorganic mercury in human brains of 27.4 years. Heavy or prolonged exposure can do irreversible damage, in particular in fetuses, infants, and young children. Young's syndrome is believed to be a long-term consequence of early childhood mercury poisoning.

Mercuric chloride may cause cancer as it has caused increases in several types of tumors in rats and mice, while methyl mercury has caused kidney tumors in male rats. The EPA has classified mercuric chloride and methyl mercury as possible human carcinogens (ATSDR, EPA)

It is difficult to differentiate the effects of low level metal poisoning from the environment with other kinds of environmental harms, including nonmetal pollution. Generally, increased exposure to heavy metals in the environment increases risk of developing cancer.

Without a diagnosis of metal toxicity and outside of evidence-based medicine, but perhaps because of worry about metal toxicity, some people seek chelation therapy to treat autism, cardiovascular disease, Alzheimer's disease, or any sort of neurodegeneration. Chelation therapy does not improve outcomes for those diseases.

The second outbreak of Minamata disease in Niigata Prefecture was discovered in a very similar way to the original outbreak in Kumamoto Prefecture. From the autumn of 1964 to the spring of 1965, cats living along the banks of the Agano River had been seen to go mad and die: "...one cat ran into a small clay cooking stove containing burning charcoal. With the pupils of its eyes dilated, salivating, convulsing and uttering a strange cry, the cat breathed its last breath." These strange symptoms eventually began to appear in people, too. Professor Tadao Tsubaki of Niigata University examined two patients in April and May 1965 and suspected Minamata disease. One patient's hair was found to have a mercury level of 390 ppm. On 31 May, he reported an outbreak of organic mercury poisoning in the Agano River basin to the prefectural government and made his findings public on 12 June.

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, as a side-effect of estrogen birth control pills, or other environmental sources. It can also result from the genetic condition Wilson's disease.

Minamata disease remains an important issue in contemporary Japanese society. Lawsuits against Chisso and the prefectural and national governments are still continuing and many regard the government responses to date as inadequate. The company's "historical overview" in its current website makes no mention of their role in the mass contamination of Minamata and the dreadful aftermath. Their 2004 Annual Report however reports an equivalent of about US$50 million (5,820 million yen) in "Minamata Disease Compensation Liabilities". From 2000 to 2003, the company also reported total compensation liabilities of over US$170 million. Their 2000 accounts also show that the Japanese and Kumamoto prefectural governments waived an enormous US$560 million in related liabilities. Their FY2004 and FY2005 reports refer to Minamata disease as "mad hatter's disease", a term coined from the mercury poisoning experienced by hat-makers of the last few centuries (cf. Erethism).

A memorial service was held at the Minamata Disease Municipal Museum on 1 May 2006 to mark 50 years since the official discovery of the disease. Despite bad weather, the service was attended by over 600 people, including Chisso chairman Shunkichi Goto and Environment Minister Yuriko Koike.

On Monday, March 29, 2010, a group of 2,123 uncertified victims reached a settlement with the government of Japan, the Kumamoto Prefectural government, and Chisso Corporation to receive individual lump-sum payments of 2.1 million yen and monthly medical allowances.

Most congenital patients are now in their forties and fifties and their health is deteriorating. Their parents, who are often their only source of care, are into their seventies or eighties or already deceased. Often these patients find themselves tied to their own homes and the care of their family, effectively isolated from the local community. Some welfare facilities for patients do exist. One notable example is , a vocational training centre for congenital patients as well as other disabled people in the Minamata area. Hot House members are also involved in raising awareness of Minamata disease, often attending conferences and seminars as well as making regular visits to elementary schools throughout Kumamoto Prefecture.

Bright's disease was historically 'treated' with warm baths, blood-letting, squill, digitalis, mercuric compounds, opium, diuretics, laxatives, and dietary therapy, including abstinence from alcoholic drinks, cheese and red meat. Arnold Ehret was diagnosed with Bright's disease and pronounced incurable by 24 of Europe's most respected doctors; he designed "The Mucusless Diet Healing System", which apparently cured his illness. William Howard Hay, MD had the illness and, it is claimed, cured himself using the Hay diet.

Bright's disease is a historical classification of kidney diseases that would be described in modern medicine as acute or chronic nephritis. It was characterized by swelling, the presence of albumin in the urine and was frequently accompanied by high blood pressure and heart disease.

]

Disease mongering is a term for the practice of widening the diagnostic boundaries of illnesses and aggressively promoting their public awareness in order to expand the markets for treatment.

Among the entities benefiting from selling and delivering treatments are pharmaceutical companies, physicians, alternative practitioners and other professional or consumer organizations. It is distinct from the promulgation of bogus or unrecognised diagnoses.

The term “monger” has ancient roots, providing the basis for many common compound forms such as cheesemonger, fishmonger, and fleshmonger for those who peddle such wares respectively. “Disease mongering” as a label for the "invention" or promotion of diseases in order to capitalize on their treatment was first used in 1992 by health writer Lynn Payer, who applied it to the Listerine mouthwash campaign against halitosis (bad breath).

Payer defined disease mongering as a set of practices which include the following:

- Stating that normal human experiences are abnormal and in need of treatment

- Claiming to recognize suffering which is not present

- Defining a disease such that a large number of people have it

- Defining a disease's cause as some ambiguous deficiency or hormonal imbalance

- Associating a disease with a public relations spin campaign

- Directing the framing of public discussion of a disease

- Intentionally misusing statistics to exaggerate treatment benefits

- Setting a dubious clinical endpoint in research

- Advertising a treatment as without side effect

- Advertising a common symptom as a serious disease

The incidence of conditions not previously defined as illness being medicalised as "diseases" is difficult to scientifically assess due to the inherent social and political nature of the definition of what constitutes a disease, and what aspects of the human condition should be managed according to a medical model. For example, halitosis, the condition which prompted Payer to coin the phrase "disease mongering", isn't merely an imagined social stigma but can stem from any of a wide spectrum of conditions spanning from bacterial infection of the gums to kidney failure, and is recognized by the Scientific Council of the American Dental Association as "a recognizable condition which deserves professional attention".

In laboratory animals, prevention includes a low-stress environment, an adequate amount of nutritional feed, and appropriate sanitation measurements. Because animals likely ingest bacterial spores from contaminated bedding and feed, regular cleaning is a helpful method of prevention. No prevention methods are currently available for wild animal populations.

Pogosta disease is a viral disease, established to be identical with other diseases, Karelian fever and Ockelbo disease. The names are derived from the words Pogosta, Karelia and Ockelbo, respectively.

The symptoms of the disease include usually rash, as well as mild fever and other flu-like symptoms; in most cases the symptoms last less than 5 days. However, in some cases, the patients develop a painful arthritis. There are no known chemical agents available to treat the disease.

It has long been suspected that the disease is caused by a Sindbis-like virus, a positive-stranded RNA virus belonging to the Alphavirus genus and family Togaviridae. In 2002 a strain of Sindbis was isolated from patients during an outbreak of the Pogosta disease in Finland, confirming the hypothesis.

This disease is mainly found in the Eastern parts of Finland; a typical Pogosta disease patient is a middle-aged person who has been infected through a mosquito bite while picking berries in the autumn. The prevalence of the disease is about 100 diagnosed cases every year, with larger outbreaks occurring in 7-year intervals.

Although Tyzzer’s disease is commonly found in laboratory animals worldwide, infected wild animal populations have been identified in North America and Australia. Specific locations where the disease has been reported in the United States include Connecticut, Idaho, Iowa, Maryland, Michigan, Montana, Ohio, Wisconsin, and Wyoming. In Canada, it has been reported in British Columbia, Manitoba, Ontario, and Saskatchewan. Outbreaks in these locations are primarily attributed to muskrat populations; however infected cottontail rabbits have been discovered in Maryland.

Fields' disease is considered to be one of the rarest known diseases in the world, with only two diagnosed cases in history. The frequency of this disease is therefore 1 in approximately 3.75 billion (although since the disease manifested in identical twins, the actual frequency is 1 in approximately 7.5 billion). It is named after Welsh twins Catherine and Kirstie Fields, of Llanelli. Fields' disease is a neuromuscular disease, causing muscular degeneration.

The disease was first noticed when the twins were around the age of four. Doctors have been unable to identify it and have not been able to match it to any known diseases. As a result, the Fields sisters have undergone numerous tests, but no treatment has yet been found. No definitive cause has been determined and doctors have generally concluded that they were born with it.

The disease appears to be progressive in nature. The Fields twins started having problems when they were four years old. By the time they had reached the age of nine, they were having difficulty walking and needed frames to assist them with walking. Their muscles have been gradually deteriorating over time. The disease affects the twins' nerves, causing them to make involuntary muscle movements such as trembling in the hands.

The extent of the disease is still unknown as the two women are only 21. However, the disease has had no apparent effect on their brains or personalities. Doctors do not know if the disease is fatal and, if so, what the life expectancy of one with this disease is. If the cause of the disease is genetic, there is a chance that the twins could pass it on to their future children.

Pacheco's disease is an acute and often lethal infectious disease in psittacine birds. The disease is caused by a group of herpesviruses, "Psittacid herpesvirus 1" (PsHV-1), which consists of four genotypes. Birds which do not succumb to Pacheco's disease after infection with the virus become asymptomatic carriers that act as reservoirs of the infection. These persistently infected birds, often Macaws, Amazon parrots and some species of conures, shed the virus in feces and in respiratory and oral secretions. Outbreaks can occur when stress causes healthy birds who carry the virus to shed it. Birds generally become infected after ingesting the virus in contaminated material, and show signs of the disease within several weeks.

The main sign of Pacheco's disease is sudden death, sometimes preceded by a short, severe illness. If a bird survives Pacheco's disease following infection with PsHV-1 genotypes 1, 2 or 3, it may later develop internal papilloma disease in the gastrointestinal tract.

Susceptible parrot species include the African gray parrot, and cockatoo. Native Australian birds, such as the eclectus parrot, Bourke's parrot, and budgerigar are susceptible to Pacheco's disease, although the disease itself has not been found in Australia.

White band disease (Acroporid white syndrome) is a coral disease that affects acroporid corals and is distinguishable by the white band of dead coral tissue that it forms. The disease completely destroys the coral tissue of Caribbean acroporid corals, specifically elkhorn coral ("Acropora palmata") and staghorn coral ("A. cervicornis"). The disease exhibits a pronounced division between the remaining coral tissue and the exposed coral skeleton. These symptoms are similar to white plague, except that white band disease is only found on acroporid corals, and white plague has not been found on any acroporid corals. It is part of a class of similar disease known as "white syndromes", many of which may be linked to species of "Vibrio" bacteria. While the pathogen for this disease has not been identified, "Vibrio carchariae" may be one of its factors. The degradation of coral tissue usually begins at the base of the coral, working its way up to the branch tips, but it can begin in the middle of a branch.

Life expectancy with Fabry disease for males was 58.2 years, compared with 74.7 years in the general population, and for females 75.4 years compared with 80.0 years in the general population, according to registry data from 2001 to 2008. The most common cause of death was cardiovascular disease, and most of those had received kidney replacements.

In infantile Krabbe disease, death usually occurs in early childhood. A 2011 study found 1, 2, 3 year survival rates of 60%, 26%, and 14%, respectively. A few survived for longer and one was still alive at age 13. Patients with late-onset Krabbe disease tend to have a slower progression of the disease and live significantly longer.