The illness is generally self-limiting. Management on the whole is preventative, by limiting exposure to mouldy environments with ventilation, or by wearing respiratory protection such as facemasks.

Treatment of mild metal fume fever consists of bedrest, keeping the patient well hydrated, and symptomatic therapy (e.g. aspirin for headaches) as indicated. In the case of non-allergic acute lung injury, standard or recommended approaches to treatment have not been defined.

The consumption of large quantities of cow's milk, either before or immediately after exposure is a traditional remedy. However, the United Kingdom Health and Safety Executive challenges this advice, warning, "Don’t believe the stories about drinking milk before welding. It does not prevent you getting metal fume fever."

Prevention of metal fume fever in workers who are at risk (such as welders) involves avoidance of direct contact with potentially toxic fumes, improved engineering controls (exhaust ventilation systems), personal protective equipment (respirators), and education of workers regarding the features of the syndrome itself and proactive measures to prevent its development.

In some cases, the product's design may be changed so as to eliminate the use of risky metals. NiCd rechargeable batteries are being replaced by NiMH. These contain other toxic metals, such as chromium, vanadium and cerium. Cadmium is often replaced by other metals. Zinc or nickel plating can be used instead of cadmium plating, and brazing filler alloys now rarely contain cadmium.

It was recognised as a distinct clinical syndrome in the 1980s. Previously, cases had been reported and given various names such as pulmonary mycotoxicosis, silo unloader’s syndrome, grain fever, toxin fever, humidifier fever, mill fever, toxic alveolitis or allergic alveolitis. In 1994, the National Institute for Occupational Safety and Health published case reports and highlighted the urgency for study of the syndrome.

Research and data collection in the agricultural industry is difficult, as many workers are casual.

Studies have shown that people who are atopic (sensitive), already suffer from allergies, asthma, or compromised immune systems and occupy damp or moldy buildings are at an increased risk of health problems such as inflammatory and toxic responses to mold spores, metabolites and other components. The most common health problem is an allergic reaction. Other problems are respiratory and/or immune system responses including respiratory symptoms, respiratory infections, exacerbation of asthma, and rarely hypersensitivity pneumonitis, allergic alveolitis, chronic rhinosinusitis and allergic fungal sinusitis. Severe reactions are rare but possible. A person's reaction to mold depends on their sensitivity and other health conditions, the amount of mold present, length of exposure and the type of mold or mold products.

Some molds also produce mycotoxins that can pose serious health risks to humans and animals. The term "toxic mold" refers to molds that produce mycotoxins, such as "Stachybotrys chartarum", not to all molds. Exposure to high levels of mycotoxins can lead to neurological problems and in some cases death. Prolonged exposure, e.g., daily workplace exposure, can be particularly harmful.

The five most common genera of indoor molds are "Cladosporium", "Penicillium", "Aspergillus", "Alternaria" and "Trichoderma".

Damp environments which allow mold to grow can also produce bacteria and help release volatile organic compounds.

Mold health issues are potentially harmful effects of molds.

Molds (US usage; British English "moulds") are ubiquitous in the biosphere, and mold spores are a common component of household and workplace dust. The United States Centers for Disease Control and Prevention reported in its June 2006 report, 'Mold Prevention Strategies and Possible Health Effects in the Aftermath of Hurricanes and Major Floods,' that "excessive exposure to mold-contaminated materials can cause adverse health effects in susceptible persons regardless of the type of mold or the extent of contamination." When mold spores are present in abnormally high quantities, they can present especially hazardous health risks to humans after prolonged exposure, including allergic reactions or poisoning by mycotoxins, or causing fungal infection (mycosis).

Prevention of aspergillosis involves a reduction of mold exposure via environmental infection-control. Anti-fungal prophylaxis can be given to high-risk patients. Posaconazole is often given as prophylaxis in severely immunocompromised patients.

The current medical treatments for aggressive invasive aspergillosis include voriconazole and liposomal amphotericin B in combination with surgical debridement.

For the less aggressive allergic bronchopulmonary aspergillosis findings suggest the use of oral steroids for a prolonged period of time, preferably for 6–9 months in allergic aspergillosis of the lungs. Itraconazole is given with the steroids, as it is considered to have a "steroid sparing" effect, causing the steroids to be more effective, allowing a lower dose.,

Other drugs used, such as amphotericin B, caspofungin (in combination therapy only), flucytosine (in combination therapy only), or itraconazole,

are used to treat this fungal infection. However, a growing proportion of infections are resistant to the triazoles. "A. fumigatus", the most commonly infecting species, is intrinsically resistant to fluconazole.

Thunderstorm asthma is the triggering of an asthma attack by environmental conditions directly caused by a local thunderstorm. It has been proposed that during a thunderstorm, pollen grains can absorb moisture and then burst into much smaller fragments with these fragments being easily dispersed by wind. However, there is no experimental evidence confirming this theory. While larger pollen grains are usually filtered by hairs in the nose, the smaller pollen fragments are able to pass through and enter the lungs, triggering the asthma attack.

There have been events where thunderstorms have caused asthma attacks across cities such that emergency services and hospitals have been overwhelmed. The phenomenon was first recognised and studied after three recorded events in the 1980s; in Birmingham, England, in 1983 and in Melbourne, Australia in 1987 and 1989. Since then there have been further reports of widespread thunderstorm asthma in Wagga Wagga, Australia; London, England; Naples, Italy; Atlanta, United States; and Ahvaz, Iran. A further outbreak in Melbourne, in November 2016, that overwhelmed the ambulance system and some local hospitals, resulted in at least nine deaths. There was a similar incident in Kuwait in early December, 2016 with at least 5 deaths and many admissions to the ICU.

Many of those affected during a thunderstorm asthma outbreak may have never experienced an asthma attack before.

It has been found 95% of those that were affected by thunderstorm asthma had a history of hayfever, and 96% of those people had tested positive to grass pollen allergies, particularly rye grass. A rye grass pollen grain can hold up to 700 tiny starch granules, measuring 0.6 to 2.5 μm, small enough to reach the lower airways in the lung.

The effect of mercury took some time – the latent period between ingestion and the first symptoms (typically paresthesia – numbness in the extremities) was between 16 and 38 days. Paresthesia was the predominant symptom in less serious cases. Worse cases included ataxia (typically loss of balance), blindness or reduced vision, and death resulting from central nervous system failure. Anywhere between 20 and 40 mg of mercury has been suggested as sufficient for paresthesia (between 0.5 and 0.8 mg/kg of body weight). On average, individuals affected consumed 20 kg or so of bread; the 73,000 tonnes provided would have been sufficient for over 3 million cases.

The hospital in Kirkuk received large numbers of patients with symptoms that doctors recognised from the 1960 outbreak. The first case of alkylmercury poisoning was admitted to hospital on 21 December. By 26 December, the hospital had issued a specific warning to the government. By January 1972, the government had started to strongly warn the populace about eating the grain, although dispatches did not mention the large numbers already ill. The Iraqi Army soon ordered disposal of the grain and eventually declared the death penalty for anyone found selling it. Farmers dumped their supplies wherever possible, and it soon got into the water supply (particularly the River Tigris), causing further problems. The government issued a news blackout and released little information about the outbreak.

The World Health Organization assisted the Iraqi government through the supply of drugs, analytical equipment and expertise. Many new treatments were tried, since existing methods for heavy metal poisoning were not particularly effective. Dimercaprol was administered to several patients, but caused rapid deterioration of their condition. It was ruled out as a treatment for this sort of poisoning following the outbreak. Polythiol resins, penicillamine and dimercaprol sulfonate all helped, but are believed to have been largely insignificant in overall recovery and outcomes. Dialysis was tested on a few patients late in the treatment period, but they showed no clinical improvement. The result of all treatments was varied, with some patients' blood mercury level being dramatically reduced, but a negligible effect in others. All patients received periods of treatment interspersed with lay periods; continuous treatment was suggested in future cases. Later treatment was less effective in reducing blood toxicity.

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.

Evidence suggests that the decline in lung function observed in chronic bronchitis may be slowed with smoking cessation. Chronic bronchitis is treated symptomatically and may be treated in a nonpharmacologic manner or with pharmacologic therapeutic agents. Typical nonpharmacologic approaches to the management of COPD including bronchitis may include: pulmonary rehabilitation, lung volume reduction surgery, and lung transplantation. Inflammation and edema of the respiratory epithelium may be reduced with inhaled corticosteroids. Wheezing and shortness of breath can be treated by reducing bronchospasm (reversible narrowing of smaller bronchi due to constriction of the smooth muscle) with bronchodilators such as inhaled long acting β-adrenergic receptor agonists (e.g., salmeterol) and inhaled anticholinergics such as ipratropium bromide or tiotropium bromide. Mucolytics may have a small therapeutic effect on acute exacerbations of chronic bronchitis. Supplemental oxygen is used to treat hypoxemia (too little oxygen in the blood) and has been shown to reduce mortality in chronic bronchitis patients. Oxygen supplementation can result in decreased respiratory drive, leading to increased blood levels of carbon dioxide (hypercapnia) and subsequent respiratory acidosis.

Prevention is by not smoking and avoiding other lung irritants. Frequent hand washing may also be protective. Treatment of acute bronchitis typically involves rest, paracetamol (acetaminophen), and NSAIDs to help with the fever. Cough medicine has little support for its use and is not recommended in children less than six years of age. There is tentative evidence that salbutamol may be useful in those with wheezing; however, it may result in nervousness and tremors. Antibiotics should generally not be used. An exception is when acute bronchitis is due to pertussis. Tentative evidence supports honey and pelargonium to help with symptoms. Getting plenty of rest and fluids is also often recommended.

Removal of ergot bodies is done by placing the yield in a brine solution; the ergot bodies float while the healthy grains sink. Infested fields need to be deep plowed; ergot cannot germinate if buried more than one inch in soil and therefore won't release its spores into the air. Rotating crops using non-susceptible plants helps reduce infestations since ergot spores only live one year. Crop rotation and deep tillage, such as deep moldboard ploughing, are important components in managing ergot, as many cereal crops in the 21st Century are sown with a "no-till" practice (new crops are seeded directly into the stubble from the previous crop to reduce soil erosion). Wild and escaped grasses and pastures can be mowed before they flower to help limit the spread of ergot.

Chemical controls can also be used, but are not considered economical especially in commercial operations, and germination of ergot spores can still occur under favorable conditions even with the use of such controls.

Prevention is mainly the role of the state, through the definition of strict rules of hygiene and a public services of veterinary surveying of animal products in the food chain, from farming to the transformation industry and delivery (shops and restaurants). This regulation includes:

- traceability: in a final product, it must be possible to know the origin of the ingredients (originating farm, identification of the harvesting or of the animal) and where and when it was processed; the origin of the illness can thus be tracked and solved (and possibly penalized), and the final products can be removed from the sale if a problem is detected;

- enforcement of hygiene procedures such as HACCP and the "cold chain";

- power of control and of law enforcement of veterinarians.

In August 2006, the United States Food and Drug Administration approved Phage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns, because without mandatory labelling consumers would not be aware that meat and poultry products have been treated with the spray.

At home, prevention mainly consists of good food safety practices. Many forms of bacterial poisoning can be prevented by cooking it sufficiently, and either eating it quickly or refrigerating it effectively. Many toxins, however, are not destroyed by heat treatment.

Techniques that help prevent food borne illness in the kitchen are hand washing, rinsing produce, preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between , called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containers

for quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of or until hot or steaming to kill bacteria.

Historically, eating grain products, particularly rye, contaminated with the fungus "Claviceps purpurea" was the cause of ergotism.

The toxic ergoline derivatives are found in ergot-based drugs (such as methylergometrine, ergotamine or, previously, ergotoxine). The deleterious side-effects occur either under high dose or when moderate doses interact with potentiators such as erythromycin.

The alkaloids can pass through lactation from mother to child, causing ergotism in infants.

Globally, infants are a population that are especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventative measure for protection of foodborne infections in infants.

Prevention of Kashin–Beck disease has a long history. Intervention strategies were mostly based on one of the three major theories of its cause.

Selenium supplementation, with or without additional antioxidant therapy (vitamin E and vitamin C) has been reported to be successful, but in other studies no significant decrease could be shown compared to a control group. Major drawbacks of selenium supplementation are logistic difficulties (daily or weekly intake, drug supply), potential toxicity (in case of less controlled supplementation strategies), associated iodine deficiency (that should be corrected before selenium supplementation to prevent further deterioration of thyroid status) and low compliance. The latter was certainly the case in Tibet, where a selenium supplementation has been implemented from 1987 to 1994 in areas of high endemicity.

With the mycotoxin theory in mind, backing of grains before storage was proposed in Guangxi province, but results are not reported in international literature. Changing from grain source has been reported to be effective in Heilongjiang province and North Korea.

With respect to the role of drinking water, changing of water sources to deep well water has been reported to decrease the X-ray metaphyseal detection rate in different settings.

In general, the effect of preventive measures however remains controversial, due to methodological problems (no randomised controlled trials), lack of documentation or, as discussed above, due to inconsistency of results.

Alimentary Toxic Aleukia was first characterized in the early 19th century after affecting a large population in the Orenburg district of the former U.S.S.R. during World War II. The sick people had eaten overwintered grain colonized with Fusarium sporotrichioides and Fusarium poae

Shortly after the incident, in September 1951, scientists writing in the "British Medical Journal" declared that “the outbreak of poisoning” was due to eating bread made from rye grain that was infected with the fungus. The victims appeared to have one common connection. They had eaten bread from the bakery of Roch Briand who was subsequently blamed for using flour made from rye.

Treatment of KBD is palliative. Surgical corrections have been made with success by Chinese and Russian orthopedists. By the end of 1992, Médecins Sans Frontières—Belgium started a physical therapy programme aiming at alleviating the symptoms of KBD patients with advanced joint impairment and pain (mainly adults), in Nyemo county, Lhasa prefecture. Physical therapy had significant effects on joint mobility and joint pain in KBD patients. Later on (1994–1996), the programme has been extended to several other counties and prefectures in Tibet.

Recent research suggests that sulfur amino acids have a protective effect against the toxicity of ODAP.

Eating the chickling pea with grain having high concentrations of sulphur-based amino acids reduces the risk of lathyrism if grain is available. Food preparation is also an important factor. Toxic amino acids are readily soluble in water and can be leached. Bacterial (lactic acid) and fungal (tempeh) fermentation is useful to reduce ODAP content. Moist heat (boiling, steaming) denatures protease inhibitors which otherwise add to the toxic effect of raw grasspea through depletion of protective sulfur amino acids. During times of drought and famine, water for steeping and fuel for boiling is frequently also in short supply. Poor people sometimes know how to reduce the chance of developing lathyrism but face a choice between risking lathyrism or starvation.

The underlying cause for excessive consumption of grasspea is a lack of alternative food sources. This is a consequence of poverty and political conflict. The prevention of lathyrism is therefore a socio-economic challenge.

The 1951 Pont-Saint-Esprit mass poisoning, also known as Le Pain Maudit, occurred on 15 August 1951, in the small town of Pont-Saint-Esprit in southern France. More than 250 people were involved, including 50 persons interned in asylums and resulted in 7 deaths. A foodborne illness was suspected, and among these it was originally believed to be a case of "cursed bread" ("pain maudit").

Most academic sources accept ergot poisoning as the cause of the epidemic, while a few theorize other causes such as poisoning by mercury, mycotoxins, or nitrogen trichloride.

Alimentary toxic aleukia, or Aleukia, is a mycotoxin-induced condition characterized by nausea, vomiting, diarrhea, leukopenia (aleukia), hemorrhaging, skin inflammation, and sometimes death. Alimentary Toxic Alekia almost always refers to the human condition associated with presence of T2 Toxin.

The European Food Safety Authority concluded that chromium is not an essential nutrient, making this the only mineral for which the United States and the European Union disagree. The proposed mechanism for cellular uptake of Cr via transferrin has been called into question. There is no proof that chromium supplementation has physiological effects on body mass or composition, and its use as a supplement may be unsafe. A 2014 systematic review concluded that chromium supplementation had no effect on glycemic control, fasting plasma glucose levels, or body weight in people with or without diabetes.

Chromium may be needed as an ingredient in total parenteral nutrition (TPN), since deficiency may occur after months of intravenous feeding with chromium-free TPN. For this reason, chromium is added to normal TPN solutions for people with diabetes, and in nutritional products for preterm infants.