Specific treatments for acute pesticide poisoning are often dependent on the pesticide or class of pesticide responsible for the poisoning. However, there are basic management techniques that are applicable to most acute poisonings, including skin decontamination, airway protection, gastrointestinal decontamination, and seizure treatment.

Decontamination of the skin is performed while other life-saving measures are taking place. Clothing is removed, the patient is showered with soap and water, and the hair is shampooed to remove chemicals from the skin and hair. The eyes are flushed with water for 10–15 minutes. The patient is intubated and oxygen administered, if necessary. In more severe cases, pulmonary ventilation must sometimes be supported mechanically. Seizures are typically managed with lorazepam, phenytoin and phenobarbitol, or diazepam (particularly for organochlorine poisonings).

Gastric lavage is not recommended to be used routinely in pesticide poisoning management, as clinical benefit has not been confirmed in controlled studies; it is indicated only when the patient has ingested a potentially life-threatening amount of poison and presents within 60 minutes of ingestion. An orogastric tube is inserted and the stomach is flushed with saline to try to remove the poison. If the patient is neurologically impaired, a cuffed endotracheal tube inserted beforehand for airway protection. Studies of poison recovery at 60 minutes have shown recovery of 8%–32%. However, there is also evidence that lavage may flush the material into the small intestine, increasing absorption. Lavage is contra-indicated in cases of hydrocarbon ingestion.

Activated charcoal is sometimes administered as it has been shown to be successful with some pesticides. Studies have shown that it can reduce the amount absorbed if given within 60 minutes, though there is not enough data to determine if it is effective if time from ingestion is prolonged. Syrup of ipecac is not recommended for most pesticide poisonings because of potential interference with other antidotes and regurgitation increasing exposure of the esophagus and oral area to the pesticide.

Urinary alkalinisation has been used in acute poisonings from chlorophenoxy herbicides (such as 2,4-D, MCPA, 2,4,5-T and mecoprop); however, evidence to support its use is poor.

Current antidotes for OP poisoning consist of a pretreatment with carbamates to protect AChE from inhibition by OP compounds and post-exposure treatments with anti-cholinergic drugs. Anti-cholinergic drugs work to counteract the effects of excess acetylcholine and reactivate AChE. Atropine can be used as an antidote in conjunction with pralidoxime or other pyridinium oximes (such as trimedoxime or obidoxime), though the use of "-oximes" has been found to be of no benefit, or possibly harmful, in at least two meta-analyses. Atropine is a muscarinic antagonist, and thus blocks the action of acetylcholine peripherally. These antidotes are effective at preventing lethality from OP poisoning, but current treatment lack the ability to prevent post-exposure incapacitation, performance deficits, or permanent brain damage. While the efficacy of atropine has been well-established, clinical experience with pralidoxime has led to widespread doubt about its efficacy in treatment of OP poisoning.

Enzyme bioscavengers are being developed as a pretreatment to sequester highly toxic OPs before they can reach their physiological targets and prevent the toxic effects from occurring. Significant advances with cholinesterases (ChEs), specifically human serum BChE (HuBChE) have been made. HuBChe can offer a broad range of protection for nerve agents including soman, sarin, tabun, and VX. HuBChE also possess a very long retention time in the human circulation system and because it is from a human source it will not produce any antagonistic immunological responses. HuBChE is currently being assessed for inclusion into the protective regimen against OP nerve agent poisoning. Currently there is potential for PON1 to be used to treat sarin exposure, but recombinant PON1 variants would need to first be generated to increase its catalytic efficiency.

One other agent that is being researched is the Class III anti-arrhythmic agents. Hyperkalemia of the tissue is one of the symptoms associated with OP poisoning. While the cellular processes leading to cardiac toxicity are not well understood, the potassium current channels are believed to be involved. Class III anti-arrhythmic agents block the potassium membrane currents in cardiac cells, which makes them a candidate for become a therapeutic of OP poisoning.

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."

Chelation therapy for acute inorganic mercury poisoning can be done with DMSA, 2,3-dimercapto-1-propanesulfonic acid (DMPS), -penicillamine (DPCN), or dimercaprol (BAL). Only DMSA is FDA-approved for use in children for treating mercury poisoning. However, several studies found no clear clinical benefit from DMSA treatment for poisoning due to mercury vapor. No chelator for methylmercury or ethylmercury is approved by the FDA; DMSA is the most frequently used for severe methylmercury poisoning, as it is given orally, has fewer side-effects, and has been found to be superior to BAL, DPCN, and DMPS. α-Lipoic acid (ALA) has been shown to be protective against acute mercury poisoning in several mammalian species when it is given soon after exposure; correct dosage is required, as inappropriate dosages increase toxicity. Although it has been hypothesized that frequent low dosages of ALA may have potential as a mercury chelator, studies in rats have been contradictory. Glutathione and "N"-acetylcysteine (NAC) are recommended by some physicians, but have been shown to increase mercury concentrations in the kidneys and the brain.

Chelation therapy can be hazardous if administered incorrectly. In August 2005, an incorrect form of EDTA (edetate disodium) used for chelation therapy resulted in hypocalcemia, causing cardiac arrest that killed a five-year-old autistic boy.

Treatment is supportive with the use of antibiotics, blood products, colony stimulating factors, and stem cell transplant as clinically indicated. Symptomatic measures may also be employed.

Accidental poisonings can be avoided by proper labeling and storage of containers. When handling or applying pesticides, exposure can be significantly reduced by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Safety protocols to reduce exposure include the use of personal protective equipment, washing hands and exposed skin during as well as after work, changing clothes between work shifts, and having first aid trainings and protocols in place for workers.

Personal protective equipment for preventing pesticide exposure includes the use of a respirator, goggles, and protective clothing, which have all have been shown to reduce risk of developing pesticide-induced diseases when handling pesticides. A study found the risk of acute pesticide poisoning was reduced by 55% in farmers who adopted extra personal protective measures and were educated about both protective equiment and pesticide exposure risk. Exposure can be significantly reduced when handling or applying pesticides by protecting certain parts of the body where the skin shows increased absorption, such as the scrotal region, underarms, face, scalp, and hands. Using chemical-resistant gloves has been shown to reduce contamination by 33–86%.

Experimental findings have demonstrated an interaction between selenium and methylmercury, but epidemiological studies have found little evidence that selenium helps to protect against the adverse effects of methylmercury.

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.

Where radioactive contamination is present, a gas mask, dust mask, or good hygiene practices may offer protection, depending on the nature of the contaminant. Potassium iodide (KI) tablets can reduce the risk of cancer in some situations due to slower uptake of ambient radioiodine. Although this does not protect any organ other than the thyroid gland, their effectiveness is still highly dependent on the time of ingestion which would protect the gland for the duration of a twenty-four-hour period. They do not prevent acute radiation syndrome as they provide no shielding from other environmental radionuclides.

The mainstays of treatment are removal from the source of lead and, for people who have significantly high blood lead levels or who have symptoms of poisoning, chelation therapy. Treatment of iron, calcium, and zinc deficiencies, which are associated with increased lead absorption, is another part of treatment for lead poisoning. When lead-containing materials are present in the gastrointestinal tract (as evidenced by abdominal X-rays), whole bowel irrigation, cathartics, endoscopy, or even surgical removal may be used to eliminate it from the gut and prevent further exposure. Lead-containing bullets and shrapnel may also present a threat of further exposure and may need to be surgically removed if they are in or near fluid-filled or synovial spaces. If lead encephalopathy is present, anticonvulsants may be given to control seizures, and treatments to control swelling of the brain include corticosteroids and mannitol. Treatment of organic lead poisoning involves removing the lead compound from the skin, preventing further exposure, treating seizures, and possibly chelation therapy for people with high blood lead concentrations.

A chelating agent is a molecule with at least two negatively charged groups that allow it to form complexes with metal ions with multiple positive charges, such as lead. The chelate that is thus formed is nontoxic and can be excreted in the urine, initially at up to 50 times the normal rate. The chelating agents used for treatment of lead poisoning are edetate disodium calcium (CaNaEDTA), dimercaprol (BAL), which are injected, and succimer and d-penicillamine, which are administered orally.

Chelation therapy is used in cases of acute lead poisoning, severe poisoning, and encephalopathy, and is considered for people with blood lead levels above 25 µg/dL. While the use of chelation for people with symptoms of lead poisoning is widely supported, use in asymptomatic people with high blood lead levels is more controversial. Chelation therapy is of limited value for cases of chronic exposure to low levels of lead. Chelation therapy is usually stopped when symptoms resolve or when blood lead levels return to premorbid levels. When lead exposure has taken place over a long period, blood lead levels may rise after chelation is stopped because lead is leached into blood from stores in the bone; thus repeated treatments are often necessary.

People receiving dimercaprol need to be assessed for peanut allergies since the commercial formulation contains peanut oil. Calcium EDTA is also effective if administered four hours after the administration of dimercaprol. Administering dimercaprol, DMSA (Succimer), or DMPS prior to calcium EDTA is necessary to prevent the redistribution of lead into the central nervous system. Dimercaprol used alone may also redistribute lead to the brain and testes. An adverse side effect of calcium EDTA is renal toxicity. Succimer (DMSA) is the preferred agent in mild to moderate lead poisoning cases. This may be the case in instances where children have a blood lead level >25μg/dL. The most reported adverse side effect for succimer is gastrointestinal disturbances. It is also important to note that chelation therapy only lowers blood lead levels and may not prevent the lead-induced cognitive problems associated with lower lead levels in tissue. This may be because of the inability of these agents to remove sufficient amounts of lead from tissue or inability to reverse preexisting damage.

Chelating agents can have adverse effects; for example, chelation therapy can lower the body's levels of necessary nutrients like zinc. Chelating agents taken orally can increase the body's absorption of lead through the intestine.

Chelation challenge, also known as provocation testing, is used to indicate an elevated and mobilizable body burden of heavy metals including lead. This testing involves collecting urine before and after administering a one-off dose of chelating agent to mobilize heavy metals into the urine. Then urine is analyzed by a laboratory for levels of heavy metals; from this analysis overall body burden is inferred. Chelation challenge mainly measures the burden of lead in soft tissues, though whether it accurately reflects long-term exposure or the amount of lead stored in bone remains controversial. Although the technique has been used to determine whether chelation therapy is indicated and to diagnose heavy metal exposure, some evidence does not support these uses as blood levels after chelation are not comparable to the reference range typically used to diagnose heavy metal poisoning. The single chelation dose could also redistribute the heavy metals to more sensitive areas such as central nervous system tissue.

A 2006 systematic review and a 2005 review by the UK Health Protection Agency each evaluated the evidence for various medical, psychological, behavioral, and alternative treatments for EHS and each found that the evidence-base was limited and not generalizable. The conclusion of the 2006 review stated: "The evidence base concerning treatment options for electromagnetic hypersensitivity is limited and more research is needed before any definitive clinical recommendations can be made. However, the best evidence currently available suggests that cognitive behavioural therapy is effective for patients who report being hypersensitive to weak electromagnetic fields."

As of 2005, WHO recommended that people presenting with claims of EHS be evaluated to determine if they have a medical condition that may be causing the symptoms the person is attributing to EHS, that they have a psychological evaluation, and that the person's environment be evaluated for issues like air or noise pollution that may be causing problems.

There is no cure for berylliosis; the goals of treatment are to reduce symptoms and slow the progression of disease.

Although the evidence that stopping exposure to beryllium decreases progression of the disease, it is still considered to be an accepted approach to treatment in any stage of disease.

People with early stages of disease, without lung function abnormalities or clinical symptoms, are periodically monitored with physical exams, pulmonary function testing and radiography.

Once clinical symptoms or significant abnormalities in pulmonary function testing appear, treatments include oxygen and oral corticosteroids and whatever supportive therapy is required.

Prevention measures include avoidance of the irritant through its removal from the workplace or through technical shielding by the use of potent irritants in closed systems or automation, irritant replacement or removal and personal protection of the workers.

Chronic exposure to human nail dust is a serious occupational hazard that can be minimized by not producing such dust. Best practice is to avoid electrical debridement or burring of mycotic nails unless the treatment is necessary. When the procedure is necessary, it is possible to reduce exposure by using nail dust extractors, local exhaust, good housekeeping techniques, personal protective equipment such as gloves, glasses or goggles, face shields, and an appropriately fitted disposable respirators to protect against the hazards of nail dust and flying debris.

Once a nickel allergy is detected, the best treatment is avoidance of nickel-releasing items. It is important to know the main items that can cause nickel allergy, which may be remembered using the mnemonic "BE NICKEL AWARE". The top 13 categories that contain nickel include beauty accessories, eyeglasses, money, cigarettes, clothes, kitchen and household, electronics and office equipment, metal utensils, aliment, jewelry, batteries, orthodontic and dental appliances, and medical equipment. Other than strict avoidance of items that release free nickel, there are other treatment options for reduction of exposure. The first step is to limit friction between skin and metallic items. Susceptible people may try to limit sweating while wearing nickel items, to reduce nickel release and thus decrease chances for developing sensitization and/or allergy. Another option is to shield electronics, metal devices, and tools with fabric, plastic, or acrylic coverings. Dermatological application tests has shown that barrier creams effectively prevent the symptoms of nickel allergy, such as the Nidiesque™.

There are test kits that can be very helpful to check for nickel release from items prior to purchasing. The ACDS providers can give a guidance list of safe items. In addition to avoidance, healthcare providers may prescribe additional creams or medications to help relieve the skin reaction.

There have been numerous accounts of patients with "trichophyton" fungal infections and associated asthma, which further substantiates the likelihood of respiratory disease transmission to the healthcare provider being exposed to the microbe-laden nail dust In 1975, a dermatophyte fungal infection was described in a patient with severe tinea. The resulting treatment for mycosis improved the patient’s asthmatic condition. The antifungal treatment of many other "trichophyton" foot infections has alleviated symptoms of hypersensitivity, asthma, and rhinitis.

Some medications that can be used for erethism are Traid and Ritalin. Methylphenidate (Ritalin) is a stimulant drug approved for therapy of attention-deficit hyperactivity disorder, postural orthostatic tachycardia syndrome and narcolepsy. It may also be prescribed for off-label use in treatment-resistant cases of lethargy, depression (mood), or neural insult.

One treatment of mercury poisoning was to admit fresh air to the patient by having him go outside daily as much as possible. Stimulants such as ammonia have also been documented to help restore pulse to a normal rhythm. For a more comprehensive reading of treatment, see Mercury poisoning, 'Treatment' section.

Pesticides exposure cannot be studied in placebo controlled trials as this would be unethical. A definitive cause effect relationship therefore cannot be established. Consistent evidence can and has been gathered through other study designs. The precautionary principle is thus frequently used in environmental law such that absolute proof is not required before efforts to decrease exposure to potential toxins are enacted.

The American Medical Association recommend limiting exposure to pesticides. They came to this conclusion due to the fact that surveillance systems currently in place are inadequate to determine problems related to exposure. The utility of applicator certification and public notification programs are also of unknown value in their ability to prevent adverse outcomes.

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.

Typical levels of beryllium that industries may release into the air are of the order of , averaged over a 30-day period, or of workroom air for an 8-hour work shift. Compliance with the current U.S. Occupational Safety and Health Administration (OSHA) permissible exposure limit for beryllium of has been determined to be inadequate to protect workers from developing beryllium sensitization and CBD. The American Conference of Governmental Industrial Hygienists (ACGIH), which is an independent organization of experts in the field of occupational health, has proposed a threshold limit value (TLV) of in a 2006 Notice of Intended Change (NIC). This TLV is 40 times lower than the current OSHA permissible exposure limit, reflecting the ACGIH analysis of best available peer-reviewed research data concerning how little airborne beryllium is required to cause sensitization and CBD.

Because it can be difficult to control industrial exposures to beryllium, it is advisable to use any methods possible to reduce airborne and surface contamination by beryllium, to minimize the use of beryllium and beryllium-containing alloys whenever possible, and to educate people about the potential hazards if they are likely to encounter beryllium dust or fumes. It is important to damp wipe meallographic preparation equipment to prevent accumulation of dry particles. Sectioning, grinding, and polishing must be performed under sufficiently vented hoods equipped with special filters.

On 29 January 2009, the Los Alamos National Laboratory announced it was notifying nearly 2,000 current and former employees and visitors that they may have been exposed to beryllium in the lab and may be at risk of disease. Concern over possible exposure to the material was first raised in November 2008, when a box containing beryllium was received at the laboratory's short-term storage facility.

People may be exposed to toxic chemicals or similar dangerous substances from pharmaceutical products, consumer products, the environment, or in the home or at work. Many toxic tort cases arise either from the use of medications, or through exposure at work.

Pharmaceutical injuries can occur when a person is injured by a dangerous, defective or contaminated medication. Many pharmaceutical toxic injury cases are mass tort cases, as most medications are consumed by thousands of people. The cases are often litigated against drug manufacturers and distributors, and potentially against prescribing physicians. When prosecuted against drug manufacturers and distributors, pharmaceutical toxic tort cases differ from medical malpractice suits in that pharmaceutical toxic tort cases are essentially product liability cases, the defective product being the drug.

Depending on the severity of the symptoms, FLD can last from one to to weeks, or they can last for the rest of one’s life. Acute FLD has the ability to be treated because hypersensitivity to the antigens has not yet developed. The main treatment is rest and reducing the exposure to the antigens through masks and increased airflow in confined spaces where the antigens are present. Another treatment for acute FLD is pure oxygen therapy. For chronic FLD, there is no true treatment because the patient has developed hypersensitivity meaning their FLD could last the rest of their life. Any exposure to the antigens once hypersensitivity can set off another chronic reaction.

Short-acting beta-agonists like salbutamol or terbutaline or long-acting beta-agonists like salmeterol and formoterol dilate airways which relieve the symptoms thus reducing the severity of the reaction. Some patients also use it just before work to avoid a drop in the FEV.

Anti-inflammatory agents like corticosteroids, LKTRA or mast cell stabilizers can also be used depending on the severity of the case.

Once chloracne has been identified, the primary action is to remove the patient and all other individuals from the source of contamination. Further treatment is symptomatic.

Secondary infections on severe or persistent lesions may need to be treated with oral antibiotics or isotretinoin. However, chloracne itself can be highly resistant to any treatment.

The course of the disease is highly variable. In some cases the lesions may disappear within two years or so; however, in other cases the lesions may be effectively permanent (mean duration of lesions in one 1984 study was 26 years, with some workers remaining disfigured over three decades after exposure).