Cadmium poisoning Health Dictionary

This illness is characterised by vomiting, diarrhoea and abdominal pain, and results from eating food contaminated with metallic or chemical poisons, certain micro-organisms or microbial products. Alternatively, the foods – such as undercooked red kidney beans or ?sh of the scombroid family (mackerel and tuna) – may contain natural posions. Food poisoning caused by chemical or metallic substances usually occurs rapidly, within minutes or a few hours of eating. Among micro-organisms, bacteria are the leading cause of food poisoning, particularly Staphylococcus aureus, Clostridium perfringens (formerly Cl. welchii), Salmonella spp., Campylobacter jejuni, and Escherichia coli O157.

Staphylococcal food poisoning occurs after food such as meat products, cold meats, milk, custard and egg products becomes contaminated before or after cooking, usually through incorrect handling by humans who carry S. aureus. The bacteria produce an ENTEROTOXIN which causes the symptoms of food poisoning 1–8 hours after ingestion. The toxin can withstand heat; thus, subsequent cooking of contaminated food will not prevent illness.

Heat-resistant strains of Cl. perfringens cause food poisoning associated with meat dishes, soups or gravy when dishes cooked in bulk are left unrefrigerated for long periods before consumption. The bacteria are anaerobes (see ANAEROBE) and form spores; the anaerobic conditions in these cooked foods allow the germinated spores to multiply rapidly during cooling, resulting in heavy contamination. Once ingested the bacteria produce enterotoxin in the intestine, causing symptoms within 8–24 hours.

Many di?erent types of Salmonella (about 2,000) cause food poisoning or ENTERITIS, from eight hours to three days after ingestion of food in which they have multiplied. S. brendeny, S. enteritidis, S. heidelberg, S. newport and S. thompson are among those commonly causing enteritis. Salmonella infections are common in domesticated animals such as cows, pigs and poultry whose meat and milk may be infected, although the animals may show no symptoms. Duck eggs may harbour Salmonella (usually S. typhimurium), arising from surface contamination with the bird’s faeces, and foods containing uncooked or lightly cooked hen’s eggs, such as mayonnaise, have been associated with enteritis. The incidence of human S. enteritidis infection has been increasing, by more than 15-fold in England and Wales annually, from around 1,100 a year in the early 1980s to more than 32,000 at the end of the 1990s, but has since fallen to about 10,000. A serious source of infection seems to be poultry meat and hen’s eggs.

Although Salmonella are mostly killed by heating at 60 °C for 15 minutes, contaminated food requires considerably longer cooking and, if frozen, must be completely thawed beforehand, to allow even cooking at a su?cient temperature.

Enteritis caused by Campylobacter jejuni is usually self-limiting, lasting 1–3 days. Since reporting of the disease began in 1977, in England and Wales its incidence has increased from around 1,400 cases initially to nearly 13,000 in 1982 and to over 42,000 in 2004. Outbreaks have been associated with unpasteurised milk: the main source seems to be infected poultry.

ESCHERICHIA COLI O157 was ?rst identi?ed as a cause of food poisoning in the early 1980s, but its incidence has increased sharply since, with more than 1,000 cases annually in the United Kingdom in the late 1990s. The illness can be severe, with bloody diarrhoea and life-threatening renal complications. The reservoir for this pathogen is thought to be cattle, and transmission results from consumption of raw or undercooked meat products and raw dairy products. Cross-infection of cooked meat by raw meat is a common cause of outbreaks of Escherichia coli O157 food poisoning. Water and other foods can be contaminated by manure from cattle, and person-to-person spread can occur, especially in children.

Food poisoning associated with fried or boiled rice is caused by Bacillus cereus, whose heat-resistant spores survive cooking. An enterotoxin is responsible for the symptoms, which occur 2–8 hours after ingestion and resolve after 8–24 hours.

Viruses are emerging as an increasing cause of some outbreaks of food poisoning from shell?sh (cockles, mussels and oysters).

The incidence of food poisoning in the UK rose from under 60,000 cases in 1991 to nearly 79,000 in 2004. Public health measures to control this rise include agricultural aspects of food production, implementing standards of hygiene in abattoirs, and regulating the environment and process of industrial food production, handling, transportation and storage.... food poisoning

See SEPTICAEMIA.... blood-poisoning

See FUNGUS POISONING.... mushroom poisoning

Lead and lead compounds are used in a variety of products including petrol additives (in the UK, lead-free petrol is now mandatory), piping (lead water pipes were once a common source of poisoning), weights, professional paints, dyes, ceramics, ammunition, homeopathic remedies, and ethnic cosmetic preparations. Lead compounds are toxic by ingestion, by inhalation and, rarely, by skin exposures. Metallic lead, if ingested, is absorbed if it remains in the gut. The absorption is greater in children, who may ingest lead from the paint on old cots

– although lead-containing paints are no longer used for items that children may be in contact with.

Acute poisonings are rare. Clinical features include metallic taste, abdominal pain, vomiting, diarrhoea, ANOREXIA, fatigue, muscle weakness and SHOCK. Neurological effects may include headache, drowsiness, CONVULSIONS and COMA. Inhalation results in severe respiratory-tract irritation and systemic symptoms as above.

Chronic poisonings cause gastrointestinal disturbances and constipation. Other effects are ANAEMIA, weakness, pallor, anorexia, insomnia, renal HYPERTENSION and mental fatigue. There may be a bluish ‘lead line’ on the gums, although this is rarely seen. Neuromuscular dysfunction may result in motor weakness and paralysis of the extensor muscles of the wrist and ankles. ENCEPHALOPATHY and nephropathy are severe effects. Chronic low-level exposures in children are linked with reduced intelligence and behavioural and learning disorders.

Treatment Management of patients who have been poisoned is supportive, with removal from source, gastric decontamination if required, and X-RAYS to monitor the passage of metallic lead through the gut if ingested. It is essential to ensure adequate hydration and renal function. Concentrations of lead in the blood should be monitored; where these are found to be toxic, chelation therapy should be started. Several CHELATING AGENTS are now available, such as DMSA (Meso-2,3dimercaptosuccinic acid), sodium calcium edetate (see EDTA) and PENICILLAMINE. (See also POISONS.)... lead poisoning

A metallic element which, when molten, gives o? fumes that can cause serious irritation of the lungs if inhaled.... cadmium

Around 2,000 mushrooms (toadstools) grow in England, of which 200 are edible and a dozen are classi?ed as poisonous. Not all the poisonous ones are dangerous. It is obviously better to prevent mushroom poisoning by ensuring correct identi?cation of those that are edible; books and charts are available. If in doubt, do not eat a fungus.

Severe poisoning from ingestion of fungi is very rare, since relatively few species are highly toxic and most species do not contain toxic compounds. The most toxic species are those containing amatoxins such as death cap (Amanita phalloides); this species alone is responsible for about 90 per cent of all mushroom-related deaths. There is a latent period of six hours or more between ingestion and the onset of clinical effects with these more toxic species. The small intestine, LIVER and KIDNEYS may be damaged – therefore, any patient with gastrointestinal effects thought to be due to ingestion of a mushroom should be referred immediately to hospital where GASTRIC LAVAGE and treatment with activated charcoal can be carried out, along with parenteral ?uids and haemodialysis if the victim is severely ill. In most cases where effects occur, these are early-onset gastrointestinal effects due to ingestion of mushrooms containing gastrointestinal irritants.

Muscarine is the poisonous constituent of some species. Within two hours of ingestion, the victim starts salivating and sweating, has visual disturbances, vomiting, stomach cramps, diarrhoea, vertigo, confusion, hallucinations and coma, the severity of symptoms depending on the amount eaten and type of mushroom. Most people recover in 24 hours, with treatment.

‘Magic’ mushrooms are a variety that contains psilocybin, a hallucinogenic substance. Children who take such mushrooms may develop a high fever and need medical care. In adults the symptoms usually disappear within six hours.

Treatment If possible, early gastric lavage should be carried out in all cases of suspected poisoning. Identi?cation of the mushroom species is a valuable guide to treatment. For muscarine poisoning, ATROPINE is a speci?c antidote. As stated above, hospital referral is advisable for people who have ingested poisonous fungi.... fungus poisoning

The toxic effect of mercury has been known since days of the medieval alchemists. Charles II presented all the symptoms we now recognise as mercurial poisoning, presumably the result of medication received over many years. Its symptoms simulate multiple sclerosis, when chronic. They are: constant fatigue, pins and needles in the limbs, resting tremor, nausea, dizziness, ataxia, pains in the bones and joints, drooling (excessive salivation), blue line along the gums. In children they may include all kinds of vague aches and pains, chorea, hyperthyroidism and facial neuralgia. Weakness, walking difficulties, metallic taste in the mouth, thirst, mental deterioration. It is now known to cause a number of serious nerve dystrophies.

Mercury has an affinity for the central nervous system. Soon it concentrates in the kidney causing tubular damage. A common cause is the mercurial content (50 per cent) in the amalgam fillings in teeth which, under certain conditions, release a vapour. Fortunately, its use in dentistry is being superceded by an alternative composite filling.

A common cause of poisoning was demonstrated in 1972 when 6,000 people became seriously ill (600 died) from eating bread made from grain treated with a fungicide containing methylmercury. For every fungus in grain there is a mercuric compound to destroy it. The seed of all cereal grain is thus treated to protect its power of germination.

Those who are hypersensitive to the metal should as far as possible avoid button cells used in tape recorders, cassette players, watch and camera mechanisms. As the mercury cells corrode, the metal enters the environment and an unknown fraction is converted by micro organisms to alkylmercury compounds which seep into ground waters and eventually are borne to the sea. When cells are incinerated, the mercury volatilises and enters the atmosphere. (Pharmaceutical Journal, July 28/1984)

Mercury poisoning from inhalation of mercury fumes goes directly to the brain and pituitary gland. Autopsies carried out on dentists reveal high concentrations of mercury in the pituitary gland. (The Lancet, 5-27-89,1207 (letter))

Treatment. For years the common antidote was sulphur, and maybe not without reason. When brought into contact sulphur and mercury form an insoluble compound enabling the mercury to be more easily eliminated from the body. Sulphur can be provided by eggs or Garlic.

Old-time backwoods physicians of the North American Medical School used Asafoetida, Guaiacum and Echinacea. German pharmacists once used Bugleweed and Yellow Dock. Dr J. Clarke, USA physician recommends Sarsaparilla to facilitate breakdown and expulsion from the body.

Reconstructed formula. Echinacea 2; Sarsaparilla 1; Guaiacum quarter; Asafoetida quarter; Liquorice quarter. Dose: Liquid Extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: 500mg (two 00 capsules or one-third teaspoon). Thrice daily.

Chelation therapy.

Formula. Tinctures. Skullcap 2-15 drops; Pleurisy root 20-45 drops; Horehound 5-40 drops. Mercurial salivation. Thrice daily. (Indian Herbology of North America, by Alma Hutchens) Dental fillings: replace amalgam with safe alternative – ceramic, etc. Evidence of a link between tooth fillings containing mercury and ME has caused the use of dental amalgam to be banned in Sweden. ... mercury poisoning

ASPIRIN is a commonly available analgesic (see ANALGESICS) which is frequently taken in overdose. Clinical features of poisoning include nausea, vomiting, TINNITUS, ?ushing, sweating, HYPERVENTILATION, DEHYDRATION, deafness and acid-base and electrolyte disturbances (see ELECTROLYTES). In more severe cases individuals may be confused, drowsy and comatose. Rarely, renal failure (see KIDNEYS, DISEASES OF), PULMONARY OEDEMA or cardiovascular collapse occur. Severe toxicity may be delayed, as absorption of the drug may be prolonged due to the formation of drug concretions in the stomach. Treatment involves the repeated administration of activated CHARCOAL, monitoring of concentration of aspirin in the blood, and correction of acid-base and electrolyte imbalances. In more severely poisoned patients, enhanced excretion of the drug may be necessary by alkalinising the urine (by intravenous administration of sodium bicarbonate – see under SODIUM) or HAEMODIALYSIS.... aspirin poisoning

See ATROPINE; BELLADONNA POISONING.... atropine poisoning

Atropa belladonna (deadly nightshade) is a relatively rare plant and severe poisoning is not common. The berries, which are black, ripen from August to October and are the most commonly ingested part of the plant. However, all parts of the plant are toxic. The berries contain ATROPINE and other unidenti?ed ALKALOIDS, the leaves HYOSCINE and atropine, and the roots hyoscine. All these alkaloids have an ANTICHOLINERGIC e?ect which may cause a dry mouth, dilated pupils with blurred vision, TACHYCARDIA, HALLUCINATIONS and PYREXIA. There may also be ATAXIA, agitation, disorientation and confusion. In severe cases there may be CONVULSIONS, COMA, respiratory depression and ARRHYTHMIA. Clinical effects may be delayed in onset for up to 12 hours, and prolonged for several days. Treatment is supportive.... belladonna poisoning

Cyanide inhibits cellular RESPIRATION by binding rapidly and reversibly with the ENZYME, cytochrome oxidase. E?ects of poisoning are due to tissue HYPOXIA. Cyanide is toxic by inhalation, ingestion and prolonged skin contact, and acts extremely quickly once absorbed. Following inhalation of hydrogen cyanide gas, death can occur within minutes. Ingestion of inorganic cyanide salts may produce symptoms within 10 minutes, again proceeding rapidly to death. On a full stomach, effects may be delayed for an hour or more. Signs of cyanide poisoning are headache, dizziness, vomiting, weakness, ATAXIA, HYPERVENTILATION, DYSPNOEA, HYPOTENSION and collapse. Loss of vision and hearing may occur, then COMA and CONVULSIONS. Other features include cardiac ARRHYTHMIA and PULMONARY OEDEMA. Patients may have a lactic ACIDOSIS. Their arterial oxygen tension is likely to be normal, but their venous oxygen tension high and similar to that of arterial blood.

Treatment Administration of oxygen when available is the most important ?rst-aid management. Rescuers should be trained, must not put themselves at risk, and should use protective clothing and breathing apparatus. In unconscious victims, establish a clear airway and give 100 per cent oxygen. If breathing stops and oxygen is unavailable, initiate expired-air resuscitation. If cyanide salts were ingested, mouth-to-mouth contact must be avoided and a mask with a one-way valve employed instead. Some commercially available ?rst-aid kits contain AMYL NITRATE as an antidote which may be employed if oxygen is unavailable.

Once in hospital, or if a trained physician is on the scene, then antidotes may be administered. There are several di?erent intravenous antidotes that may be used either alone or in combination. In mild to moderate cases, sodium thiosulphate is usually given. In more severe cases either dicobalt edetate or sodium nitrite may be used, followed by sodium thio-sulphate. Some of these (e.g. dicobalt edetate) should be given only where diagnosis is certain, otherwise serious adverse reations or toxicity due to the antidotes may occur.... cyanide poisoning

Ergot poisoning, or ergotism, occasionally results from eating bread made from rye infected with the fungus, Claviceps purpurea. Several terrible epidemics (St Anthony’s Fire), characterised by intense pain and hallucinations, occurred in France and Germany during the Middle Ages (see ERYSIPELAS). Its symptoms are the occurrence of spasmodic muscular contractions, and the gradual production of gangrene in parts like the ?ngers, toes and tips of the ears because of constriction of blood vessels and therefore the blood supply.... ergot poisoning

When LYSOL is swallowed it burns the mouth and throat. Brown discoloration of the affected tissues, accompanied by the characteristic smell of lysol on the breath, is typical.

Treatment This is urgent. If the skin has been contaminated with the lysol, it must be washed with water, and any lysol-contaminated clothing must be taken o?. Do not make the victim vomit if he or she has swallowed a corrosive substance such as lysol or phenol. Call an ambulance and say what the victim has taken. See APPENDIX 1: BASIC FIRST AID.... lysol poisoning

Poisoning by saxitoxin, a toxin present in some shellfish, usually in tropical or subtropical seas. Symptoms of respiratory arrest, or brain involvement occur in some 8% of cases, resulting in death. Saxitoxin is related to tetrodotoxin.... paralytic shellfish poisoning

See CYANIDE POISONING.... prussic acid poisoning

This occurs from eating poorly preserved scromboid ?sh such as tuna, mackerel and other members of the mackerel family. In such ?sh, a toxic histamine-like substance is produced by the action of bacteria or histidine, a normal component of ?sh ?esh. This toxin produces nausea, vomiting, headache, upper abdominal pain, di?culty in swallowing, thirst, itching and sometimes URTICARIA. The condition settles as a rule in 12 hours. ANTIHISTAMINE DRUGS sometimes ameliorate the condition.... scrombotoxin poisoning

See POISONS.... self-poisoning

Most antifreeze in the contains ethylene glycol, which is poisonous.

Drinking antifreeze initially produces effects similar to alcohol intoxication, but vomiting, stupor, seizures, and coma may follow; acute kidney failure may occur within 24–36 hours.

Antifreeze poisoning requires immediate medical attention.... antifreeze poisoning

MORPHINE and CODEINE are natural opium ALKALOIDS found in the opium poppy (Papaver somniferum). The other opioids are either synthetic or semi-synthetic analogues of these. Their main use is in the treatment of moderate to severe PAIN, but they are also used as antidiarrhoeal and antitussive agents. As a result of induced tolerance (see DEPENDENCE) and great individual variability, the amount of opioid substances required to cause serious consequences varies enormously.

The most common effects of opioid overdose are vomiting, drowsiness, pinpoint pupils, BRADYCARDIA, CONVULSIONS and COMA. Respiratory depression is common and may lead to CYANOSIS and respiratory arrest. HYPOTENSION occurs occasionally and in severe cases non-cardiogenic pulmonary oedema and cardiovascular collapse may occur. Cardiac ARRHYTHMIA may occur with some opioids. Some opioids have a HISTAMINE-releasing e?ect which may result in an urticarial rash (see URTICARIA), PRURITUS, ?ushing and hypotension. Activated CHARCOAL should be given following overdose and NALOXONE administered to reverse respiratory depression and deep coma.... opioid poisoning

Paracetamol is one of the safest drugs when taken in the correct dosage, but overdose may occur inadvertently or deliberately. Initially there may be no symptoms or there may be nausea, vomiting, abdominal pain and pallor. Then, 16–24 hours after ingestion, liver damage becomes evident and by 72–120 hours the patient may have JAUNDICE, COAGULATION abnormalities, hepatic failure (see LIVER, DISEASES OF), renal failure (see KIDNEYS, DISEASES OF), ENCEPHALOPATHY and COMA. Treatment involves the administration of antidotes such as METHIONINE (within 8 hours) orally or intravenous ACETYLCYSTEINE.

An overdose of paracetamol is a common choice of those attempting to commit suicide. Since the government restricted the number of paracetamol tablets an individual may purchase over the counter, the incidence of people taking the drug in overdose with the intention of taking their lives has fallen sharply.... paracetamol poisoning

In the United Kingdom this occurs in two main forms. Shell?sh may be the cause of typhoid fever (see ENTERIC FEVER) as a result of their contamination by sewage containing the causative organism. They may also be responsible for what is known as paralytic shell?sh poisoning. This is caused by a toxin, or poison, known as saxotoxin, which is present in certain planktons which, under unusual conditions, multiply rapidly, giving rise to what are known as ‘red tides’. In these circumstances the toxin accumulates in mussels, cockles and scallops which feed by ?ltering plankton. The manifestations of such poisoning are loss of feeling in the hands, tingling of the tongue, weakness of the arms and legs, and di?culty in breathing. There is also growing evidence that some shell?sh poisoning may be due to a virus infection. (See also FOOD POISONING.)... shellfish poisoning

The toxic effects of chemicals present in some defoliant weedkillers. Ingesting chlorates can cause kidney and liver damage, corrosion of the intestine, and methaemoglobinaemia (a chemical change in haemoglobin in the blood). Small doses of chlorates can prove fatal. Symptoms of poisoning include ulceration in the mouth, abdominal pain, and diarrhoea.... chlorate poisoning

The toxic effects of plant poisons that cause leaves to drop off.

Defoliants are poisonous if swallowed.

Widely used defoliants include sodium chlorate, potassium chlorate, phenoxy herbicides, and paraquat.... defoliant poisoning

The toxic effects that occur as a result of swallowing the cleaning agents in shampoos, laundry powders, and cleaning liquids.... detergent poisoning

See food poisoning.... shellfish poisoning

See mushroom poisoning.... toadstool poisoning

A Harvard study links coffee consumption with cancer of the pancreas. No association has been found between tea-drinkers and cancer. Some authorities claim coffee is not carcinogenic until roasted.

While an internal mechanism slows down the body, caffeine in tea, cola and coffee restores alertness. Caffeine acts by blocking the action of the compound, adenosine – one of the building blocks of DNA which promotes cell energy. Caffeine interferes with natural metabolic processes. In the aged, coffee increases production of uric acid, causing irritation of the kidneys, joint and muscle pains. vCaffeinism is responsible for a wide range of disorders. Increases the heart beat, promotes excessive stomach acid and increases flow of urine. It may give rise to birth defects and should be taken with caution in pregnancy.

Symptoms. Restlessness, nervous agitation, extreme sensitiveness. Intolerance of pain, nervous palpitation, all senses acute.

To antidote. Chamomile tea.

Practitioner. Tincture Nux vom BP: 10 drops to 100ml water. Dose: 1 teaspoon thrice daily. Inhalation: Strong spirits of Camphor.

Diet. Plenty asparagus. ... caffeine poisoning

The harmful effects on the body as a result of an excessive dose of a drug. Accidental poisoning is most common in young children. In adults, it usually occurs in elderly or confused people who are unsure about their treatment and dosage requirements. Accidental poisoning may also occur during drug abuse. Deliberate self-poisoning is usually a cry for help (see suicide; suicide, attempted). The drugs that are most commonly taken in overdose include benzodiazepine drugs and antidepressant drugs. Anyone who has taken a drug overdose and any child who has swallowed tablets that belong to someone else should seek immediate medical advice. It is important to identify the drugs that have been taken. Treatment in hospital may involve washing out the stomach (see lavage, gastric). Charcoal may be given by mouth to reduce the absorption of the drug from the intestine into the bloodstream. To eliminate the drug, urine production may be increased by an intravenous infusion. Antidotes are available only for specific drugs. Such antidotes include naloxone (for morphine) and methionine (for paracetamol).

Drug poisoning may cause drowsiness and breathing difficulty, irregular heartbeat, and, rarely, cardiac arrest, fits, and kidney and liver damage.

Antiarrhythmic drugs are given to treat heartbeat irregularity.

Fits are treated with anticonvulsants.

Blood tests to monitor liver function and careful monitoring of urine output are carried out if the drug is known to damage the liver or kidneys.... drug poisoning

Poisons may be swallowed, inhaled, absorbed through skin, or injected under the skin (as with an insect sting).

Poisons may also originate in the body, as when bacteria produce endotoxins, or when metabolic disorders produce poisonous substances or allow them to build up.

Poisoning may be acute (a large amount of poison over a short time) or chronic (gradual accumulation of poison that is not eliminated quickly).

Unintentional poisoning occurs mainly in young children.

Adults may be poisoned by mistaking the dosage of a prescribed drug (see drug poisoning), by taking very high doses of vitamin or mineral supplements, by exposure to poisonous substances in industry, or by drug abuse.

Poisoning may also be a deliberate attempt to commit suicide.... poisoning

Strychnine is a poisonous chemical found in the seeds of Strychnos species (tropical trees and shrubs). Its main use is as an ingredient in some rodent poisons; most cases of strychnine poisoning occur in children who accidentally eat such poisons.

Symptoms begin soon after ingestion and include restlessness, stiffness of the face and neck, increased sensitivity of hearing, taste, and smell, and photosensitivity, followed by alternating episodes of seizures and floppiness. Death may occur from respiratory arrest.

The victim is given intravenous injections of a tranquillizer or a barbiturate, with a muscle-relaxant drug if needed.

Breathing may be maintained by a ventilator.

With prompt treatment, recovery usually occurs in about 24 hours.... strychnine poisoning