Ammonia Colourless, highly irritating gas with a pungent, suffocating odour Lighter than air, flammable at high concentrations and temperatures Dissolves in water and forms ammonium hydroxide - an alkaline corrosive solution Exposure to ammonia may be fatal if it is inhaled - ammonia's odour threshold is fortunately sufficiently low to provide adequate warning of its presence NH 3 present in non-ionized (NH 3 – toxic) and ionized form NH 4 +
Clinical signs: -Even low concentrations of ammonia produce rapid eye and nose irritation -Skin contact with concentrated ammonia solutions can cause serious corrosive injury -Throat irritation, cough, bronchospasm. -More severe clinical signs include immediate laryngospasm and laryngeal oedema resulting in upper airway obstruction, pulmonary oedema can occur Swallowing causes immediate burning in the mouth and throat, chest, and abdomen with swallowing difficulty, drooling, and vomiting. Perforation of the oesophagus or stomach may occur
Pathological examination: -Mucosas hyperaemic, congested, swollen, signs of burning, perforations in GIT Treatment: -Fresh air, supplemental oxygen if available, inhalation of aerosol containing 2 % of citric acid and 1 % procain -In p.o. intake neutralise stomach content – solution of 1-2 % acetic acid
Ammonia + nitrite intoxication In fish Aquarium or pond - especially when immediately stocked to full capacity Nitrification bacteria is not able to convert all ammonia to nitrates and nitrites to nitrates Treatment is complicated, prevention very easy – small number of fish, increase aeration
Ammonia autointoxication Also in fish Happens when there are big changes in temperatures within a few minutes or hours In decreased temperature – decreased metabolism and excretion Cummulation of ammonia inside of the body, poisoning – congestion and oedema of gills, incoordination, seizures
Urea - alimentary intoxication by ammonia Urea used as an fertilizer and feed additive in ruminants Exchange for dietary salt Ammonia released in rumen by bacterial microflora. In small amount used by microflora. In huge amounts causes immediate and strong alkalinization of rumen content In alkaline environment, most of ammonia is in non-ionized toxic form – absorption to blood, transport to liver Mechanism of action: -In liver it is normally converted back to endogenous urea, but the process is limited -In excess it goes to blood – here formation of glutamine and asparagine from glutamic and asparigic acid. If this is not sufficient too – pure ammonia goes to CNS – blockage of Krebs cycle – depletion of α-ketoglutarate and glutamate!
Clinical signs: -apathy, hyperaesthesia, incoordination, muscle tremors, sternal recumbency, convulsions, death -rumen stasis, hypersalivation, increased defecation and urination, dehydration, dyspnoe, arrhytmias -If eaten a lethal dose, death comes very quickly Pathological examination: -gastritis, enteritis, peribronchial haemorrhage, nephritis, hyperaemia and haemorrhage in brain Treatment: -Neutralisation of rumen content – solution of acetic acid -Large amounts of fluids -Symptomatic
Cyanides One of the most potent poisons Release HCN Bitter-almond smell Cyanides are not available for common population – poisonings mainly from cyanogenic glucosides found in plants Lecture on food toxins
Fluorosis Biogenic element Intoxications rare: endemic due to soil content – India, or near aluminium works Except humans, the most sensitive species are cattle and honey bees Absorption by inhalation or orally Deposition in bones and teeth, thyroid gland Increased density of bone tissue, exostosis, hypercalcification, deformation of bones and teeth Excreted in faeces, cross placenta, excreted in milk
Clinical signs: Acute poisoning: - very rare - decreased breathing, GIT symptoms, tremor, convulsions, paralysis of vasomotoric centre and death Chronic poisoning: - inappetence, decreased milk yield, painful movement, exostoses, damage of hoofs, teeth Pathological examination: - damage of GIT mucosa, degeneration of liver, inflammatory changes on kidneys and bladder, deformation of teeth, hyperostosis, thickening of mandibula Treatment: - no antidote, acute form – symptomatic, chronic changes irreversible
CO 2 – carbon dioxide CO 2 concentration in air is 0,03% CO 2 is heavier than air, thus is occurs downstairs Colourless, odourless It is generated during complete combustion of organic substances, during fermentative processes It occurs in caves, mines, during excavation of wells, sillage holes Haemoglobin is occupied – formation of carbaminohaemoglobin, but CO 2 is also transported freely in blood. Most commonly the reason of poisoning is just lack of oxygen Death due to suffocation
Concentration: about 5% - narcotic effect, tachypnoe, increased blood pressure, decreased body temperature over 20% - induces rapid apneusis and death (used for euthanasia of fish and some other small animals) Therapy – fresh air, inhalation of oxygen, analeptics to increase the frequency of breathing (in rapid intoxication)
Sulphane – H 2 S Heavier than air Smell of rotten eggs In high concentration paralysis of olfactory nerve – impossible detection High concentration in waste containers in pig farms, from industry Reacts with metaloenzymes, most important is bond to Fe 3+ in cytochrome-oxidase – similarly to cyanides – inhibition of cell respiration Irritation of eyes, cough, dyspnea, lung oedema, damage to CNS. Long-term exposure: exhaustion, inappetence, confusion Treatment same as in cyanides – methaemoglobin formation, then it reacts with sulphur - thiosulphates
Poisoning possible also by SO 2 (industry, used in wine production, dried fruits, seed treatment, as a bleach) – irritation, corrosion, lung oedema, allergic reaction Nitrosamines – from nitrates and nitrites, nitrous acid is formed in guts – in acidic pH nitroso cations are released. They react with secondary amines (aminoacids, glucosamines etc.) and form carcinogenic nitrosamines. They can be produced also during meat smoking.