Toxic Substances – Chapter 3: Mercury, Lead, Arsenic, CO, NOx, Acids & Bases

Toxic Substances – Chapter 3: Mercury, Lead, Arsenic, CO, NOx, Acids & Bases

I. Mercury (Hg)

1. Characteristics:

• Group A Metal: Hg, Pb, Cd, Se, As

• Form of existence: Liquid metal, highly volatile.

• Solubility: Insoluble in water, alkalis, common acids. Partially soluble in concentrated HNO3, concentrated hot H2SO4, lipids, and pentane.

• Forms of existence:

• Elemental mercury or vapor in air

• Inorganic compounds: HgS (cinnabar), HgSe (tiemannite), HgTe (tiemanite), Hg2Cl2 (calomel)

• Organic compounds: Methylmercury (most toxic to aquatic organisms)

• Applications: Electrode production, chlorine and NaOH production via electrolysis, electrical equipment, ore processing.

• Effects of HgS: Psychological calming.

• Effects of HgX: Antiseptic.

• Effects of Hg(NO3)2: Cauterization (burning) of inflamed areas.

• Formula of Thimerosal: Ethylmercury (antibacterial, preservative).

• Form of mercury present in marine organisms: Methylmercury.

2. Causes of Poisoning:

• Intentional: Although it has a pungent odor, it can be used for suicide.

• Accidental: Confusion with other metals.

• Occupational: Direct exposure during production processes.

• Environmental pollution: Production of NaOH, Cl2, application of fungicides and herbicides, paper production, electrical equipment manufacturing.

3. Mechanism of Toxicity:

• Most toxic form: Inorganic Hg > organic Hg, Hg(II) is the most toxic.

• Routes of poisoning: Skin, digestive system, respiratory system.

• Toxic form: Only toxic in the gaseous form. 80% of inhaled Hg enters the lungs and causes central nervous system (CNS) toxicity.

• Effects on CNS: Only elemental and organic Hg affect the CNS. Inorganic Hg has limited CNS impact, causing kidney toxicity if ingested in large quantities.

• Sites of action for organic Hg: CNS, kidneys, digestive system, fetus. Methylmercury causes CNS damage and birth defects.

• Mechanisms:

• Tissue degeneration due to the formation of highly soluble protein complexes.

• Enzyme inhibition through the SH group.

• Hg(II) cannot cross biological membranes but binds to hemoglobin and albumin.

• Accumulation in: Kidneys.

• Accumulated form: Hg2+.

• Salt causing poisoning through digestion: HgCl2.

• Reason for difficult recovery: Severe organ damage and long-term persistence of Hg in the body.

4. Management:

• Acute poisoning: Through inhalation or ingestion.

• Chronic poisoning: Due to organic Hg.

• Detoxification: Ingest egg whites or rogalit solution, ingest activated charcoal.

• Mechanism of removal: Conversion of Hg salts into Hg to reduce absorption.

• Mechanism of neutralization: BAL and DMSA have SH groups to bind with Hg.

• DMSA application: All cases of Hg poisoning.

• BAL application: Only for inorganic Hg, not for Hg vapor or organic Hg.

5. Quantification:

• Qualitative methods:

• Formation of an alloy with copper metal.

• Stable reddish-orange color with dithizone.

• Precipitation with KI in a neutral or slightly acidic medium to form red HgI2, soluble in excess KI.

• Precipitation with SnCl2 in an acidic medium.

• Quantitative methods: AAS (Atomic Absorption Spectroscopy) using the cold vapor technique.

II. Lead (Pb)

1. Characteristics:

• Mineral: Pb3O4 (combination of 2PbO.PbO2).

• Characteristics of Pb oxides: Soluble in alkalis, slightly soluble in water.

• Pb salts in medicine and laboratories: Lead acetate.

• Cause of acute poisoning: Sucking on toys, storing NaCl in lead-containing glass bottles.

• Pb compounds in gasoline: Pb(C2H5)2.

• Causes of chronic poisoning: Ingesting food, working in printing, battery, gasoline, and paint factories.

• More dangerous poisoning: Chronic poisoning.

• Main source of Pb in urban areas: Food.

2. Mechanism of Toxicity:

• Enzyme inhibition: Involved in heme transport and synthesis.

• Inhibition of ALA dehydrase: Increases ALA, leading to heme deficiency and decreased Hb synthesis.

• Pb amount causing anemia: 0.8 ppm.

• New substance in blood due to Pb poisoning: Coproporphyrin.

• Distribution:

• Acute: Liver

• Chronic: Corneal epithelium

• Characteristic abdominal pain: Episodic upper abdominal pain.

• Vomiting: Vomiting white matter (PbCl2).

• First symptom: Blue line at the gum, unpleasant breath odor.

• Pb location: Digestive system.

• Normal Pb levels:

• Blood: 0.06 mg/100 ml

• Urine: 0.08 mg in 24 hours

3. Management:

• Management: Normal gastric lavage.

• Pb removal: Intravenous Calcium EDTA administration.

• Combined with BAL: In patients with brain damage.

• DMSA use: In patients without brain damage.

• Mannitol, Dexamethasone injection: In patients with increased intracranial pressure.

• Pb dissolution in air: Using HNO3.

• Treatment of organ samples: Sulfonitric, then dissolve in acetic acid.

4. Quantification:

• Qualitative methods:

• Formation of a red-violet precipitate with dithizone.

• Precipitation with KI: Formation of a yellow precipitate (golden rain reaction).

• Formation of black potassium copper lead 6NO2 complex.

• Formation of black PbS.

• Formation of yellow PbCrO4 precipitate, insoluble in acetic acid, soluble in inorganic acids and alkalis.

• Quantitative methods: AAS or ICP emission (Inductively Coupled Plasma).

• Wavelength: 283.3 nm.

III. Arsenic (As)

1. Characteristics:

• Most important compound: Arsenic trioxide (As2O3).

• Oxidation in air: Forms As2O3, burning with a garlic-like odor.

• Arsenides: Salts of arsenic acid, green in color, used for dyeing paper.

• Arsenates: Salts of arsenic acid.

• Sodium salts: Used in gunpowder.

• Copper salts: Used for dyeing paper (green color).

• Potassium and calcium salts: Used as pesticides.

• Arsine: AsH3 (gas with a garlic-like odor, highly toxic).

• Organic compounds: Chemical warfare agents, pesticides.

• Excretion: Mainly through kidneys and intestines (slow).

• Causes of poisoning:

• Poisoning: Due to lack of odor and taste.

• Accidental ingestion.

• Occupational exposure.

• Suicide.

• Medication, pesticides, water containing As.

• Absorption and excretion: Rapid absorption, slow excretion.

• Most toxic form: As(III) > As(V), inorganic As > organic As.

2. Mechanism of Toxicity:

• Enzyme inhibition:

• As(III): Through SH groups.

• As(V): Replacing phosphate groups.

• Lethal dose of As2O3: 2 mg/kg.

• Confirming poisoning: Finding As in blood, urine, hair, and nails.

• Normal As levels:

• Blood: Below 30 mcg/l.

• Hair, nails: Below 1 ppm.

• As levels in organs:

• cg: Conclusive evidence of As poisoning.

• mg: Inquire about the patient’s use of As-containing medications.

• Maximum permissible As levels:

• Body: 2 mcg/kg.

• Water: 0.01 mg/L.

• Most severely affected organ: Digestive system.

3. Management:

• Acute management: Vomiting, gastric lavage with egg whites.

• Neutralization: Substances with sulfite groups, Fe3+ salts, Mg oxide, BAL injection, DMSA ingestion.

• Inorganic oxidation: Sulfonitric.

• Qualitative methods:

• DDTC-Ag: Using Zn to convert As(III) to AsH3, passing the gas through a DDTC-Ag solution, measuring the absorbance of the resulting solution.

• Marsh’s test: Formation of AsH3 gas, passing it through a glass tube, burning at 600°C to form As deposited on the tube wall as a black ring. Removing the ring and burning it reveals the characteristic shape of As2O3.

• Cribier’s test: AsH3 gas reacts with HgCl2 and HgBr2-impregnated paper, forming yellow-orange or brown colors, then immersed in KI to fix the color.

• Quantitative methods: AAS using the hydride generation technique.

• AAS wavelength: 193.7 nm.

IV. CO (Carbon Monoxide)

1. Characteristics:

• Produced in the body: Derived from the metabolism of dichloromethane in the liver or the conversion of heme to biliverdin.

• Sources of CO production:

• Incomplete combustion of C-containing compounds.

• Smelting.

• Cigarette smoke.

• Traffic.

• Deep wells.

• Forest fires.

• Recognition: Colorless, odorless, non-irritating.

• Flame color: Blue (Barium gives a green flame).

• Solubility: Very slightly soluble in water, soluble in ethanol and benzene.

• Do not use activated charcoal to detoxify CO: CO is not absorbed by activated charcoal and can pass through normal gas masks.

• Mask detoxification: Using metal oxides, as these substances oxidize CO.

• Causes of poisoning: Suicide, accidental ingestion, occupational exposure, environmental pollution.

2. Mechanism of Toxicity:

• Binding to Hb: Forms carboxy Hb, impairing O2 transport and causing tissue hypoxia.

• Enzyme inhibition: Cytochrome oxidase, inhibiting cellular respiration.

• Binding to myoglobin: Reduced cardiac muscle contraction, hypotension, cerebral ischemia.

• Fatty acid peroxidation: Causes brain edema and necrosis.

• Fetal anemia:

• Reduced O2 supply from mother to fetus.

• Higher affinity for HbF than HbA.

• Slower CO elimination in fetuses than adults.

• Main toxicity: Tissue hypoxia and ischemia.

• Most affected organs: Brain and heart.

• Cadaver characteristics: Red lips, crimson stains on the thighs and abdomen due to the bright red color of CO-infected blood.

• Affinity: CO for Hb and Mb > O2 (250-60).

3. Management:

• Prompt treatment: Patients may recover but can still experience neurological sequelae.

• Carbogen: O2 gas with 5% CO2.

• Management: Keep warm, quiet.

• Rapid quantification: Using I2O5.

• CO quantification in blood: Directly (releasing CO from Hb and using gas chromatography), indirectly (measuring carboxyHb absorbance).

V. NOx (Nitrogen Oxide)

1. Characteristics:

• Mixture: 5 gases: NO, NO2, N2O3, N2O4, N2O5.

• Most toxic gases: NO and NO2.

• Sources of NOx:

• Reactions of organic substances with HNO2 and HNO3.

• Combustion of nitrocellulose.

• Color, odor, solubility:

• NO: Colorless, odorless.

• NO2: Brown, pungent odor.

• Higher toxicity: NO2.

• Combustion: Non-combustible but can promote the combustion of flammable materials.

• Route of poisoning: Respiratory system.

• Systemic effects: Regardless of the route, it causes systemic effects.

• Most affected organ: Lungs.

2. Mechanism of Toxicity:

• Lung damage:

• Formation of corresponding acids in the peripheral airway system, damaging lung cells and structures.

• Formation of free radicals that oxidize proteins, peroxidize peptides, and damage cell membranes.

• Alteration of immune system function, making infections more likely.

• Differences between NO and NO2: NO2 causes more severe damage, NO forms MetHb more strongly and rapidly.

3. Management:

• Stage of fatal poisoning: Irrespective of the stage.

• Treatment medication: No antidote.

• Methylene blue: When the victim has signs of tissue hypoxia, MetHb levels above 30%.

• Gastric lavage: Do not perform gastric lavage if NOx is ingested.

• Metabolism and excretion: NO2- and NO3- through urine.

• Monitoring: MetHb, chest X-ray, urine for NO2- and NO3- levels.

VI. Acids & Bases

1. Acid (HF)

• Toxic concentration: 1% is still dangerous.

• Effects: Corrosion, burns, necrosis.

• Mechanism: Coagulation-type, causing microvascular obstruction, dehydration, collagen loss in cells.

• Absorption through skin: Can be absorbed through the skin to enter the bloodstream and cause systemic effects.

• Hypocalcemia: HF can cause hypocalcemia.

• Neutralization:

• Digestive system: MgO, soapy water (do not use NaHCO3 as it produces CO2, which can cause stomach perforation).

• Skin, mucous membranes: NaHCO3 (after thorough washing).

• Qualitative determination: Color development to identify presence, followed by reactions to differentiate acids.

2. Strong base (NH4OH)

• Mechanism of necrosis: Liquefaction-type: Saponification of fats and mucous membranes, dissolution of albumin and collagen, dehydration, blood clot formation, capable of penetrating deeply to damage tissues.

• Neutralization: Weak acid: Dilute lemon juice, citric acid.

• Gastric lavage, inducing vomiting: Do not perform gastric lavage, do not induce vomiting, give ice to suck.

Note: This content has been condensed from the original data and may lack some information.