Hydrocarbon Toxicity PDF

Chemical and Environmental Toxicity POISONING BY HYDROCARBONS Dr. Rasha Fadhel Hydrocarbons toxicity Hydrocarbons are organic compounds that contain hydrogen and carbon. They may be divided into aliphatic (straight chain)...

Chemical and Environmental Toxicity POISONING BY HYDROCARBONS Dr. Rasha Fadhel Hydrocarbons toxicity Hydrocarbons are organic compounds that contain hydrogen and carbon. They may be divided into aliphatic (straight chain) aromatic (benzene ring) halogenated (aliphatic and aromatic) hydrocarbons. They can come in the form of a gas, liquid , & solid Exposure to these substances can cause significant health risks Toxic exposure to hydrocarbons primarily impacts the respiratory and central nervous system Hydrocarbon exposure Hydrocarbon exposure in the symptomatic patient will typically occur three ways. First, the unintentional ingestion of household products by children Second, dermal or inhalation occupational exposure. Lastly, the intentional recreational inhalation of hydrocarbons by adolescents  Toxicity of hydrocarbons Toxicity of hydrocarbons is directly related to their physical properties, specifically the viscosity , volatility, surface tension , and chemical activity -Lower viscosity is associated with a higher chance of aspiration , Low viscosity allows for deeper penetration into the lungs -surface tension is also inversely related to aspiration risk , Low surface tension can allow compounds to spread easily over large areas. -The degree of volatility is directly related with risk of aspiration *Aspiration potential increases with low viscosity, low surface tension, and high volatility. Aliphatic Hydrocarbons - The aliphatics are used primarily as fuels, polishes, and solvents. - At room temperature, methane, propane, & butane are gases; pentane & hexadecane are Liquid and longer chains are solids. Aliphatic Hydrocarbons Pathophysiology: -Gaseous aliphatic: lowers the oxygen partial pressure causes hypoxia. - The lung is the primary target organ affected by a aliphatic hydrocarbon ingestion. pulmonary injury results from aspiration of the hydrocarbon and not from gastrointestinal absorption. Aspiration occurs during either initial ingestion or subsequent emesis. - Aliphatic hydrocarbons within the intestinal tract are poorly absorbed and exert minimal toxicity.  Aliphatic Hydrocarbons -Initial pulmonary damage is probably due to the chemical destruction of surfactant in the alveoli and distal airways. Leading to early airway closure, Pulmonary edema with subsequent hypoxia , pneumonitis, necrosis & death Aliphatic Hydrocarbons -Central Nervous System (CNS) effects: are not due to direct CNS toxicity of the hydrocarbon but rather to the hypoxia. Hypoxia caused by pulmonary injury -GIT pathology is mild : Irritation of the pharynx, intestinal inflammation and superficial ulceration -Fatty infiltration of the liver may develop after ingestion of aliphatic but frank necrosis uncommon -Renal toxicity uncommon Clinical Presentation Most patients are asymptomatic, Common symptoms include: Respiratory symptoms : cyanosis: common for gaseous toxin CNS symptoms : occur only in presence of aspiration of aliphatic hydrocarbons Mild: ( irritability or drowsiness) Moderate: (lethargy, flaccidity) Severe : (stupor, coma , seizures GIT: Initial pharynx irritation and hyperemia Vomiting, abdominal pain, and diarrhea.  Diagnosis 1-Chest radiography: for all symptomatic with doubt of hydrocarbon Aspiration 2-Mild clinical symptoms : Pulse oximetry and cardiac monitoring Arterials blood gas assessment in patients moderate to severe respiratory distress CBC Serum electrolyte determination Urinalysis, and renal and liver function may need to be evaluated over 48 -72 hours Treatment - Supplemental oxygen with intubation. -Skin contamination should be treated by removal of hydrocarbon contaminated clothing, followed by cleansing with soap or shampoo and copious H2O irrigation Treatment *Contraindicated therapies - Emesis/ lavage / activated charcoal - Epinephrine or other nonselective agents with both α- and β-adrenergic activity are not recommended because of possible myocardial sensitization to catecholamines and potential induction of ventricular dysrhythmias  Treatment - Bronchospasm may be treated with aerosolized selective β2-adrenergic agonist bronchodilators (e.g., albuterol, terbutaline, metaproterenol). Halogenated Hydrocarbons Halogenated hydrocarbons, also known as halocarbons, are hydrocarbon compounds in which at least one hydrogen atom is replaced by a halogen (bromine, chlorine, fluorine) They are encountered as solvent, degreasing agents remove Most are liquid at room temperature, but they are high volatile , one commonly used anesthetic gas , halothane, is Alkyl Halide Halogenated hydrocarbons vapors are well absorbed through lungs and rapidly distributed to the brain and other organs fat content. Pathophysiology CNS toxicity occurs by direct damage to nerve cell membranes, thereby altering neurotransmission briefly or permanently, depending on toxin concentrations & duration of exposure. Cardiac: exposure actually stabilizes the myocardial cell membrane to depolarization, this block impulses transmission and increases risk of dysrhythmia  Pulmonary: simple asphyxia is most common as theses volatile decreases the partial pressure of O2 in inhaled air Following ingesting , the risk of aspiration is less that associated with many aliphatic due to the higher viscosity of h-Hydrocarbons Renal: renal toxicity is less remarkable than hepatic damage In the liver Halogenated hydrocarbons can produce significant hepatic damage, including necrosis, and cirrhosis. *Relative hepatotoxicity of halogenated hydrocarbons Tetrachloroethane Carbon tetrachloride Trichloroethane Chloroform Perchloroethylene TCE ( trichloroethylene) Methylene chloride Methyl chloroform * from most to least hepatotoxic Carbon tetrachloride (CCl4) and halothane produce toxicity by production of reactive free radicals. Halothane: The hepatic cytochrome P450 system bio transforms the halothane into free radicals (Trifluoroacetyl halide) which bind covalently to liver proteins & initiated an immune complex- mediated hepatitis  Skin toxicity: includes drying and cracking of the skin , However, significant burns have been reported from an acute exposure. Systemic toxicity does not typically result from dermal exposure, with the exception of carbon tetrachloride, which can be trans dermally absorbed in quantities sufficient to cause systemic toxicity. Clinical presentation Acute inhalation Rapid state of consciousness intoxication ( with rapid recovery) Early excitatory phase : euphoria, disorientation,and hallucinations Progressive CNS depression: stupor, coma , cardiac dysrhythmia , sudden death Ingestion Nausea, vomiting, abdominal pain, and diarrhea Drowsiness Hepatic or renal toxicity ( hours to days ) Dermal exposure Skin drying or cracking, Huffer's rash( area of erythema around mouth or on the hands Chronic toxicity CNS dysfunction Hepatic or renal dysfunction ( usually mild and reversible) Diagnosis 1- Diagnosis of toxicity is usually made by the clinical presentation 2-Chest X ray : if pulmonary symptoms present at the Presentation 3- ECG , arterial blood gas , head ( ct ) scan, & lumbar puncture (CSF) when CNS effect present 4- Renal and liver function may need to be evaluated over 48 -72 hours  Treatment 1- It is necessary to maintain airway, breathing, and circulation. -Following inhalation exposure, the victim should be moved to fresh air and given assisted ventilation with supplemental oxygen as needed. 2-The patient should be monitored for potential cardiac dysrhythmias, Lidocaine and amiodarone are recommended for the treatment of halogenated hydrocarbon dysrhythmias. Treatment 3-Gastric decontamination with nasogastric tube aspiration ingestion is recent. 4-Remove contaminated. Clothing and decontamination. with copious H2O irrigation 5-Hemodialysis for renal failure 6-N- Acetylcysteine to prevent hepatic damage given after CCl4 exposure Aromatic Hydrocarbons Aromatic Hydrocarbons Benzene Benzene has been used in the shoe making, glue manufacture, and petroleum industries. Absorption of benzene occurs rapidly by ingestion, inhalation, and dermal routes. -Exposure : usually intentional abuse of toluene and xylene -Non occupational exposure: automobile emissions and cigarette smoke It is classified as a human carcinogen benzene is metabolism in the liver and excreted in urine.  Pathophysiology aromatic hydrocarbons (especially benzene) can lead to an increased risk of aplastic anemia, multiple myeloma, and acute myelogenous leukemia. In addition, hemolysis has been reported following the acute ingestion of various types of hydrocarbons. Pathophysiology - Exposure to benzene stimulates the cytochrome P-450, which is responsible for oxygenation of benzene, which generates oxygen-free radicals. These radicals are a major cause of benzene toxicity. Clinical presentation Acute toxicity: Inhalation exposure: euphoria, ataxia, headache, and respiratory depression. Massive exposure to high concentrations : pulmonary edema , haemorrhagic pneumonitis , cardiac dysrhythmias, seizures, coma, and death have been reported. Acute ingestion: burning of the oral pharynx, esophagus, and gastric mucosa results, with nausea, vomiting and abdominal pain.  Aromatic Hydrocarbons Dermal exposure. Cutaneous burns, erythema, and blistering may occur. Chronic toxicity: Fatigue, anorexia, and dizziness are common, aplastic anemia and acute leukemia have been reported Laboratory studies 1- CBC Monitor for thrombocytopenia, anemia, leukopenia, pancytopenia 2-Marrow’ biopsies: may show acute myelogenous leukemia 3- Liver profile , BUN, creatinine, and urinalysis 4- Monitor ECG for evidence of cardiac toxicity Treatment: - it is necessary to maintain airway, breathing, and circulation. - Emesis with syrup of ipecac is not recommended for acute ingestion since benzene may cause respiratory depression and seizures. - Hypotension: fluid resuscitation and pressor agent as needed  Treatment: - Gastric aspiration and activated charcoal are indicated with recent oral exposures. -Monitor the patient for cardiac dysrhythmias. Use epinephrine cautiously.