Central nervous system respiratory effects

The benzodiazepine antagonist flumazenil is sometimes used to accelerate recovery from excessive sedative actions of intravenous benzodiazepines, but reversal of respiratory depression by flumazenil is less predictable. Its short duration of action (< 90 minutes) may necessitate multiple doses to prevent recurrence of central nervous system depressant effects of longer-acting benzodiazepines. 

Chronic exposure results in eye damage, kidney degeneration, and central nervous system (CNS) effects. It is a carcinogen to nasal passages, pharynx, and respiratory tract. A dose-response relationship exists between exposure and damage to the reproductive system. Age or stage of sexual development also mediated damage. 

Acute toxicity induced by pentazocine is primarily associated with central nervous system (CNS) effects that include dizziness, anxiety, hallucinations, mood alterations, and seizures. Respiratory depression, increased PaCOi levels, pulmonary edema, and apnea may occur. Tachycardia, increased systolic and diastolic blood pressure, pinpoint pupils, nausea, vomiting, and abdominal pain have also been reported. In a recently published case series, 40% of acute pentazocine overdose patients did not have the classic opioid toxidrome of CNS and respiratory depression with miosis. 

CHRONIC HEALTH RISKS effects on peripheral nervous system and central nervous system respiratory system effect liver damage. 

ACUTE HEALTH RISKS irritation of eyes, nose and throat irritation to respiratory tract coughing shortness of breath headache nausea vomiting diarrhea may affect the central nervous system narcotic effects in high concentrations may cause dermatitis possible comeal bums eye damage pulmonary changes. 

ACUTE HEALTH RISKS irritation of skin, eyes, and respiratory system cough headache sore throat shortness of breath cyanosis narcosis nausea pulmonary edema pulmonary irritation effects on central nervous system respiratory failure rapid evaporation of the liquid may cause frostbite death in high concentrations. 

The acute inhalation toxicity is of low order. Since it is a gas, the route of exposure is primarily inhalation. The target organs are the liver, central nervous system, respiratory system, and blood. Exposure to high concentrations can produce narcosis. A 30-minute exposure to 30% vinyl chloride in air was fatal to experimental animals. Chronic exposure produced minor injury to the liver and kidneys. Such effects were noted at a 7-hour exposure daily to 200 ppm for 6 months. 

Poisoning may effect the skeleton, kidneys, and central nervous system. Respiratory tract irritation, coughing, choking, and bums of the mucous membranes can be expected. 

Health and Safety Factors. Carbonyl sulfide is dangerously poisonous, more so because it is practically odorless when pure. It is lethal to rats at 2900 ppm. Studies show an LD q (rat, ip) of 22.5 mg/kg. The mechanism of toxic action appears to iavolve breakdowa to hydrogea sulfide (36). It acts principally on the central nervous system with death resulting mainly from respiratory paralysis. Little is known regarding the health effects of subacute or chronic exposure to carbonyl sulfide a 400-p.g/m max level has been suggested until more data are available (37). Carbon oxysulfide has a reported inhalation toxicity in mice LD q (mouse) = 2900 ppm (37). 

Overexposure to tetrachloroethylene by inhalation affects the central nervous system and the Hver. Dizziness, headache, confusion, nausea, and eye and mucous tissue irritation occur during prolonged exposure to vapor concentrations of 200 ppm (15). These effects are intensified and include incoordination and dmnkenness at concentrations in excess of 600 ppm. At concentrations in excess of 1000 ppm the anesthetic and respiratory depression effects can cause unconsciousness and death. A single, brief exposure to concentrations above 6000 ppm can be immediately dangerous to life. Reversible changes to the Hver have been reported foUowing prolonged exposures to concentrations in excess of 200 ppm (16—22). Alcohol consumed before or after exposure may increase adverse effects. 

Air-poUutant effects on neural and sensory functions in humans vary widely. Odorous pollutants cause only minor annoyance yet, if persistent, they can lead to irritation, emotional upset, anorexia, and mental depression. Carbon monoxide can cause death secondary to the depression of the respiratory centers of the central nervous system. Short of death, repeated and prolonged exposure to carbon monoxide can alter sensory protection, temporal perception, and higher mental functions. Lipid-soluble aerosols can enter the body and be absorbed in the lipids of the central nervous system. Once there, their effects may persist long after the initial contact has been removed. Examples of agents of long-term chronic effects are organic phosphate pesticides and aerosols carrying the metals lead, mercury, and cadmium. 

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