Toxicology Exam 3

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Carbon monoxide gas
- colorless
- tasteless
- non-irritating
Common sources of human exposure to carbon monoxide
- smoke inhalation in fires
- automobile exhaust fumes
- faulty or poorly ventilated charcoal
- kerosene or gas stoves
- cigarette smoke
- methylene chloride
Mechanism of toxicity with carbon monoxide
- cellular hypoxia and ischemia
- CO binds hemoglobin in place of oxygen decreasing oxygen carrying capacity
- CO directly inhibits cytochrome oxidase C
- binds myoglobin preventing contraction of muscles
Carbon monoxide binds hemoglobin with an affinity ____ times that of oxygen

250
Damage from CO is most severe in

the brain
CO intoxication correlates with

severity of systemic hypotension
More sensitive to binding CO

fetal hemoglobin
Recommended workplace limit (ACGIH TLV-TWA) for CO

25 ppm as an 8 hour TWA
Level of CO immediately dangerous to life or heath (IDLH)

1200 ppm (0.12%)
Several minutes of exposure to 1000 ppm (0.1%) may result in

50% saturation of carboxyhemoglobin
Symptoms of CO intoxication
- predominantly in high O₂ consumption organs such as brain and heart
- headache
- dizziness
- nausea
Predisposing factor for CO intoxication

congestive heart failure
Survivors of serious CO exposure may suffer from
- neurological sequelae consistant with hypoxic ischemia
- parkinsonism
- persistant vegetative state
- personality or memory disorders
CO exposure during pregnancy may result in

fetal death
first sign of CO poisoning

headache
Diagnosis of CO poisoning
- cherry red skin
- bright venous blood (smokers may have too)
- carboxyhemoglobin level
Fetal hemoglobin may produce falsely elevated levels of ____ in young infants that may last up to ____ years.
- carboxyhemoglobin
- may last up to 2 years
Treatment of CO poisoning
- maintain open airway
- assist ventilation
Because smoke often contains other toxic gases, considter the posibility of ____, ____ and ____ along with CO intoxication.
- cyanide poisoning
- methemoglobinemia
- irritant gas injury
Specific drugs/antidotes for CO intoxication

Administration of 100% oxygen for approximately 1 hour at normal temp and pressure
Hyperbaric 100% oxygen at ____ atm can spead elimination of CO to ____ min.
- 2-3 atm
- 20-30 min
Applications for Cyanide
- chemical synthesis
- laboratory analysis
- metal plating
_____ used in plastic manufacturing are metabolized to CN.
- Aliphatic nitriles
- acrylonitrile
- propionitrile
Natural sources of cyanide
- amygdalin from apricot pits
- cassava
- plants in africa (tuber)
In order to eat tuber from africa

must ferment to release HCN
component of artificial nail glue that has caused several pediatric deaths
- acetonitrile
- releases CN in the child
Hydrogen Cyanide
- gas generated by mixing hydrogen with cyanide salts
- common product of burning plastics or wools
HCN poisoning is an important cause of
- death from structural fires
- homicide
- suicide
Mechanism of CN toxicity
- chemical asphyxiant
- binds cytochrome oxidase to block aerobic utilization of oxygen in the muscle
Difference between CO and CN mechanisms
- CO acts on mitochondrial oxidase C in the mitochondria
- CN acts on cytochrom oxidase in the muscle
Unbound CN is detoxified by metabolism to ____ which is excreted in the ___.
- thiocyanate
- urine
Air level of CN considered immediately dangerous to life or health

50 ppm
Fatal level of CN if exposed

150-200 ppm
Solutions of CN salts
- can be absorbed through skin
- 200 mg ingested can be fatal
CN poisoning can result from ____ but is rare.
- nitroprusside infusion
- amygdalin-containing seeds
Hallmark sign of cyanide poisoning

abrupt onset of profound toxic effects
symptoms of CN poisoning
- headache
- nausea
- dyspnea
- confusion
When CN is ingested as a salt, as a capsule or with food

brief delay in symptoms may occur
clinical symptoms of CN poisoning
- lactic acidosis
- bitter almond odor may or may not be noted based on genetics
Whole blood levels of CN ranging from ____ are considered toxic

0.5-1 mg/L
Smokers may have normal blood CN levels of ____.

0.1 mg/L
Rapid nitroprusside infusion may result in blood CN levels of ____ along with ____.
- 1 mg/L
- metabolic acidosis
Cyanide antidote package consists of
- amyl and sodium nitrites
- sodium thiosulfate
Amyl and sodium nitrite mechanism of action
- break a pearl of amyl nitrite under the nose of the pt
- infuse sodium nitrite 300 mg IV
- causes conversion of hemoglobin to methemoglobin which binds CN
Mechanism of sodium thiosulfate
- administer 12.5 g IV
- accelerates conversion of cyanide to thiocyanate
Given empirically even if CN poisoning diagnosis is uncertain

sodium thiosulfate
useful in mitigating nitroprusside toxicity

sodium thiosulfate
Most promising alternative antidote
- hydroxocobalamin
- synthetic form of vitamin B₁₂
mechanism of action for hydroxocobalamin

hydroxocobalamin exchanges its hydroxyl group with free cyanide in the plasma to produce non-toxic cyanocobalamin
side effects of hydroxocobalamin

bodily fluids become brownish-red
hydroxocobalamin availability

investigational orphan drug in the US
most visible form of air pollution

smoke
sources of air pollution

burning fossil fuels, coal and oil.
Five major pollutants which account for 98% of all air pollution from highest to lowest
- CO (52%)
- Sulfur Oxides (18%)
- Hydrocarbons (12%)
- Particulates (10%)
- Nitrogen Oxidases (6%)
Major air pollutants are generated from
- fuels used in electric power plants and industry
- car exhaust
- waste/refuse disposal
Average air CO concentration

0.1 ppm
in heavy traffic CO concentrations can reach

100 ppm
Sulfur Dioxide

colorless irritant gas generated from combustion of sulfur-containing fossil fuels
sulfur dioxide forms ____ on contact with mucous membranes

sulfurous acid
Primary signs of sulfur dioxide exposure

conjunctival and bronchial irritations
____ ppm sulfur dioxide can cause severe bronchospasm

5-10 ppm
Treatment for SO₂ exposure
- removal from contaminated air
- treatment of irritation and inflammation
Nitrogen dioxide is formed in
- fires
- fresh silage on farms
Effects of nitrogen dioxide
- deep lung irritation capable of producing pulmonary edema
- irritation of eyes, nose and throat
- death of farmers in silos
Treatment of nitrogen dioxide poisoning
- no specific treatment
- reduce inflammation and pulmonary edema
Ozone
- O₃
- bluish irritant gas
- produced in air and water purification devices and in electrical fields
Exposure to ____ ppm Ozone causes irritation and dryness of mucous membranes.

0.1 ppm
Higher concentrations of Ozone exposure may result in

impaired pulmonary function
Chronic Ozone exposure may result in
- bronchitis
- bronchiolitis
- fibrosis
- emphysema
Treatment for Ozone poisoning
- no specific treatment
- reduce inflammation
- reduce pulmonary edema

Author

Rx2013

77645

Card Set

Toxicology Exam 3

Description

CO/CN & Air Pollution

Updated

2011-04-06T00:11:15Z

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