|
Module 3: Toxicology -
Section
10: Toxic Gases |
TOX 10.3: Specific Toxic
Gases |
SPECIFIC TOXIC GASES:
I. Physical asphyxiants:
See: La Dou
II. Chemical asphyxiants:
1. Carbon monoxide (CO):
Source:
- Environmental/domestic: fuel
burning in unventilated spaces
- Smokers: Carboxyhaemoglobin
around 4 - 5 % (may reach 10%)
- Occupational: vehicle
exhaust, (methylene chloride) unvented combustion: e.g. vehicle
workshops, tollbooth workers in tunnels
Clinical:
Acute effects:
- Tissue hypoxia
- Hyperventilation
- Vasodilatation-syncope
- Nonspecific: headache,
nausea, etc
Chronic effects:
- Neuropsychiatric
abnormalities
Ix:
Carboxyhaemoglobin. Note: PO2
may be normal.
Rx:
100% 02.
Observe.
Control:
As per source. R-OEL: 50 ppm, (STEL 300 ppm)
Note: You are not expected to remember
any specific numbers. However you do need to know where to look it up.
Hydrogen cyanide (HCN, prussic
acid):
Source:
- Fumigation,
- Metal plating/cleaning
- Chemical manufacture. (nylon)
- Firefighting
Clinical:
Acute:
(a) Mucous membrane skin irritation (b) Hypoxia due to binding of
cytochrome oxidase in cells. Bitter taste, headache, nausea and
vomiting, dyspnoea, agitation, respiratory arrest.
Post-acute:
Delayed CNS damage
Chronic:
Persistent symptoms, neurologic deficit, goitre
Ix:
Suspicion, blood thiocyanate
Rx:
100% 02, Amyl nitrite / Na nitrite IV, followed by Na thiosulphate IV
Control:
Engineering, PPE, decontamination/evac. procedures. C-OEL: STEL (only)
10 ppm
Note: Hydrogen cyanide has a Control -
OEL (C-OEL). Revise this concept.
3. Hydrogen sulphide (H2S):
Source:
- Decay of sulphur containing
materials (sewage, manure, animal/fish)
- Refining sulphur containing
petroleum
- (Smell of rotten eggs, but
not at high concentrations)
Clinical:
Acute:
Irritant (eyes, URT) plus cellular asphyxiant.
Post acute:
CNS deficits
Chronic:
?
Diagnosis:
History
Rx:
100% 02,
Na nitrite (as an antidote).
Control:
- Strict controls (do not
underestimate toxicity)
- Evacuation protocol.
- R-OEL: 10 ppm (STEL 15 ppm)
III. Irritant gases:
Sulphur dioxide (SO2):
Source:
- Fuel burning
- Refineries
- Smelters
- Food manufacture (starch)
Clinical:
Acute:
- URT irritation
- Systemic: nausea
- LRT: bronchospasm
(asthmatics!)
Post acute:
Reactive Airways Dysfunction Syndrome (RADS)
Chronic:
Chronic bronchitis/COPD?
Ix:
Airways function
Rx:
Bronchodilators, systemic steroids
Control:
As for source. R-OEL: 2 ppm (STEL 5 ppm)
Oxides of nitrogen (NO, NO2):
Source:
- Vehicle exhaust (component
of photochemical smog)
- Grain fermentation (Look up:
Silo filler’s disease).
- Welding
- Underground blasting
Clinical
Acute:
Relatively little impact on URT (low solubility) LRT damage! Delayed up
to 24 hrs - bronchiolitis, alveolitis, pulmonary oedema.
Post acute:
Obliterative bronchiolitis (Medics: look this up).
Chronic:
?Emphysema
Ix:
Serial examinations; close monitoring for 24-48 hrs (Admit if unsure).
Follow up at 1 month
Rx:
Systemic steroids, O2,
ventilation.
Control:
Local ventilation (welders) in closed spaces.
Flushing of silos with fresh air. R-OEL: 3ppm (STEL 5ppm)
Ozone (O3):
Source:
- Arc welding
- Photochemical reactions
- Photocopiers
[Note: same gas as
stratospheric ("good") ozone, but in wrong place, viz. at ground level]
Clinical:
Acute:
- Irritant plus insoluble
"Bleach" odour. URT, then LRT if concentration high enough.
- Reversible decrement in lung
function
Chronic:
"Lung aging", i.e. accelerated decline in lung function?
Ix/Rx:
As for general respiratory measures.
Control:Readily
reactive with most surfaces, (e.g. tubing) where it is converted to O2.
R-OEL: 0.1 ppm (STEL 0.3 ppm)
Ethylene oxide:
Source:
Sterilising agent (health care workers!), fumigation chemical industry
Clinical:
URT; skin irritant/allergen
Chronic:
mutagenic
clastogenic
carcinogenic in
animals
? carcinogenic
(leukaemia)
?? teratogenic
(Revise these terms)
Ix/Rx:
As per circumstances
Control:
Enclosure/extraction. C-OEL: 5 ppm. Monitor exposed workers (See Task
below).
Note: this is a problem in
hospitals
Phosgene (COCl2):
Source:
Chemical manufacture, heating chlorinated solvents, (chemical weapon)
Clinical:
Acute:
Lower RT irritant (low solubility), ARDS, delayed pulmonary oedema.
Post-acute:
lung function abnormality.
Ix:
Suspicion, assess severity.
Rx:
Observe, Rx early as for respiratory distress /pulmonary oedema.
Controls:
Strict. R-OEL: 0.1 ppm
Glossary of lung injury:
Adult
Respiratory Distress Syndrome (ARDS):
diffuse parenchymal lung injury resulting in severe respiratory
distress and hypoxaemic respiratory failure.
Bronchitis:
Inflammation of the bronchial tree
Bronchiolitis:
Inflammation of the bronchioles, i.e. the smallest branches of the
bronchial tree
Alveolitis:
Inflammation of the gas exchange part of the lung
Pulmonary oedema:
Filling of the gas exchange part of the lung with fluid. Occurs with
lung injury but also in heart failure
Emphysema:
Breakdown of the gas exchange part of the lungs including the
respiratory bronchioles, so that the alveoli become non-functional in
that area.
Assignment:
Hazardous gases
Question
1:
Someone rushes in to tell you that there has been an ammonia leak and
that one of the workers who was near the tank at the time has
collapsed.
Outline ALL the steps needed in
the management of this problem from an occupational health perspective.
Include all the elements of a management system needed to deal with
this sort of situation, including prevention of future episodes.
Question
2:
What medical surveillance would you do, if any, for employees exposed
to ethylene dioxide in hospital sterilising units?
REFERENCES:
- Occupational
and Environmental Medicine,. La
Dou J. 33, Pages 571-583. Gases and other inhalants.
Postgraduate Diploma in Occupational Health (DOH) - Modules 3:
Occupational Medicine & Toxicology (Basic) by Profs Mohamed
Jeebhay and Rodney
Ehrlich,
Health
Sciences UCT is licensed under a
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Major contributors: Mohamed Jeebhay, Rodney Ehrlich, Jonny Myers,
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Last updated Jan 2007.
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