PROFESSIONAL POISONING WITH TOXIC GASES

advertisement
CURRICULUM FOR THE HEALTH SCIENCES IN SOUTH EASTERN EUROPE
Number (unit, topic): U4-T4
Review – Status: D
ECTS (suggested):
Title
Professional Poisoning with Toxic Gases
Author(s), degree,
institution(s)
Asst. Prof. Bela Prokes, MD, PhD
specialist in occupational medicine
Department of Occupational Medicine,
Medical Faculty Novi Sad
Asst. Prof. Bela Prokes, MD, PhD
Address for
correspondence
Keywords
Learning objectives
Department of Occupational Medicine,
Medical Faculty Novi Sad
Futoska 121
Novi Sad
Tel +381 21 614-277, 613-998, fax 624-128
E-mail zzzrns@eunet.yu
Poisoning, Toxic Gases, Sulphurdioxide, Ammonia,
Chlorine, Phosgene, Nitrogen oxides, Methane, Carbon
dioxide, Sulphurated hydrogen, Hydrogen Cyanide,
Arsenic Hydride
Prevention of poisonings with gases appearing in
occupational environment and how to recognize an early
signs of intoxication.
Synopsis (Abstract)
This topic covers:
Teaching methods
Transparency presentation, Oral lecture, Distribution of the
literature to small group of students, Discussion about target
themes, Presentation of clinical entities
Specific
recommendations
for teacher
Assessment of students
Practical work on intoxication diagnosis and work capability
evaluation; Oral exam
Professional Poisoning with Toxic Gases
Bela Prokeš, MD, PhD, specialist in occupational medicine
Department of Occupational Medicine, Medical Faculty Novi Sad
Classification of toxic gases according to effect:
1. GASES WITH IRRITABLE EFFECT - “IRRITANTS”
a) with main effect to breathing passages:
Sulphurdioxide
Ammonia
Chlorine
b) with main effect to lung parenhim:
Phosgene
Nitrogen oxides
2. GASES WITH ASFICTIC EFFECT
a) Simple asphyctic gases:
Methane
Carbon dioxide
b) Chemical asphyctic gases
Carbon monoxide
3. MAIN TOXIC GASES
Sulphurated hydrogen
Hydrogen Cyanide
Arsenic Hydride
The basic way of penetration in organism for all of them is respiratory
tract.
SULPHUR DIOXIDE
Extent and professional risk
- appears in smelting of sulphicle ores
-
in
in
in
in
in
foundries
combustion of coal
manufacture of sulphuric acid
battery forming
bleaching, desinfection, desinsection
Effect on human body: - irritable to respiratory tract
General toxic effect:
- metabolic acidosis
- disorder in metabolism of proteins and carbohydrates (polyglobulia,
methemoglobinaemia and sulphates in urine)
Clinical features:
Acute poisoning:
Slight degree: irritation of upper breathing passages and eye mucous
membrane, ticking and aches in throat, cough, huskiness
Moderate degree: headache, cough, aphonia, aches in epigastrium,
vomiting, nausea
Hard degree: diffuse bronchitis, acute emphysema, toxic pneumonia,
lung oedema, asphyxia. Dystrophic changes of myocard, liver, kidneys.
Chronic poisoning:
Chronic rhinitis, laringitis, bronchitis, hiposmia and anosmia,
conjunctivitis, stomach and intestinal disorders, disorder in endocrinal
glands and nervous system, lung emphysema and pneumosclerosis.
AMMONIA
Extent and professional risk
- in fertiliser manufacturing (amoniumsulphate and ammonium-nitrate
- row materials
- for bleaching in textile and furniture industry
- in production of artificial fibbers, commercial refrigerant etc.
Effect on human body: Irritable (general)
Clinical features:
Acute poisoning:
Slight degree: irritation of conjunctivas and upper breathing passag es
Moderate degree: swelling of larynx mucous membrane, bronchitis,
bronchopneumonia and lung oedema, damage of cornea (ambliopia)
Hard degree: reduction in pulmonary and cordial function (exitus)
Chronic poisoning:
Chronic conjunctivitis, nasal and throat catar, anosmia, chronic
bronchitis, pneumosclerosis, dyspeptic appearnesses, anaemia of moderate
degree.
CHLORINE
Extent and professional risk
- is produced commercially by electrolysis of Sodium chloride
- desinfection of drinking and waste waters, pools
- bleaching of cotton, paper, pulp
- in manufacture of chlorine compounds, polyvinilchloride, synthetic
rubber etc.
Effect on human body: Irritable (general)
- protoplasmic poison (C12+ H2O = 2HCI+O)
- reflective - as a result of irritation of breathing passage interreceptors
Clinical features:
Acute poisoning:
Slight degree (concentration of 1-6 ppm): irritation of eye mucous
membrane, nose and throat.
In higher (concentrations around 30 ppm): reflective spasm of smooth
muscular bronchioles: sudden cough attack, retrosternal pain and vomiting,
alveolar damage - lung oedema.
Hard degree (100-1000 ppm): reflectable effect to breathing center,
exitus.
Chronic poisoning
- in concentrations of 1-5 ppm - headache, dizziness, gingivitis, over
colored teeth, caries, chronic conjunctivitis, dermatitis, eczema,
functional liver disorder
Slighter forms of chronic poisoning: chronic rhinopharingitis,
laringotracheitis, bronchitis, lung emphysema, pneumosclerosis.
Hard forms of chronic poisoning: diffuse pneumosclerosis,
bronchiectasias, bronchial asthma, chronic lung insufficiency and chronic
cardio-pulmonary insufficiency. In blood: leucocytosis, polyglobulia,
accelerated sedimentation.
Pathological changes have irreversible character and prognosis
unfavourable
PHOSGENE
Extent and professional risk:
- in application of means for fire extinguishing which contain
- tetrachlorinecarbon
- thermal degradation (breakdown) of chlorine carbohydrates:
- tetrachlorinemethane, trichlorineethylen, chloroform
Effect on human body:
- doesn't result in significant irritable effects to upper breathing
passages
- influences to bronchiole damaging an endotel of lung capillary
- lung oedema
Clinical features:
Acute form of poisoning:
- initial stadium: slight irritation of upper breathing passages
- latent period 3-6, 12, 24
- appearance of lung oedema (dispnea, cyanosis, cough, blue-gray
cyanosis/exitus caused by asphixia or cardial insufficiency).
is
Complications: pneumonia, apsces, emboli, bronchiektasia
Treatment: repose, oxygenotherapy, antibiotic therapy
NITROGEN OXIDES OR NITRIC GASES
Mixture of oxides: nitrogenoxidul (N 2 O)
nitrogenoxide (NO)
nitrogendioxide (NO 2 )
nitrogentrioxide (N 2 O,)
nitrogenpentoxide (N 2 O 5 )
- in production of nitrogen acid, anilinic colors, artificial silk,
- fertilisers
- in contact of nitrogen acid organic matters or metals
Effect on human body: damages of deep respiratory tract parts
Clinical features:
Acute poisoning:
- slight irritation of eyes, nasal and upper breathing passage’s mucous
membrane
- latent period from 0,5 to 36 hours
- appearance of lung oedema:
- alarm trias: tachicardia, tachipnea, thrombocitosis,
- cyanosis
- X ray changes
- decreased diaphragma
- unclearly edged numerous shadows
Complications: -bronchopneumonia
- infarct type pneumonia
- bronchiolitis obliterans
- -wax myocard degeneration
Chronic poisoning:
- chronic inflammation of upper breathing passages
-
chronic bronchitis
lung emphysema
asthma
vegetative dysfunction
METHANE
Extent and professional risk:
- constitutional part of "mines gas" - 90%
- pillboxes for coal sorting
- decomposition of organic matters (“mud gas”)
- in production of crude petroleum
Effect on human body:
-syndrome of oxygen insufficiency
Clinical features:
Acute poisoning:
- headache, dizziness, sleepiness, accelerated pulse and breathing,
disorder in movement co-ordination
- vomiting, loss of consciousness Objectively: coldness and pale skin
- hipotonia
- CNS changes
- leucocytosis (lymphocytopaenia)
CARBON DIOXIDE
Extent and professional risk
- in combustion of organic matters with oxygen presence
- in fermentative processes (cellars, grain elevators)
- in foundries, refrigeration plants
Effect on human body:
- irritable effect on skin and mucous membranes
- depressively on breathing center (in high concentrations)
- due to decreased oxygen - anoxemia
Clinical features:
Acute forms:
Air concentration of carbon dioxide higher:
- than 2%: headache, weakness, sleepiness
- than 5 - 8 % : irritation of mucous membrane of upper breathing
passages, buzzing in ears, dizziness, irritability, psychical disorders
- than 0 % loss of consciousness (anoxemia)
After poisoning: retrograde amnesia, headache, weakness, bronchitis and
bronchopneumonia.
CARBON MONOXIDE
Extent and professional risk:
- in combustion of matters without sufficient oxygen presence: coal
combustion, coke plants, iron and steel foundries, coal mines,
electric and autogen welding
Effect on human body:
Toxic effect is consequence of hypoxia:
2. Concerning blood:
- it is connected to hem towards which has 200- 300 times greater
affinity and produce carboxihaemoglobine (COHb).
3. Concerning tissues:
- it is connected to myoglobine producing carboximyoglobine
(COMb) which decreases oxygen transfer to muscle mythohondrias,
particularly to myocard.
- influences the enzymes that have hem group: cytohrom a3 and p450
that participate in cell respiration.
Clinical feature:
Acute poisoning:
Slight degree (20-30% COHb): headache, dizziness, ear buzzing, chest
oppression, nausea, vomiting, weakness, accelerated pulse, retarded
reactions.
Medium degree (30-35% COHb): loss of consciousness, organic
damage of CNS, weakness, muscle slackness
Hard degree (50-60 % COHb): coma and symptoms of diffuse cerebrum
damage (tonic cramps in extremities, epileptiformal attacks, pathologic
reflexes), accelerated breathing, accelerated pulse, hipotonia.
Chronic poisoning:
- appears as a result of close carbon monoxide influence to CNS
Functional cumulation - damage of center in cortex with following
symptoms: headache, dizziness, asthenia, ear buzzing, heart palpitation,
fatigue, irritability, weakened memory
- cerebrovascular, cardiovascular disorders, atherosclerosis (COHb to
11%).
SULPHURATED HYDROGEN
Extent and professional risk:
-
manufacture of sulphur types of petroleum
sewage system, waste water pools
in sugar refineries, breweries, tanneries
copper, nickel, cobalt extraction from minerals
Effect on human body:
- intensive irritable effect to mucous membrane of eyes and breathing
passages
- general toxic effect - inhibition of Warburg’s breathing ferment and
tissue anoxia
Clinical features:
Acute poisoning:
Slight degree: irritable symptoms at mucous membrane of eyes and
breathing passages
Medium degree: symptoms of respiratory effects: headache, dizziness,
weakness, nausea, vomiting, disorder in motoric coordination, irritability or
loss of consciousness, bronchitis, bronchopneumonia, tahicardia, cyanosis,
increased temperature.
Hard degree: disorder in respiratory and cardiovascular system, coma
and death.
Superacute and appoplectiform degree: paralysis of respiratory and
cardiovascular center, loss of consciousness and finally death.
Subacute form: headache, dizziness, weakness, fatigue, perspiration,
irritation of nasal and throat mucous membrane, cough, nausea, vomiting.
Chronic poisoning: headache, dizziness, weakness, perspiration, loss of
appetite, pale skin and mucous membranes, anaemia, finger tremor,
hypotonia, bradicardia etc.
HYDROGEN CYANIDE AND CYANIDES
Extend and professional risk:
-
in desinsection and deratisation
in manufacture of Hydrogen cyanide acid, salts and other compounds
in manufacture of silver, gold and mercury from minerals
galvanisation
fertiliser production
bensene, toluene, pesticide production
Ways of penetration:
- respiratory tract digestive tract skin
- mucous membranes
Excretion:
- through lungs (unchanged)
- through kidneys (like rodanides)
Effect on human body:
- blockade of respiratory ferments, cytochromoxidasis - tissue anoxia
CNS, respiratory and vasomotor center
- direct toxic effect to central nervous system
Clinical features:
Acute poisoning:
Slight form: headache, dizziness, chest pain, accelerated breathing
Hard form: loss of consciousness, widen pupil of eye, exoftalmia,
dispnea, cramps, paralysis of respiratory center
- Initial stadium: metal taste and ticking in mouths, irritation of eye
mucous membrane, weakness, headache, dizziness, nausea and
vomiting.
- Dispnoic stadium: disorder in respiratory rhythm, bradicardia,
- Convulsive stadium: clonic and tonic convulsions, jaw trismus, loss of
consciousness.
- Paralytic stadium: loss of consciousness, arreflaxia, unwillingly
urination, defecation, paralysis of respiratory center and stoppage of
heart function - exitus.
ARSENIC HYDRIDE (ARSINE)
Extend and professional risk:
- in treatment of metals with acids
- in production of metals
- in manufacture of acetylene
- melting of lead alloys
Arsenic hydride is released whenever hydrogen in “status nascenti” appears
in presence of arsenic.
Effect on human body:
Chemolitic effect - haemoglobinuria, anaemia, reticulocytosis, jaundice,
damage of kidneys.
Clinical features:
Acute form:
Latent period 3-8 hours - weakness, shivering, headache, obstructed
breathing, dispnea, tahicardia, extended liver and spleen, oliguria, reddish
urine, anaemia, leucocytosis, reticulocytosis, hiperbilirubinaemia
In urine: albumens, eritrocytes, cylinders. Disorder of central nervous
system
Consequences: arsenic polyneuritis, disorder in fat metabolism, damage
of kidneys, liver, heart and nervous system.
Chronic poisoning:
pale skin, dizziness, fatigue, obstructed breathing, anaemia, changes on
skin.
References:
1. Levy BS, Wegman DH. (eds): Occupational Health, Recognizing and
Preventing Work-Related Disease and Injury. Lippincott Williams &
Wilkins, Philadelphia, 2000.
2. LaDou J. (ed): Occupational and Environmental Medicine. Prentice -Hall
International, Inc, 1997
3. Rosenstock L, Cullen M. (eds): Textbook of Clinical Occupational and
Environmental medicine. W.B. Saunders Company, Philadelphia, 1994.
4. Stacey N. (ed): Occupational Toxicology. Taylor&Francis, London 1995.
Download