PROFESSIONAL POISONING WITH TOXIC GASES

Classification of toxic gases according to effect:

1. GASES WITH IRRITABLE EFFECT - IRRITANTS
a) with main effect to breathing passages:
Sulphur oxides (mainly sulphur dioxide)
Ammonia
Chlorine
b) with main effect to lung parenhim:
Phosgene
Nitrogen oxides
Ozone
2. GASES WITH ASFICTIC EFFECT
a) Simple asfictic gases non-toxic gases:
Nitrogen
Argon
Methane
Carbon dioxide
Some fuel gases

b) Chemical asfictic gases

Carbon monoxide
Hydrogen cyanide
3. MAIN TOXIC GASES both systemic and local effects
Hydrogen sulphid
Arsenic Hydride
Phosphin
Formaldehyde
Ethylen oxide
The basic way of penetration in organism is respiratory tract.
SULPHUR DIOXIDE
Extent and professional risk
appears in smelting of sulphide ores and alloys
in foundries
in combustion of coal
in manufacture of sulphur acid
in battery forming
in bleaching, desinfection, desinsection
Main effect - Local: - irritable to respiratory tract
General toxic effect
-metabolic acidosis
-disorder in metabolism of proteins and carbohydrates
(polyglobulia, methemoglobinemia 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 miocard, liver, kidneys.
Chronic poisoning:
Chronic rinitis, 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 (ammoniumsulphate and ammonium-nitrate - raw materials
-for bleaching in textile and furniture industry
-in production of artificial fibbers, commercial refrigerant etc.
Effect : Irritable

Clinical feature

Acute poisoning:
Slight degree: irritation of conjunctivas and upper breathing passages
Moderate degree: swelling of larynx mucous membrane, bronchitis, bronchopneunionia and lung
oedema, damage of cornea (ambliopia)
Hard degree: reduction in pulmonary and cordial function (egsitus)
Chronic poisoning:
chronic conjuctivitis, 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 natrium chloride
-desinfection of drinking and waste waters, pools
-bleaching of cotton, paper, pulp
-in manufacture of chlorine compounds, polyvinilcliloride, synthetic rubber etc.
Effect:

- irritable
- protoplasmic poison (C1 2 + H 2 O = 2HCI+O)
- reflective - as a result of irritation of breathing passage interrecep-tors

Clinical feature:
Acute poisoning:

Slighter degree: irritation of eye mucous membrane, nose and throat (1-6 ppm). In higher concentrations
(30 ppm):
reflective spasm of smooth muscular bronchioles: sudden cough attack, retrosternal pain and
vomiting, alveolar damage - lung oedema.
Hard degree: reflectable effect to breathing centre (100-1000 ppm), exitus.
Chronic poisoning
-in concentrations of 1-5 ppm - headache, dizziness, gingivitis, overcoloured teeth, caries, chronic
conjunctivitis, dermatitis, eczema, functional liver disorder
Slighter forms of chronic poisoning: chronic rhinofaringitis, laringotracheitis, bronchitis, lung
emphysema, pneumosclerosis.
Hard forms of chronic poisoning: diffuse pneumosclerosis, bronchiectasy, bronchial asthma, chronic lung
insufficiency and chronic cord.pulm. In blood: leucocitosis, polyglobulia, accelerated
sedimentation.
Pathological changes have irreversible character, prognosis -in favourable
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 to human body

-doesn't result in significant irritable effects to upper breathing passages
-influences to bronchiole damaging endotel of lung capillary
-lung oedema
Clinical feature

Acute form of poisoning:

1. initial stadium: slight irritation of upper breathing passages
2. latent period 3-6 h, 12 h, 24 h.
3. appearance of lung oedema (dispnea, cyanosis, cough, blue-grey cyanosis/egzitus caused by
asphixia or cardial insufficiency!.)
Complications: pneumonia, apsces, emboli, bronchiektasia
Treatment: repose, oxigenotherapy, 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 )

Extent and professional risk

-in production of nitrogen acid, anilinic colours, artificial silk,
fertilisers
-in contact of nitrogen acid organic matters or metals
Effect to organism
- cause damages of deep respiratory tract parts
Clinical feature

Acute poisoning:
1.Slight irritation of eyes, nasal and upper breathing passages mucous membrane
2.Llatent period from 0,5 to 36 hours
3.Appearance of lung oedema:
alarm trias: tachicardia, tachipnea, trombocitosis,
cyanosis
Rtg changes
-decreased diaphragma
-unclearly edged numerous shadows
Complications: - bronchopneumonia
- infarct type pneumonia
- bronchiolitis obliterans
- "wax" degeneration of the miocard

Chronic poisoning:
1. chronic inflammation of upper breathing passages
2. chronic bronchitis
3. lung emphysema
4. asthma
5. vegetative disfunction
OZONE
Colourless or blue gas with a pungent odour
Ozone is produced by the action of ultraviolet light (sun, UV-lamps), electric discharge (lightning,
arc welding) or ionising radiation (metal detectors, medical usage) on the atmospheric oxigen
Effect to organism
Appreciable solubility in lipids - tend to be deposited in terminal broncioles and alveoli as well as in
upper airways degradation of cellular proteins and oxidation of lipids
Clinical features

Acute poisoning:
- irritation of eyes, nasal and upper airways mucous membrane
- pulmonary oedema usually delayed for up to 30 h
- systemic effects drowsines and headache (by relatively high exposure)
Chronic exposure:

- may lead to emphysema and increased risk of infection

NITROGEN, ARGON, SOME FUEL GASES (hydrogen, propane etc)
Compressed inert gases (nitrogen, argon) are used:
- for welding
- for purging storag vessels and pipelines
- in the heat treatment of metals
Liquid forms
- to freeze and preserve foods and other materials
- for situations where very low temperatures are required
The flammable simple asphyxiants (hydrogen, propane)
- as fuels
- in many industrial processes
Effects to human body and clinical features are the same like by METHANE
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 to human body

- syndrome of oxygen insufficiency

Clinical feature

Acute poisoning
- headache,dizziness, sleepiness, accelerated pulse and breathing, disorder in movement coordination
- vomiting, loss of consciousness Objectively: coldness and pale skin
hipotonia
- CNS changes
- leucocitosis (Iimphocitopenia)
CARBON DIOXIDE
Extent and professional risk
- in combustion of organic matters with oxygen presence
- in fernientative processes (cellars, grain elevators)
- in foundries, refrigeration plants
Effect to human body
- irritable effect to skin and mucous membranes
- depressively to breathing centre (in high concentrations)
- due to decreased oxygen - anoxemia
Clinical feature

Acute forms:
Higher than: 2%: headache, weakness, sleepiness
5 - 8 % : irritation of mucous membrane of upper breathing passages, buzzing in ears,
dizziness, irritability, psychical disorders
10 %: 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 autogenic welding
Effect to human body
Toxic effect - consequence is hypoxia
1. Concerning blood it is connected to hem towards which has
200- 300 times greater affinity and produce carboxichenioglobine (COHb).
2. Concerning tissues
a) is connected to mioglobine producing carboximioglobin (COMb) which decreases oxygen
transfer to muscle mythohondries, particularly miocard.
b) influences the enzymes that have hem group: citohrom a 3 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 hard degree~ (30-35% COHb): loss of consciousness, organic damage of CNS, weakness,
muscle slackness
Hard degree: (50-60 % COMb): coma and symptoms of diffuse cerebrum damage(tonic cramps in
extremities,epileptifermal attacks, pathologic reflexes), accelerated breathing, accelerated pulse,
hipotonia.
Chronic poisoning:
- appears as a result of close CO influence to CNS Functional cumulation - damage of centre in
meninx Symptom: headache, dizziness, asthenia, ear buzzing, heart palpilation,fatigue,irritability,
weakened memory
Cerebrovascular, cardiovascular disorders, atherosclerosis (COHb to 11%).
HYDROGEN CYANIDE AND CYANIDES
Extend and professional risk
-in desinsection and deratisation
manufacture of Hydrogen cyanide acid, salts and other compounds
En manufacture of silver, gold and mercury from minerals
galvanisation
fertiliser production
bensol, toluol, pesticide production
Ways of penetration:
respiratory tract digestive tract skin
mucous membranes

Excretion
through lungs
through kidneys (rodanide)
Effect to human body
-blockade of respiratory ferments, citochromoxidasis - tissue anoxia CNS, respiratory and
vasomotor centre
-direct toxic effect to central nervous system
Clinical feature
Acute poisoning:
Slight form: headache, dizziness, chest pain, accelerated breathing
Hard form: loss of consciousness, widen pupil of eye, egzoftalmia, dispnea, cramps, paralysis of
respiratory centre
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, heatt pains.
Convulsive stadium: clonic and tonic convulsions, jaw trismus, loss of consciousness.
Paralytic stadium: loss of consciousness, areflaxia, unwillingly urination, defecation, paralysis of
respiratory centre and stoppage of heart function - exitus.
HYDROGEN SULPHID
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 to human body

1. intensive irritable effect to mucous membrane of eyes and
breathing passages
2. general toxic effect - inhibition of Warburgs breathing ferment
- tissue anoxia
Clinical feature
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 apoplectiform degree: paralysis of respiratory and cardiovascular centre, loss of
consciousness -death.
Subacute form: headache, dizziness, weakness, fatigue, perspiration, irritation of nasal and throat
mucous membrane, cough, nausea, vomiting.

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 to human body
Chemolitic effect - hemoglobinuria, anaemia, reticulocitosis, jaundice, damage of kidneys.
Clinical feature
Acute form:
Latent period 3-8 hours - weakness, shivering, headache, obstructed breathing, dispnea, tahicardia,
extended liver and spleen, oliguria, reddish urine, anaemia, leucocitosis, reticulocitosis,
hiperbilirubinemia
In urine: albumens, eritrocites, 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.

PHOSPHIN
Phosphine is a colourless, flamable gas with a caracteristic, unpleasant odour associated with the
gas due to other phosphorus compounds which are always present
Extend and professional risk
In treatment of grain as a grain fumigant
In electronics industry as a dopant, mixed with nitrogen
In manufacture of acetylene as a unwanted by-product
Effect to human body
Phosphine is a systemic and an irritant. Phosphine, probably blocks the respiratory chain by
inhibiting cytohrome oxidase in the same way as cyanide. It inhibits other enzymes, and react with
haem and copper containing proteins.
Clinical feature
Acute form:
Nervous, gastrointestinal and respiratory symptoms: vertigo, headache, tremor, impaired
muscular coordination, drowsiness, nausea, vomiting, liver dysfunction, kidney inflammation, chest
pain, shortnes of breath and cough. Death is often caused by delayed pulmonary oedema.
Chronic form:
There is scarcity of symptoms of chronic exposure.
Excreted in urine

FORMALDEHYDE
Formaldehyde is a colourless, flamable gas with a pungent odour, very soluble in water.
Extend and professional risk:
- in manufacture of pharmaceuticals, cosmetics, household cleaners, photographic solutions, dyes,
paper, rubber, fertilisers etc.
- as a desinfectant and fumigant
- for the preservation of biological and anatomical specimens
- in manufacture of polymeric resins
It is ubiquitous in environment (oxidation of methane in Earths troposphere, burning of wood,
decomposition of vegetation etc)
It is normally present in animal tissues (endogenous and exogenous)
Effect to human body
Formaldehyde is a skin, eye and respiratory irritant
Respiratory system severe irritation, difficulty in breathing, coughing bronchial asthma (rare)
Skin - a primary skin irritant (contact dermatitis) and powerful sensitiser (allergic contact dermatitis.
Eye irritation intense lachrimation
Carcinogenic effect

Rise of chromosomal aberrations

ETHYLEN OXIDE
Ethylene oxide is a colourless, flammable liquid or gas, highly reactive
Extend and professional risk:
- in manufacture of ethylene glycol (for antifreeze and polymeric resins) non ionic surfactants and
ethanolamines
- sterilising agent in hospitals and medical products
Effect to human body
Acute exposure is relatively rare symptoms: nausea, vomiting, headache, dyspnoa, irritation of the
eyes, nose and throat, and later pulmonary oedema, bronchitis and ECG abnormalities.
Chronic exposure is relatively high symptoms (low levels) numbing of the sense of smell, slight
eye irritation, and adverse effects on a number of organs, including the liver, kidneys, adrenal gland,
testes and CNS
Carcinogenic effect
Rise of chromosomal aberrations
ORGANIC SOLVENTS
Classification according to Simonen:
1. Aromatic hydrocarbons

2. Hydrocarbon halogen derivatives

3. Aliphafle hydrocarbons
4. Alcohols
5. Ethers
6. Esters
7. Aldehydes
8. Ketones
9. Carbon disulphide
10.Alicyclic hydrocarbons
CHARACTERISTICS:
-

Easy evaporation
Fat solvents
Unchangeable in reaction with water, alkalis
Must NOT have chemical reaction with matters they dissolve

APPLICATION:
-

Manufacture of varnishes
Colours
Anticorosive mixtures
Rubber, artificial leather, industrial viscose products, textile md.
Paper, wood industry
Oil, fat extracdon
Fat-removal from metal parts
Dry-cleaning of textiles
Chemical and pharmaceutical industry

PENETRATION
Main path's
1. Inhalatory
2. Gastrointestinal
3. Skin and mucous membrane
ELIMINATION
Main path's
1. Lungs mainly inchanged
2. Gastrointestinal feces fat soluble unchanged chemicals and methabolites
3. Kidney's urine water soluble unchanged chemicals and methabolites
4. Lacrimes, Sweat, Milk
CLASSIFICATION ACCORDING TO TOXIC EFFECT:
1.
2.
3.
4.

Narcotic effect (benzine, ethers, acetone)

Neurotoxic effect (CS 2 , methyl alcohol, THE)
Effect to hematopoiesis (bensol, toluol, TNT)
Effect to liver, kidneys (halog. derivatives glycols)

FIRE AND EXPLOSION DANGER

PREVENTION (PROTECTIVE MEASURES)
AROMATIC HYDROCARBONS
BENZENE

BENZENE HOMOLOGUES
BENZENE CONDENSES
DERIVATIVES OF BENZENE, HOMOLOGUES AND CONDENSES
BENZENE:
Characteristics
Application:
-Chemical reagent (for organic synthesis, manufacture of styrene, detergents, pesticides,
perfumes, explosives, fertilisers, pharmac. products).
-Fuel (By 1950 antidetonator was added to fuel in USA)
-Solvent (Industry of plastic and artif. fibbers, colours, varnishes, rubber, caoutchouc, for oil
and fat extraction, in manufacture of photographs, minors, in medicine).
PENETRATION IN ORGANISM
Main path's
1. Inhalatory
2. Gastrointestinal
3. Skin and mucous membrane
ELIMINATION
-Unchanged
-Oxidation in blood as well as oxidative product through
kidneys
-Storage (CNS, liver, endok.syst., bone marrow)

-In liver - phenol, triphenol, catehol, hydrochinol, in conjugation with H 2 SO 4 and glucuronic acid
are developed organic sulphates and glucuronates.
-Pathophysiological mechanism of effect:
-Hipoxia (without O 2 )
-Decreased ascorbic acid synthesis, C hypo-vitaminosis
-Disturbance of oxidoreductive processes
-Radiomimethic effects (DNA, RNA inhibition), cytostatic effect.
-Chromosomal aberrations
-Leukemogenic effect
POISONING
ACUTE
-Neurotrophism
-Prenarcotic
-Cater syndrome
Narcosis (Epil.spasms
spasm. paralysis)
Coma (tox. encephal.
acute, psychosis)

CHRONIC
- Chemopathiae
a) Ilyperplasia (leucosis)
b) Hypoplasia
c) Skin
d) General symptoms

COMPLICATIONS
ESTIMATION OF WORK ABILITY
Depending on poisoning severity

THERAPY - SYMPTOMATIC
CHLORINATED HYDROCARBONS:
are developed in all three physical conditions
-CL and F are less toxic than Br and J.
-Unsaturated are less toxic than saturated
-If H atom is replaced within aromatic hydrocarbon, less toxic compound is developed and with
aliphatic is inversely.
APPLICATION:
solvents, flre-exthiguishing appliances, cooling, fat-extraction, dry-cleaning, pesticides, chemical
and pharmaceutics industry, medicine - anaesthetics, colour and varnish industry
WAY OF ENTRANCE:
as before mentioned
EFFECT:
SPECIFIC
-Neurotoxic
-Hepatotoxic
-Nephrotoxic

NON-SPECIFIC
-Irritable
-Narcotic

VINYLCHLORIDE:

Application: plastic mass

WAY OF ENTRANCE:
as before mentioned
ELIMINATION:
-Unchanged
-Metabolites: Carboxymethyl cistein, Thiodiglycol acid
TOXICITY:
Astnovegetative symptomatic
Acroosteolysis
Changes on lungs
Changes in blood
Liver angiosarcom
Cancer - other localities
TETHRACHLORETAN:
Non-inflammable liquid, THE MOST TOXIC
Application: Tetrachloride ethylene, trichlorine ethylene, fat and oil solvent, in manufacture of organic
matters, bitumen, tar
WAY OF ENTRANCE:

as before mentioned
- TOXICITY:
Acute: Narcotic effect, General symphatomology of CNS, liver, heart, kidneys
Chronic: Effect to CNS (tox. encephalopathy), gastrointestinal, - liver
ALIPHATIC HYDROCARBONS
BENZINE:
- Structure hydrocarbon mixture
- Application: fuel, solvent, in rubber industty, in colour and
vanish industiy, oil extraction from seed
WAY OF ENTRANCE:
as before mentioned
TOXICITY: Narcotic (CNS)
POISONING:
ACUTE
1. Slight : headache, irritation of eyes and respiratory system, irritability (hypotonia, bradicardia,
hypothermia)
2. Hard: tremor, enlarged liver, proteinuria, comatose, hallucination, amnesia.
CHRONIC

General symptoms, depression, tremor, irritation of eyes, respiratory system and skin.
FIRST AID:
-O 2
-Artificial respiration
-Sedatives
-Cardiotonie
-Vitaminotherapy
ESTIMATION OF WORK ABILITY:
Depending on poisoning severity
PREVENTION
PETROLEUM
Toxicology:
Acute poisoning:
The same as H 2 S poisoning - if there is Sulphur in petroleum, and benzine poisoning
Chronic:
Astenovegetative syndrome, irritation of eyes, skin and respiratoiy system.
CARBON DISULPHIDE (CS 2 )
CHARACTERISTIC: colourless liquid, with ether-like odour

APPLICATION: Manufacture of viscose fibbers, cellophane, optical glass, glue, in chemical

industry, solvent, pesticide etc.
-

WAY OF ENTRANCE:
Main path is inhalatory way

ELIMINATION:
- Unchanged - through lungs
- Through urine
- Through excrement - non-organic sulphates through milk
-

POISONING:

ACUTE
Slight: intoxication, headache, dizziness, exhaustion, paresthesies.
Medium: narcotic effect, euphoria, irrational laughter, dizziness, headache, ataxia, hallucination,
delirium
Hard:
loss of consciousness, tox. coma
COMPLICATIONS: Ecephalom.and mental disorder
CHRONIC
Neurasthenia, weakness, fatigue, loss of appetite, vegetative lability, perspiration, dermographia,
palm hyperhidr., weakened sensibility.

Hard form:

-Damage of nervous system

-Encephalopathy
-Encephaloneuritis
-Damage of peripheral nervous system - Polyneuritis
-Hard sensibility disorder up to anaesthesia, weakened tendinous reflexes
-Extreme vegetative simpt.
-Damage of endocr. system (adrenal gland, thyreoidea, testis)
-Vascular disorders - arteriosclerosis, most frequently on cerebral and renal blood
vessels
TREATMENT:
Symptomatic
ESTIMATION OF WORK ABILITY:
PREVENTION
AMINO AND NITRO COMPOUNDS OF AROMATIC COLUMN
APPEAR by replacement of one or more H atoms in benzols ring or in homologue of amino - Nil 2
or nitro - NO, group.
APPLICATION: Colour industiy, explosives, pharmac. md, perfume md, rubber, soap,
shoe polish, in synthesis of pesticides, plastic mass etc.
WAY OF ENTRANCE:

1. Inhalatory
2. Skin and mucous membrane
3. Gastrointestinal (rare)
ELIMINATION:
Unchanged through lungs
Through urine in compound with H 2 SO 4 or glucuron acid.

POISONING:
-Irritable effect (skin, mucous membrane, respirat., gastroint. and urin. system).
-Hematopoiesis damage
-Parenh. org.(liver, kidneys)
-CNS
ETIOLOGY:
-Direct toxic effect of none or metabolites
-Hypoxia (met. and/or sulph. Hb)
MET- Hb
Normally: 1%
Conditioned by enzymatic system of met Hb-reductases which require DPNH and TPNH as co-enzymes,
and non-enzymatic -glutation

SULPH - Hb
Fe loses capacity of connection with 0 2 but not CO. Met and Sulph Hb result in cyanosis. Cyanosis
appears when 5 gr. Hb is reduced at 100 ml of blood. Death appears when 66 % of Hb is transformed in
Met Hb.
Within blood are present:
-Heinzs bodies
-Hemolysis
-Hypoplasia, aplasia (marrow)
-Damage of liver
-Damage of kidneys
-CNS (palidostrial syst. n.opticus)
NITRO DERIVATIVES
NITROBENZENE
Characteristics (flavour of bitter almond)
Application (colours, explosives, soap md.)
Way of entrance
Elimination
Poisoning
Acute
-Irritable symptom
-Damage of CNS with parestes.epylept. convuls. ----Coma, death as a result of breath
paralysis

-Damage of liver
Chronic
-Irritation (skin, respiratory and d,gestive system)
-MetHb
-Damage of liver and CNS
Treatment:
-Take out poisoned person
-Skin decontamination
-Oxygen therapy
-Treatment of Met I-lb with ascorbic acid methylene blue
-Transfusion
-Hepatoprotective therapy

TRINITROTOLUENE
-

Characteristics (strong,acid.powder)
Apphcation (explosive)
Way of entrance (the most important - skin, resp.and digest.syst.)
Elimination (urine)
Poisoning
-Irritable (orange coloured skin, resp.,digest.)
-Met Hb 4 Sulph. Hb
-Hemolysis

-Hypoplas. aplas. of bone marrow

-Hepatocyte necrosis
-Toxic nephrosis
Treatment
AMINO DERIVATIVES
ANILINE
Characteristics: colourless oil liquid, characteristic smell, water insoluble
Application: colour industry, explosive, perfume, pharmac.industiy, rubber and pesticide md.
Way of entrance:
Elimination: In human body it is oxidised in phenyl hydroxilamme and this in pam aminophenol which is
conjugated with H 2 S0 4 . glucuronic acid and is eliminated with urine.
Pathogenesis:
Effect of noxa itself is minimal it is effect of metabolism.
Causes:
-BPE
-Hemolysis

-MetHb
- Heinz bodies
Poisoning:
Acute: euphoria, loss of consciousness, dizziness, headache, weakness, sight disorder, skin and
mucous membrane lividity, cyanosis, dark urine.
Chronic: weakness, atonia, anaemia, BPE

FARMING
WORK CONDITIONS AND SPECIFIC PROBLEMS IN PROTECTION
OF WORKERS
The nature of farming itself tends to create a situation of increased risk.
FARMING
Agricultur
Fruit-growing
Wine-growing (grape-growing)
Cattle-breeding
AGRICULTUR
ploughing (cultivation of land)
sowing

plant disease protection (pesticide spraying)

manureing
harvest
etc
Work conditions:
often work alone
work under all weather conditions
long hours work with few breaks
hard work (rarely)
dust (organic and/or inorganic)
pesticides vapours
manure dust
noise
vibrations
exhaust gasses
very powertul equipment (injury possibility)
FRUIT- AND WINE-GROWING
Work conditions:
work under all weather conditions
long hours work with few breaks
work on height
hard work

dust (organic and/or inorganic)

pesticides vapours and dusts
manure dust
much rarely (specially on big plantages)
noise
vibrations
exhaust gasses
very powertul equipment (injury possibility)
CATTLE-BREEDING
feeding the animals (worker - grazier)
cleaning the animals
cure the animals (veterinarian doctor)
raising:
cattles, bulls, horses, muls, swines, goats, sheeps, fowls, hares, bees, silk-bugs etc
Work conditions:
uncontinued working shift
hard work
dust (organic and/or inorganic)
unpleasant odour (NH 3 , SO 2 CO 2 H2 S etc)
manure
noise

zoonoses
injury possibility
Access to emergency services and trauma treatment is very often poor in rural farming areas.
They share a common home and work environment and often are in business with relatives
and in-laws.
SIGNIFICANT HEALTH PROBLEMS
Traumatic injuries
Hearing loss
Respiratory diseases
Zoonotic diseases (40 have signifficance as occup.
diseases)
Malignant diseases
Intoxications (solvents, pesticides !!!, exhausts gasses)
Cumulative Trauma Disorderss
-Arthritis (diferent forms and intensitys)

TRAFFIC
WORK CONDITIONS AND SPECIFIC PROBLEMS IN PROTECTION
OF WORKERS
TRAFFIC
on the ground
railway transport
road teransport
in the cityes (local transport)
inter cityes
international
on the water
on rivers
on see
on seeside (local traffic, fishing)
intercontinental

in the air
passenger aviation
cargo aviation
business aviation (f.e. air-spraying, airmanureing)
sport and pleasure aviation
national destinations
international destinations
intercontinental destinations
GROUND TRAFFIC
RAILWAY CREW
engine driver
train guard
train security
reilwaymen - reilwatcher
WORK CONDITIONS
often work alone
work under all weather conditions
long hours work with few breaks
dust (mostly inorganic)
exhaust gasses
noise
vibrations

very powertul equipment

personal conflicts etc
SIGNIFICANT HEALTH PROBLEMS
Respiratory diseases (mostly upper resp. organs)
Alimentary and stomach disorders
Hearing loss
Local and whole body vibration disorders
Traumatic injuries (traumas, burns, el. burns)
Intoxications (exhausts gasses, fuel)
Psychical dificulties
ROAD TRANSPORT
truck or buss driver
truck or buss co-driver
buss conductor (local transport)
buss guard (inter city and inter national)
WORK CONDITIONS
often work alone
work under all weather conditions
long hours work with few breaks
dust (mostly inorganic)

exhaust gasses
noise
vibrations
very powertul equipment
local traffic (frequently stops)
personal conflicts etc
SIGNIFICANT HEALTH PROBLEMS
Respiratory diseases (mostly upper resp. organs)
Musculo-sceletal disorders
Alimentary and stomach disorders
Hearing loss
Local and whole body vibration disorders
Traumatic injuries (traumas, burns, el. burns)
Intoxications (exhausts gasses, fuel)
Psychical dificulties
Sexualy transmited diseases
WATER TRANSPORT
Ships crew members
Captain (Skipper)
Engine leader and engine crew (Machinists)

Radio and Radar crew

Sailor etc

WORK CONDITIONS
work under all weather conditions
work in shifts
long hours work with few breaks
relative fast changing the climate
exhaust gasses, fuel
noise
vibrations
very powerful equipment (shipengine, ship power plant, ships crane etc)
personal conflicts etc
SIGNIFICANT HEALTH PROBLEMS
Respiratory diseases
Musculo-sceletal disorders
Alimentary and stomach disorders
Hearing loss
Local and whole body vibration disorders
Traumatic injuries (traumas, burns, el. burns)
Intoxications (exhausts gasses, fuel, cargo)
Psychical dificulties
Sexualy transmited diseases

Zoonoses
AIR TRANSPORT
Plane crew members
Pilot - Captain
Co-pilot
Flight engineer
Navigator
Plane mechanic
Stuards and stuardeses
WORK CONDITIONS
work under all weather conditions
long hours work with few breaks
psychical pressure
very fast changing the climate
dekompression
acceleration and deceleration (in all directions)
exhaust gasses, fuel
noise
vibrations
personal conflicts etc

SIGNIFICANT HEALTH PROBLEMS

Respiratory diseases
Alimentary and stomach disorders
Compression or decompression disorders
Hearing loss
Local and whole body vibration disorders
Traumatic injuries (plane crash possibility)
Intoxications (exhausts gasses, fuel, cargo)
Psychical dificulties

NOISE
every desirable sound is a tone
every undesirable sound is a noise
Pavarotys singing can be a music but also can be a noise too
Sound have a physical characteristics like:

-volume
-intensity
-frequenzy
-color
-etc.
OCCUPATIONAL HEARING LOSS
Occupational hearing loss can be defined as a partial or complete hearing loss in one or both ears araising
in, or during the course of, and as the result of ones employment.
This includes -acustic traumatic injury
-noise induced hearing loss
Acustic traumatic injury araising out of traumatic injuri such as explosions or a blow to the head.
Noise levels much lower than those producing acoustic trauma may produce hearing loss if the exposure
suffitiently intense and prolonged.
Therm Noise induced hearing loss is generally used to denote the cumulative, permanent loss of hearing
that develops gradually after months or years of exposure to high level of noise.
Pathophysiological matter of hearing loss
bloodvessel spasam
or
neuromechanical damage

Earli signs of hearing loss include:

Difficulty in anderstanding spoken words in a noisy environment
Need to be near or look at the person speaking to help understand words
Familiar sounds are muffled
Complaints that people do not speak clearly
Ringing noises in the ears
Hearing loss evaluation
Audiometry is the mesurement of hearing
speech audiometry
instrumental audiometry
air conduction
bone conduction
Therapy:
-remove affected people from noisy environment
-simptomatical therapy by vitamins (b-vit),
vasodilatators, etc

Working capability:
it depends from grade of hearing loss
Noise measurement
Sound consists of small, rapid, local fluctuations in atmospheric pressure which can be detected by human
ear
Like human ear microfon is capable to detect the small fluctuations in atmospheric pressure and transform
them in electrical impulses which are corresponding to pressure level
Instruments are sound level meters
Mesurement units are decibels - dB
Decibel scale, which is logaritmic, express the magnitude of atmospheric pressure fluctuations
Hearing range is 0 - 140 dB (pain limit)
Maximal allowable noise level - 85 dB(A) -SRB-legislative
ULTRASOUND
is sound ABOVE 16-20 kHz, expansion speed is 330 m/s through the air, 1450 m/s through water, in some
tissues of human body is 1450-1600 m/s, in bones from 3360-4000 m/s.
Passing trough biological environment ultrasound has:
thermal activity - absorption
mechanical activity - particle fluctuation
cavity activity - making holes due to condensation and dilution of tissue particles.
-

USAGE:

detection of underwater objects - sonar

investigation of underwater relief
for measurement of depth' s
remote controllers for home and other equipments (alarm,
garage doors etc)
for metal cutting and welding
in medicine Doplers effect and in therapy - thermal activity
in stomatology - removing of layers - mechanical activity

Clinical features:
Symptoms of exposure to high frequency US can appear only in case of direct contact among body
(body parts) and source of ultrasound.
Exposure to low frequency US can cause local and overall symptoms

A wide range of symptoms can be present in accordance with transfered energy

Symptoms can be local
vegetativ polyneuritis
partial paralysis of fingers, hands, forearm
etc
and overall
inflamations

haemorrhagias
necrosis
INFRASOUND
is sound BELOW 16 or 20 Hz
In nature it appears during wave activity and their striking of the coast, in case of avalanche
movements, in earthquakes etc.
In industry it appears together with low frequent noise and vibrations of great power machines, at
small number of rotations, activities and striking of moving parts, in fans, gas turbines, compressors,
ships and helicopters.
Effect on human body:
- IS 8 Hz - most dangerous for human's correspond with brain alpha wave's dizzines , loss of
consciousness, even coma
- IS 1-3 Hz can cause breathlessnes and disturbances in respiration rhythm
- IS 5-9 Hz can cause chest pain and pain in low abdomen
- IS 8-12 Hz can cause loins pain
- IS 12 20 Hz can cause mouth-pain, pain in throat, bladder, rectum, some muscles etc
Clinical features:
Long term exposure: cause weakness
irritability
fatigue
sleep disturbances
working capabillity reduction

BAROMETRIC PRESSURE (BP)

is a pressure performed by atmospheric air on everything on the earth
BP is expressed in mmHg or milibars (mbar) 1 mbar = mmHg
PRESSURE (Si system) unit is Pascal (Pa)

ON THE SEA LEVEL pressure is

-

1013,25 mbar = 760mmHg = 101,3kPa = 1 Atm

EFFECTS OF DECREASED BAROMETRIC PRESSURE
(HIGH ALTITUDE SICKNESS (HAS) / SKY DISEASE)
At the sea level partial oxygen (O 2 ) pressure is 159,1 mmHg,
At 3000 m 110mmHg, which means saturation of oxyhaemoglobine 93-94%.
Further decrease of partial pressure results in stepwise hipoxia over 4000m.
For development of clinical picture of disease more significant is partial O 2 pressure in alveoluss,
which is in correlation to partial pressure of CO 2 and water vapour.
Partial CO 2 pressure in alveoluss is 30-40 mmHg, and that of water vapour is 47 mmHg.
The increase of pressure of gas mixture (e.g. air his components) cousese the increase of partial
pressure of each component of the mixture, and this increases the solubility of each component found the
mixture in the body fluids.
This means --- if total barometric pressure is decreased to 87 mmHg, (CO 2 + water vapour = 87).
----- Entrance of air in lungs becomes impossible ----- this can be prevented by breathing in pure O 2
(100%) ----- but blood oxygenation up to 93% is possible only up to heights of 10 km.
At 10.000 m barometric pressure is 198 mmHg, which is 1/4 of pressure at sea level.
There gasses spreading 4 times more in body cavities (sinuses, ear, gastrintest. tract)
Spreading of gases results in sky meteorism, sinusitis, otitis and "aerodentalgia".

In quick decompression melted gas releases in the form of bubbles.

DECOMPRESSION DISEASE is classified to:
skin form "the creeps" usualy mild and of minor significance tingling or itching in
localized areas (area of limbs or chest, thighs)
osteomioartralgic form the commonest manifestation (in more than 70% of cases) pain is
centered around a knee, shoulder, elbow, wrist or ankle (hips are much less affected).
paralytic form very rare (<1% of cases) but can involve any part of central nervous system
wide range and localisations of paresthesias, localised anesthesias and even paralysis and
convulsions are possible
cardiopulmonal form appears in about 4% of cases but they are of serious import
substernal pain, constriction in the chest and epigastrium with general and increasing weakness
can lead to death
chronic manifestations (aseptic bone necrosis)
-

TREATMENT
AS SOON AS POSSIBLE RECOMPRESSION,
then
DECOMPRESSION
(in accordance with prescribed protocol (time table))
E.G - Two protocols of decompression

"even"
every 2 min to
decrease p.
for 10 kPa

"gradual"
to decrease p. to half
then pause

ESTIMATION OF WORK ABILITY

Depending on form and difficulty of decompression disease
PREVENTION
1.
2.
3.
4.
5.
6.
7.
8.
9.

Rate of ascent or descent

Altitude or depths attained
Duration of exposure
Activity immediately prior to exposure
Dietary and fluid intake prior to exposure
Age (recommendation: 18 45 years)
Gender (forbidden for women)
Obesity
Previous injuries

INCREASED ATMOSPHERIC PRESSURE

Refresher - Normal atmospheric pressure - 101,32 kPa (1 Atm)
Exposed to increased atmospheric pressure are:
-workers in bridge work caisson workers

-workers in tunnel work

-divers
-workers in geological investigations of flora and fauna - caves
Appearance of caisson
A - pre - chamber
B - central chamber
C - tubus
D - working chamber
E - compressor unit
WATER
RIVER
BOTTOM

EFFECTS OF INCREASED ATMOSPHERIC PRESSURE

A Directly- physically
B Indirectly biological and metabolical

A. In quick compression or in case of fall of diver in depth or when air supply in scafander stops,
appears phenomenon of succinum, with difficult fractures, or ejection of diver and drowning at enormous air
addition in scafander.
B. Simultaneously with increasing of common atmospheric pressure, the partial preassures of
components of inhaled medium (gas mixtures for diving) incresing also.
Oxigen

Neurotoxicity
Pulmonary toxicity

Nitrogen

Narcotic effect - "deep sea drunkenness"

Carbondioxid

Blood hypercapnia

IN CASE OF QUICK EMERGE (DIVERS, CAISSON WORKERS) OR FAST TAKE-OFF (PILOTS)

WILL DEVELOP THE
DECOMPRESSION DISEASE
PREVENTION
PROFESSIONAL OR WORK-RELATID DISEASES CAUSED BY
NON-PHYSIOLOGICAL WORK CONDITIONS
DAMAGES OF LOCOMOTORIUM

Periarthritis of shoulder joint

Prof bursitis

Tendovaginitis crepitans
Professional miositis
Flat foot
Knee-joint deformations
Spinal deformations

Varicous veins
Abdominal hernia
Descensus and prolaps in genital organs
Professional neuritis
Coordinational neuroses
Professional lung emphysema
Professional laryngitis
Disorders in sight sense
Nistagmus at miners
Prof stigmata

CUMULATIVE TRAUMA DISORDERS

Work-related muskuloskeletal disorders commonly involve the back, cervical spine and
upper extremities.

Millions of workers are reported to be suffering from the development of cumulative

trauma disorders (CTDs) or are working in jobs which have been considered by various
authorities to be associated with an increased risk of CTDs. However, a great deal of
controversy exists about:
the definicion of CTDs,
the true incidence of the diseases,
jobs and job tasks at risk of causing CTDs,
treatment issues,
ergonomic interventions, and
prevention strategies.

Low back pain (LBP)

LBP is one of the oldest occupational health problems in history
(Ramazzini, the "founder" of occupational medicine, referred to "certain violent and
irregular motions and unnatural postures of the body by which the internal structure" is
impaired)

LBP is one of the most common health problem

( 80 % of workers will expirience LBP sometime during their active working life.
At any given moment 10-15% of adult population of the USA expiriences LBP
11 % Americans report LB impairment or a reduced ability to function
Every year 2 % of the employed lose time from work because of LBP
AMONG MEDICAL REASONS FOR WORK ABSENCE IT IS SECOND ONLY TO
UPPER RESPIRATORY INFECTIONS

PATOPHYSIOLOGY
Pain in the lubosacral spine can result from inflammatory, degenerative, neoplastic,
gynecologic, traumatic, metabolic and other types of disorders.
The great majority of LBP remain nonspecific and unknown cause

Many theories regarding the origin of nonspecific LBP have been proposed, but so far
no one has been able to prove how and where the pain arises.
Multifactorial aetiology of back pain

Diagnosis, Menagment, Prognosis Medical Rehabilitation

PREVENTION of LBP

Carpal tunnel sindrome (CTS)

It is caused by injury to the median nerve in the wrist

CTS often presents in early stages with intemietent paresthesias, hyperesthesia, or

hypoesthesia in the sensory distribution of the median nerve in the hand. Often, symptoms
are first noted in the dominant hand and may be bilateral. Occasionally, complaints are
restricted to one or two fingers, usually the middle finger or index and middle fingers.
Complaints of pain and numbness may occur later, with up to 15% of affected individuals

experiencing pain radiating to the upper arm or shoulder. Motore deficits in the abductor
pollicis brevis, opponens pollicis, or flexor pollicis brevis may be found in more severe cases
of CTS

Wrist flexion test

Tinels test

Positive nubnes and/or tingling

NONOCCUPATIONAL RISK FACTORS FOR THE DEVELOP-MENT OF CTS
Female sex, Rheumatoid arthritis, Diabetes, Myxedema, Acromegaly
Pregnancy, Hormones, Oophorectomy, Menopause, Gout, Amyloid, Multiple myeloma,
Raynaud's disease, Edema from congestive heart failure, Renal failure, Uremia and

hemodialysis, Obesity, NeopLasia (including benign tumors and lesions), Osteoarthritis,

Aberrant muscle bodies, Acute trauma, Coiles' fracture, Wrist fractures and dislocations
Improper immobilization of the wrist, Congenitally small carpal tunnel canal
THERAPY:
Nonoperative treatment (mild intermittent symptms of
short duration, without muscle atrophy)
-antiiflamatory drugs
-vitamins
-rehabilitative treatment (phisical methods)

Surgical treatment

OTHER CUMULATIVE TRAUMA DISORDERS

A brief overview of some well-recognized entities are presented here.
Tendonitis/Tenosynovitis

This is an intlammation of the tendon or the tendon sheath causing inflammation and pain.
When inflammation precludes free movement of a finger tendon, the result is stenosing
tenosynovitis, or trigger finger. De Quervain's disease results from stenosing tenosynovitis of
the abductor poilicis longus and extensor poilicis brevis. Movements which may precipitate
these effects include flexion of finger tendons with a flexed wrist (finger flexor tendons);
ulnar deviation wich outward rotation as in VDT users (finger extensor tendons); or repeated
radial or ulnar deviations as the wrist, particularly in combina- tion with force of the thumb
(de Quervain's disease). The chronic use of a screwdriver or pliers may result in de
Quervatn's disease.

Bicipicatal/Rotator Cuff Tendinitis

This disorder may be associated with work requiring abduction with or without rotation, as
well as constant or repetitive forward elevation of the arm at the shoulder.
Epicondylitis

Athloetic movements and work tasks may be associated with medial (golfer's elbow") or
lateral ("tennis elbow") epicondylitis. Contributing activities include wrist/finger extension
wich elbow extension, abrupt elbow extension or forearm supinacion as in lifting and
pushing up (lateral epicondylitis), or wrist/finger filexion with forearm pronation (medial
epicondylitis).
Ganglionic Cysts
These may arise arfter acute trauma or in a degenerative or diseased joint or tendon.
Pronator Syndrome
Proximal forearm pain with pronation of a tightly clenched fist against resistance may be
assotiated with median nerve sensory loss when the median nerve is compressed under the
pronator muscle. Repetitious, forceful pronation and figer flexion may cause this syndrome
in writers. assembly line workers, or garment workers.
Cubital Tunnel Syndrome
Compared to CTS, ulnar neuropathies at the elbow or forearm may cause more motor and
sensory deficits and fewer complaints of pain. This syndrome may be due to entrapment
through the cubical tunnel or direct trauma to the nerve at the ulnar groove. Individuals
with bilaterat symptoms often have shallow ulnar grooves. Patients may experience pain,
paresthesias, or numbness in the small and ring fingers, difficulty picking up small objects
between the thumb and index finger, wreat wrisc flexion, and atrophy of the hy- pothenar or

interosseous muscles. Tasks associated with repetitive elbow tlexion (e.g., hammering,
shoveling, lifting) or repeated tauma or pressure to the ulnar groove (e.g., leaning elbows on
a desk or workbench) are possible causal factors.
Ulnar Neuropathy
Motor and sensory symptoms may occur in the hand from injury to the palmar branch of the
ulnar nerve at the hand/wrist. Using the hand as a hammer or putting pressure on the
hypothenar eminence (as in using pliers, staplers, or pneumatic drills) can result in this
injury. When the deep motor branch is affected, weakness of the interossei and the third and
fourth lumbricales occurs without any sensory findings. This is seen most often in
electronics assembly workers, jewelers, and machinists.
Supinator or Posterior Interosseous Nerve Syndrome
Single or repeated forceful pronacion, supinacion, radial deviacion, or abrupt elbow
extension can result in radial nerve compression and injury in the supinator muscle,
Affected individuals have weak hand grip and weak wrist/finger extension without sensory
symptoms. Musicians, pitchers who throw screwballs. and construction workers who
hammer with a straight arm or lift with extended arms are at risk.

Thoracic Outlet Syndrome

Thoracic outlet syndrome may result from either impingement of the blood supply or the
nerves to the arm as they pass from the neck to the shoulder. Compression may occur in the
scalene muscle, from cervical ribs. fibrous bands, or transverse C7 verrebral processes.
Symptoms vary with vascular or neurologic compression but may include lateral arm pain,
paresthesias of the ring and small fingers, hand swelling or weakness, and a causalgia-like
syndrome. A 3-minute elevated arm stress test is helpful in diagnosis. Adson's maneuver is
often positive but may be seen in 10% of the normal population. Electrodiagnostic studies
are helpful if they demonstrate a block across the brachial plexus, between the axilla and
Erb's point, or between Erb's point and the C7 nerve root. Various activities and postures
have been associated with this disorder, including pulling the shoulders back and down, as in
military personnel standing at attencion; carrying heavy loads in the hand, as in painters,
welders, or persons carrying suitcases; and working overhead with repetitive abduction and

adduction of the shoulder and arm, as in automotive or aircraft repair workers. Once
commonly diagnosed in working populations, thoracic outlet syndrome is now felt by some to
be overdiagnosed.

PROTECTION OF WORKING WOMAN

Occupational noxae having negative influence to:
1. men and women equally

noise prof. hearing los,

sight strain prof. myopio
2. women more than men, but not disturbing reproductive function
physical strains of bone and joints neuromuscular system,
skin
3. reproductive function (toxic substances, radiation)
Influence of occupational noxae on womans health, espetially during pregnancy, lactation and
meno-pause, is due to
Disorder in liver function, increased permeability of capillaries, irritability of vegetative nervous
system, spasm of smooth musculature, increased metabolism, lung ventilation, blood circulation, which
accelerates absorption of toxic substances.
E.G.
1. Disorder in menstrual cycle (lead, mercury, arsenic, yellow phosphorus, gasoline, benzene, H 2 S,
phenol, TNT, formaldehyde causing:

2. Sterility (pb, mercury, arsenic, gasoline)

3. Pathological pregnancy due to penetration through placental membrane (Pb, mercury, Cd, P.
H,S, petrol, nicotine, pesticides).
4. Penetration of toxic substances in milk (decreased quantity, taste)
5. Embryogenesis disorder (Mn, formaldehyde, hloropren,pesticides)
PHYSICAL STRAINS:
carrying of load
vibrations and work in standing position result in:
disorder in menstrual cycle,
incontinence of urine
prolapse ofgenital organs
HIGH TEMPERATURE AND- RADIATION (IONISED) result in:
- disorder in ovarial / menstrual function
PREVENTIVE MEASURES
-

technical
hygienic
legislative - administrative
social care
medical

HEALTH CARE OF YOUNG PEOPLE

14-18 YEARS OF AGE

- increased neuroendocrinal function (pituitary gland, thyroid gland,
adrenal glands, sex glands)
- development of musculosceletal system is not finished
- rapid changes in cardiovascular and nervous system
- accelerated methabolism
- instability of vegetative nervous system
- instability of stomach secretion function
YOUNG PEOPLE UNDER 18 YEARS OF AGE
CANNOT WORK:
-in zone of ionised radiation
-in increased atmospheric pressure
-with toxic substances (Pb, mercury, Mn, benzene, pesticides)
-in raised dust (quartz, asbestos)
-overtime and night work
- physical work in 14-15 aged person represents 1/2 of physical power of adult person, and 2/3 in 16-17
aged person.
-

maximal alowed load:

constant up to 4 kg
single, occurring once men 16kg
women 10kg

from 16 to 18
years of age

from 15- 16 years of age 2 times less

noise maximal:
15-20dB less than adult persons,
if not possible, up to 95dB short time exposition
PREVENTION
-

technical
hygienic
legislative - administrative
social care
medical

PROFESSIONAL ORIENTATION