HAZARDOUS GASES AND THEIR HEALTH EFFECTS:

The common gases that are present in a refinery industry are:

•Ammonia

•Benzene

•Carbon monoxide

•Chlorine

•Hydrogen sulfide

•Nitrogen oxides

•Sulfur dioxide
1. AMMONIA:

It is pungent having suffocating odor irritant gas, colorless, liquids under

pressure.

Elevated temperature may cause containers to explode. The threshold

value of ammonia is 25 ppm.

TOXICITY:

Chronic poisoning is less common. In industries acute poisoning occurs

mostly.

Above 100mg/m3 , it is severe irritant to eyes.

Eyes- corneal irritation. Serious eye injury or death of eye ball or

blindness if liquid.

In the respiratory tract it causes chest pain, bronchospasm, pulmonary

oedema, bronchitis.

Escape in large quantities may cause explosion.

SAFETY AND HEALTH HAZARD:

Mainly fire and explosion hazard occurs hence:

Process plant should be constructed in open air and only

compressors should be allowed to house inside the building

Preservation in material which are not affected by high pressure or

corrosion.

Reduction of corrosion in cooling system by use of air rather than

the water.

Regular plant maintenance.

Adequate measures for explosion and fire fighting.

Use of filter type respiratory device to absorb CO, H2S and NH3
While working in closed/ confined space one must use respiratory
device and safety belt.
TREATMENT:
•Removal from exposure place.

•If liquid splash, immediately flush eyes lifting upper and lower eyelids
and skin with water

•Remove contaminated clothing’s

•If it falls on skin –vigorous wash with water followed by lotion of 5%

acetic / tartaric/salicylic acid.

•If ingestion of liquid accidentally – allow to take plenty of water to dilute

if conscious. Don’t induce vomiting if unconscious.

•Area of spill should be ventilated to allow evaporation

•If inhaled- shift victim to fresh air, give warm vapour inhalation with
vinegar/ citric acid, should be watched for the visual disturbances,
upper airway obstruction

•Hospitalization for 72 hours for watch on delayed onset of pulmonary

oedma.
2. BENZENE:

It is clear, colorless liquid, a characteristic pleasant odour at

lower concentration but unpleasant/disagreeable at high
concentration.

A highly inflammable and explosive mixture with air. Fairly

stable but readily undergoes substitution reactions to form
halogen, nitrate and sulfonate. The TLV is 10 ppm.

TOXICITY:

Benzene is irritant to skin.

Defatting of keratin layer causes erythema, vesiculation, dry

and scaly dermites.

The inhalation is most prevalent means of intoxication.

Effects vary following repeated exposure rather than single
one.
With depletion of protective enzymes, a small part is excreted or
exhaled as such.

Rest undergoes oxidation in liver to form phenol, catechol or quinor.

Phenol subsequently conjugates with to sulphate to phynyl sulphate.

ACUTE EXPOSURE:

The sighn of staging gait, vomiting, somnolence, shallow, rapid pulse,

loss of consiousness and later delirium with subsequent chemical
pneumunitis, serious collapse due to initial stimulation , hyper-
excitement followed by flushing , weakness, headache,
breathlessness, constriction of the chest pain and fear of impending
death.

Visual disturbances and convulsions are frequent, inhalation of 200

ppm for 5 minutes is fatal immediately.

Recovery depends on the initial concentration and exposure time, but

sysmtoms may persists for several week.
The main sign of intoxication are manifested by drowsiness,
dizziness, headache, vertigo and delirium and may be proceed to
loss of consciousness.

At first time moderate exposure to benzene may produce typical

prenacrosis syndrome, headache, giddiness and sometime
transient mild irritation of the respiratory and alimentary tract.

Acute high exposure may cause dysnae inebriation (habitual

Intoxication) with euphoria ( a feeling of great) and tetanus
which rapidly leads to typical deep anesthesia.

If not treated leads to respiratory arrest, muscular switching and

terminal convulsions ( fatal, shake uncontrollably) as well.

CHRONIC EXPOSURE:
A. Inhalation: The level to produce effects vary widely with the
individuals. Contributing factors are poor nutrition, certain
immunological tendencies, consumption of alcohol and drugs.
Documented are hyperbilirubinimia speeleno and
adernomegaly. Blood dyscrasuos.

Metabolism under chronic exposure. The main effect appears

to be the involvment like abnormal caloric labyrinth irritiblity
and impairment of hearing.

Its carcinogenic and teratogenic property is not confirmed.

B. haematologic effects:

Effects on the hamatopoietic systems have been known for

many years.

Effects are not uniform symptoms and laboratory findings are

not parallel. Blood dyscrasia like thrmobocttosis, pancytopenia
and aplastic anemia may occour.

At this stage, if diagnosed and treated, the effects are

reversible.
SUBCELLUAR EFFECTS:

The aberrations found in peripheral lymphocytes classified as

chromatid and chromosome type were found to increase with years
of exposure.

It interferes on the molecular level of DNA replication, inhibits

polyribosome, protein synthesis.

IMMUNOLOGIC RESPONSE:

Decreased phagocytic activity reduced bactericidal activity of the

skin. Lowered lysozyme and blood cholinesterase activity are some
of following exposure.

BLOOD CHANGE:
Earliest changes noticed during benzene exposure in human are on
hemopoitic system primarily.
Initial changes are reduction in platelet count (less than 1 lac/cu
mm), increase in bleeding time and clotting time, lecucopaemia and
anaemia.
TREATMENT:

Sound health at the time of induction

Previous occupational history-especially – specially of solvents

No person below 18yrs or pregnant/ lactating woman

Medical check up schedule- 0,3,6,12 months

Through physical check up specially of target organs like liver, bone

marrow ,skin

Investigations – urine for DHP, haematological: Hb%, platelets count,

BT, CT, TLC, DLC, ESR, SGOT, SGPT etc.
3. CARBON MONOXIDE:

It is a colorless, tasteless, odorless gas, which s lighter than air

with a blue flame. The threshold value for this gas is 35 ppm.

TOXICITY:

This gas is easily absorbed thru lungs into the blood and
combines with Hb to form carboxyHb (COHb).

The affinity of human Hb for CO is about 240 times that of its

affinity with O2. the formation of COHb has two undesirable
effects.

It blocks oxygen carriage by inactivating Hb

MEDICAL PREVENTION AND TREATMENT:

Pre-employment medical exame, must be performed with special

attention to CVS diseases ,anemia, respiratory efficiency, any
other diseases or medical condition which could be exacerbated
by the hypoxic effect of CO.

pregnant woman should not be employed in the tasks where

there is a risk of dangerous concentration of CO in the air.

Biomedical repair starts if the victim is breathing. Therefore

victim should immediately be moved from contaminated to fresh
air.

If breathing is stopped, revival should be started without delay

using mouth to mouth and if necessary external cardiac massage.

Stimulant drugs / methylene blue should be avoided.

Absolute rest in bed for 48 hrs should be ensured. Avoiding early
physical activity may be prophylactic as to possible late
complications of CO poisoning.

After recovery patient must be watched for late neurological/ cardio

logical complications.

4. CHLORINE:

It is yellowish green gas, irritant pungent odour. Amber colour liquid

under pressure, bleach like, highly oxidizing agent, slightly soluble
in water , very soluble in alkalis.

Can cause moderate fires and explosions. The TLV is 1ppm.it is

widely occurred in nature –earth crust, sea water and natural
deposits.

It is commonly used for bleaching of paper, pulp, textiles, cellulose

fibers. It is also used as disinfectant for drinking water, swimming
pool.
TOXICITY

It reacts with moist surface to form acids/ strong irritant to

eyes, respiratory tract. High concentration exposure occurs
due to leakages, spills, but toxicity is rare due to enough time
to escape due to smell irritant to eyes, nose throat, spreads to
chest, cough with chest pain and may cause vomiting.

If escape is not possible lung oedema, decrease BP, cardiac

arrest may occur. Breathing distress and pain subsidies within
72 hours.

Cough increases in severity and frequency after 2-3 days,

cough becomes thick and disappears after 14 days.

Liquid chlorine cause burns of eyes leading to loss of sight.

Very high concentration causes irritation to eyes as severe
burning, pricking, inflammation and blister formation.
FIRE & EXPLOSION:

Flammable, explosive with hydrogen, hydrocarbons, alcohols,

ether sometimes exothermic reactions may take place.

TREATMENT:

Immediate removal from exposure site.

If breathing has stopped, give artificial respiration ( never

mouth to mouth)

Hospitalization

Oxygen inhalation

If obstruction is due to block/oedema, clear the way by

intubations and start mechanical ventilation.

.
If skin irritation-lightly wash with soap and water. Remove
contaminated clothing

If eyes are irritating – flush with water for 30 minutes.

If both inhalation and contact has occurred, first aid for

inhalation should be given first

5. HYDROGENSULFIDE:

It is colourless, flammable gas with rotten egg odour. The TLV of

hydrogen sulphide is 10 ppm.
TOXICITY:
Hydrogensulphide has general toxic action and inhibits
respiratory cytochrome oxidase activity.

This inhibition is fatal for cellular respiration. On contact of

mucous membranes. It forms caustic sulphide.

Acute poisoning –low concentration of 200 ppm for prolonged

exposure. Dulls the sense of smell and makes the odor very
unreliable means of warning.

There is no accumulation phenomenon & elimination occurs

thru intestine, urine and expired air.

In slight poisoning of 500 ppm, headache for several hours,

pain in legs and rarely loss of consciousness for few minutes
but no respiratory distress.

In severe poisoning probably as a result of carotid sinus

stimulation , the subject
Acute poisoning –low concentration of 200 ppm for prolonged
exposure. Dulls the sense of smell and makes the odor very
unreliable means of warning.

There is no accumulation phenomenon & elimination occurs thru

intestine, urine and expired air.

In slight poisoning of 500 ppm, headache for several hours, pain

in legs and rarely loss of consciousness for few minutes but no
respiratory distress.

In severe poisoning probably as a result of carotid sinus

stimulation , the subject

drops into profound coma.

SUBACUTE POISIONING:

The signs may be nausea, stomach distress, foetid eructations,

rotten egg breath and diarrhea.
Also accompanied are balance disorders, vertigo, dryness,
irritation of throat with mucopurulent sputum and diffuse rales
and ronchi. Retrosternal pain like angina may occur showing
transient changes in ECG .

in chronic poisioning there is headache , asthenia, eye disorders,

chronic bronchitis and grey green line on gums.

In acute poisoning ocular symptoms predominate.

MEDICAL PREVENTION AND TREATMENT:

In acute poisoning the victim should be removed from exposure

site and should be provided with 100% O2.

the respiratory centre may be stimulated by injection lobelin and

niketinamide. Vitamin C may be injected.

Eyes should be washed with boric acid solution or isotonic

physiological solution and olive oil drops be instilled. For more
serious cause 1% adrenalin solution and hot –cold compressed is
considered.
6. NITROGEN OXIDE:

Oxides of nitrogen are generated in some manufacturing process as

intermediate or as rejected wastes products.

These are also produced as UV light of arc welding flame or CO2 gas
cutting welding.

As these oxides amy undergo interconversion by decomposition,

interaction or reaction with O2. they occour as mixture .

in refinerires this mixture exists as N2O3, NO2, N2O4. N2O3 dissociate

as N2O3  2NO2.

The TLV is 3 ppm.

TOXICITY:
Nitrogen dioxide, with its associated dinitrogen tetra oxide is a powerful
lung irritant and it is probable that the hazard from “ nitrous fumes” is
due mainly to this component.

Exposure to high concentrations of 100-500 ppm may lead to sudden

death from brochospasm and respiratory failure.

A more typical death from delayed pulmonary oedema, the initial signs
on exposure being no more than moderate irritation of eyes and
respiratory tract.

A third type of death may ensue several weeks after exposure and may
be associated with inflammatory changes termed bronchiolitis fibrosa
obliterans.

Moderate steady exposure results in the region of 20-50 ppm may lead to
some form of chronic diseases.
There is some evidence that such concentrations can lead to complaints
ofdrowsiness, dizziness or vomiting and this may be associated with the
presence of meth-haemoglobinaemia.
MEDICAL TREATMENT:

Immediate and completes rest is essential after suspected excessive

exposure and the patient should be kept under continuous observation,
even if he feels quite well.

O2 should be administered as soon as there are sign of pulmonary

insufficiency, with artificial ventilation if necessary.

If pulmonary oedema develops, may be reduced by tracheobroncheal

suction. Acute oedema is unlikely to occur more than 24 hrs.

after exposure. But the patient should be observed for 2-3 weeks, with
occasional chest X-rays.

Hydrocortisone should be administered by endotrachial instillation or

neubillsation followed by course of intravenous injections, together with
prophylactic treatment by a broad spectrum antibiotic.
7. SULFURDIOXIDE:

It is colorless gas, non flammable, pungent and having acidic taste. It is

soluble in organic solvents/ H2SO4, very soluble in water, readily
combines with water to form H2SO3 and then slowly into H2SO4.

The threshold value is 2 ppm.

It is used as a bleaching agent for sugar, fibres, leather,glues.

It is also used as preservation of organic materials in wine industry.

it mixed with ammonia and environment mist to form ammonium sulfate

mist to protect crops against night frost.
TOXICITY:
Most widely encountered contaminated released in large quantities in
manufacture of H2SO4 liquid sulfur dioxide, cast iron, refining of sulfur
rich minerals, combustion of sulfur rich coals.

Also produced in production of cellulose, sugar, super-phosphates, food

preservation, petroleum refining, bleaching disinfectant.

Effects are due to formation of H2SO3/ H2SO4 on contact with mucous

membrane.

Enters in lungs thru inhalation or got thru dissolving in saliva. 90% of

inhaled gas is absorbed thru upper respiratory tract.
Due to high solubility may reach blood thru lungs/ moist skin
forming metha-haemoglobulin.

Liquefied sulfur dioxide on skin produces skin burn. Liquefied

sulfur dioxide under pressure – if splashed on eyes causes
corneal burns and opafications.

Acute poisoning: inhalation of high concentration , normally

accidental causes irritation of eyes, breathlessness, blue skin
followed by consciousness disorders.

Chronic poisoning: very common burning, dryness and pain in

nose throat , altered smell secretions, from nose and salivation-
occasional blood streak.

Dry cough leading to chronic bronchitis, chronic emphysema.

Swelling and redness of nose, pharynx, larynx and tonsils.
Ulceration of nasal septum may bleed.
Nervous disorders- usually functional- may due to toxic effect on whole
body

Dental carries- rapid and painless dental destruction, loss of filling,

increased tooth sensitivity, loss of brilliance, skin irritation due to formation
of H2SO3 in sweat

TREATMENT:

Should be targeted to decrease SO2 in emission.

Total enclosure of process with exhaust ventilation

Respiratory PPE

Good hygiene – bathing and cleaning teeth after work.

Physical exercise to maintain lung functions

Rinse mouth with 10% soda bicarbonate solution during working
hours

Pre-employment – person with chronic bronchitis, chronic

conjunctivitis, laryngitis, bronchial asthma, blood disorders
should be avoided

First aid-evacuation to fresh air

O2 therapy-shift to hospital

If eyes are affected: wash with 2% soda bicarbonate solution and

2-3% ephedrine nasal drops.