Phenol is a toxic compound discovered in 1834 that has a variety of industrial and medical uses. It is absorbed through the skin, lungs, and gastrointestinal tract, distributing widely in the body before being metabolized and excreted in urine. Acute exposure can cause rapid nervous system effects like seizures and coma, while chronic exposure is associated with damage to the kidneys, liver, heart and skin. Phenol was also used by Nazis during World War II for individual executions by injection.

1. Phenol -Overview
• By Dr. Ashok Laddha
• Emergency Medicine
• Occupational health physician

2. Content
• History
• History of second world war
• Introduction
• Physical properties
• Chemical properties
• Hazardous Characteristics
• Phenol in environment
• Uses
• Medical application
• Physiopathology & Toxicology
• Target organ
• First Aid
• Medical treatment
• Preventive Measures

3. History
• Phenol was discovered in 1834 by Friedlieb Ferdinand
Runge, who extracted it (in impure form) from Coal Tar.
• Runge called phenol "Karbolsäure" (coal-oil-acid, carbolic
acid).
• Coal tar remained the primary source until the
development of the petrochemical industry.
• In 1841, the French chemist Auguste Laurent obtained
phenol in pure form.
• In 1836, Auguste Laurent coined the name "phène" for
benzene; this is the root of the word "phenol" and
“phenyl".
• In 1843, French chemist charles Gerhardt coined the name
"phénol"

4. History of Second world war
• The toxic effect of phenol on the central nervous system,
causes sudden collapse and loss of consciousness in both
humans and animals; a state of cramping precedes these
symptoms because of the motor activity controlled by the
central nervous system.
• Injections of phenol were used as a means of individual
execution by the Nazis during the 2 nd world war
• It was originally used by the Nazis in 1939 .
• Maximilian Kolbe was also killed with a phenol injection
after surviving two weeks of dehydration and starvation
in Auschwitz when he volunteered to die in place of a
stranger.
• Approximately one gram is sufficient to cause death

5. Introduction
• Natural, obtained from coal tar, or as a degradation
product of benzene. Synthetic, made by fusing sodium
benzenesulfonate with NaOH, or by heating
monochlorobenzene with aqueous NaOH under high
pressure
• Phenol is also a product of auto exhaust, and therefore,
areas of high traffic likely contain increased levels of
phen ol.
• Phenol has been detected in surface waters, rainwater,
sediments, drinking water, groundwater, industrial
effluents, urban runoff, and at hazardous waste

6. Chemical Properties
• Phenol is the simplest member of a family of
compounds in which an -OH group is attached
directly to a benzene ring. Phenol itself is the
only one of the family that you are likely to
need to know about for UK A level purposes.
• Chemical formula-C6-H6-0/C6H5OH
• Molecular weight—94.11
• IUPAC Name-Phenol

7. Structure of phenol

8. Physical Properties
• The crystals turn pink or red on exposure to
air and light, hastened in presence of alkalinity
(Windholz, 1983). Phenol has an acrid smell
and a sharp burning taste.
• Melting point is 43°C, the commercial product
has an impurity that increases the melting
point
• Boiling point: 181.75°C
• Flash point: 80°C

9. Hazardous characteristics
• Autoignition temperature is 715°C. Phenol is a volatile,
combustible solid that when heated gives off flammable
vapours and carbon dioxide.
• Explosive or violent reactions occur with acetylaldehyde;
aluminium chloride plus nitrobenzene; aluminium chloride-
nitromethane; butadine; calcium hypochlorite;
peroxomonosulphuric acid; peroxodisulphuric acid; sodium
nitrate; and sodium nitrate-trifluoroacetic acid .
• Phenol is sensitive to oxidising agents. Splitting of the
hydrogen atom from the phenolic hydroxyl group is
followed by resonance stabilization of the resulting
phenyloxy radical. The radical that is formed can be further
oxidised. This makes phenol suitable as an antioxidant,
functioning as a radical trapping agent

10. Physical Properties
• In the molten state, it is a clear, colourless
liquid with a low viscosity.
• It is soluble in most organic solvents, and
solubility is limited in aliphatic solvents.
• Phenol's solubility. In water is limited at room
temperature, above 68°C it is entirely water
soluble.
• The vapour is heavier than air

11. Phenol in the Environment
• Phenol enters the air, water, and soil as a result of its
manufacture and use.
• Phenol has a short half-life in air, less than 1 day. In air, it
reacts with photochemically-produced hydroxyl radicals.
• Phenol generally remains in soil only about 2–5 days. In
soil, phenol biodegrades under both aerobic and anaerobic
conditions.
• Phenol is rapidly degraded in water, but it can remain in
water for a week or more if present in high concentrations.
• Phenol does not accumulate in fish, other animals, or in
plants

12. Synonyms
• Acidum carbolicum
• Acidum phenolicum
• Aacidum phenylicum
• Bbaker's P & S liquid ointment
• Bbenzaphenol
• Benzene phenol
• Benzenol carbolic acid
• Carbolic acid
• Hhydroxybenzene (IUPAC)
• Monohydroxybenzene
• Monophenol
• NCI-C50124
• Oxybenzene
• Phenic acid;
• Phenol alcohol
• Pphenyl hydrate
• Phenyl hydroxide
• Phenylic acid
• Phenylic alcohol

13. Phenol includes---------
• chlorophenol;
• cresol;
• lysol;
• creosote;
• butylphenol;
• resorcinol;
• pyrocatechol;
• hydroquinone and others.

14. Uses-1
• The main use of phenol is as a feedstock for phenolic resins,
bisphenol A and caprolactam (an intermediate in the
production of nylon-6). It is used in the manufacture of
many products including insulation materials, adhesives,
lacquers, paint, rubber, ink, dyes, illuminating gases,
perfumes, soaps and toys (IARC, 1989; WHO, 1994).
• Also used in embalming and research laboratories.
• It is a product of the decomposition of organic materials,
liquid manure, and the atmospheric degradation of
benzene
• Phenol and its derivatives like dinitrophenol and
pentachlorophenol (carbolic acid) are widely used as
insecticides,.

15. Uses-2-Medical application
• It is found in some commercial disinfectants, antiseptics,
lotions and ointments.
• Phenol is active against a wide range of microorganisms,
and there are some medical and pharmaceutical
applications including topical anesthetic and ear drops,
sclerosing agent.
• It is also used in the treatment of ingrown nails in the "nail
matrix phenolization method" (Kimata et al., 1995).
• Another medical application of phenol is its use as a
neurolytic agent, applied in order to relieve spasms and
chronic pain (Wood, 1978; Geller, 1997).
• It is used in dermatology for chemical face peeling.

16. High Risk Group
• Petroleum industry
• Manufacture of nylon, epoxy resins and
polycarbonates,
• Herbicides,
• Wood preservatives,
• Hydraulic fluids,
• Heavy-duty surfactants,
• Lube-oil additives,
• Tank linings and coatings,
• and intermediates for plasticizers and other specialty
chemicals

17. Causes of Phenol Poisoning
• violation of safety procedures during the work with them;
• accidental use of a poisonous substance;
• suicide attempt;
• violation of dosages and rules for the use of medicinal
products;
• violation of rules for storage of medicines, disinfectants and
household chemicals in places accessible to children;
• the use of toys by children from plastics that do not comply
with GOST (in recent years, children have been poisoned by
puppets, even expensive ones made in China and Thailand).

18. Routes of Exposure
• Dermal
• Ingestion
• Inhalation
• Ocular
• paraentral

19. Target Organs-Toxicity
• Blood
• Bone Marrow
• Lung
• Liver
• Kidney
• Spleen
• thymus

20. TOXICOKINETICS
• Phenol is readily absorbed and widely distributed following
inhalation, oral, and dermal exposure.
• The distribution of phenol is thought to be dependent on blood
flow. Conjugates with glucuronic acid and sulfate are the major
metabolites of phenol, although small amounts of the hydroxylation
products catechol and hydroquinone are also produced.
• Sulfotransferase and glucuronyltransferases are present in most
tissues, although the major sites of phenol conjugation are the
gastrointestinal tract, liver, lung, and kidney.
• Because of the large capacity of the intestines and liver to
conjugate phenol, the fact that the first-pass effect occurs following
oral exposure but not following dermal exposure may contribute to
the greater potential for phenol to result in adverse effects
following dermal exposure.
• Phenol and its conjugates are predominantly excreted in the urine.

21. Health effect
• Acute exposure
• Chronic Exposure

22. Caution
• Phenol (carbolic acid) is an aromatic acid
alcohol that is a highly reactive and corrosive
contact poison.

23. Acute exposure
• As a corrosive substance, phenol denatures proteins and
generally acts as a protoplasmic poison.
• Phenol may also cause peripheral nerve damage (i.e.,
demyelination of axons).
• Systemic poisoning can occur after inhalation, skin contact,
eye contact, or ingestion. Typically, transient CNS excitation
occurs, then profound CNS depression ensues rapidly.
• Damage to the nervous system is the primary cause of
death from phenol poisoning. However, damage to other
organ systems (e.g., acid-base imbalance and acute kidney
failure) may complicate the condition. Symptoms may be
delayed for up to 18 hours after exposure.

24. Chronic exposure
• Repeated phenol exposure in the workplace has caused
• renal damage including kidney inflammation, swelling
in the kidney tubules and cells, and degenerative
changes in glomeruli.
• Liver damage
• pigment changes of the skin have been noted in some
workers.
• Chronic exposure has also been correlated with an
increased risk of coronary artery disease and
insufficient blood supply to the heart in workers.

25. CNS Effect
• Initial signs and symptoms may include nausea,
• excessive sweating,
• headache,
• dizziness, and
• ringing in the ears.
• Seizures,
• loss of consciousness,
• coma,
• respiratory depression, and death may ensue. Coma and
seizures usually occur within minutes to a few hours after
exposure but may be delayed up to 18 hours.

26. Chronic exposure characteristic
• increased fatigue;
• sweating;
• sleep disturbance;
• headache;
• nausea and digestive disorders;
• dermatitis;
• irritability.

27. Cardiovascular effect
• Phenol exposure causes
• initial blood pressure elevation,
• then progressively severe low blood pressure
and shock.
• Cardiac arrhythmia and bradycardia have also
been reported following dermal exposure to
phenol.

28. Respiratory effect
• Mild exposure may cause
• upper respiratory tract irritation.
• With more serious exposure, swelling of the
throat, inflammation of the trachea, tracheal
ulceration, and an accumulation of fluid in the
lungs can occur.
• Ingestion may lead to death from respiratory
failure.

29. Gastrointestinal effect
• Nausea, vomiting, abdominal pain, and
diarrhea are common symptoms after
exposure to phenol by any route.
• Ingestion of phenol can also cause severe
corrosive injury to the mouth, throat,
esophagus, and stomach, with bleeding,
perforation, scarring, or stricture formation as
potential sequelae.

30. Renal Effect
• Renal failure has been reported in acute
poisoning.
• Urinalysis may reveal the presence of protein
(i.e., albuminuria), casts, and a green to-
brown discoloration of the urine.

31. Haematological effect
• Components of the blood and blood-forming organs
can be damaged by phenol.
• Most hematologic changes
• Hemolysis,
• Meth- Hemoglobinemia,
• bone marrow suppression,
• and anemia) can be detected by blood tests or simply
by the color or appearance of the blood.
• Heinz body hemolytic anemia and hyperbilirubinemia
have been reported occasionally (WHO, 1994).

32. Dermal Effect
• When phenol is applied directly to the skin, a white
covering of precipitated protein forms. This soon turns red
and eventually sloughs, leaving the surface stained slightly
brown. If phenol is left on the skin, it will penetrate rapidly
and lead to cell death and gangrene. If more than 60 square
inches of skin are affected, there is risk of imminent death.
• Phenol appears to have local anesthetic properties and can
cause extensive damage before pain is felt.
• Because of their relatively larger surface area:body weight
ratio, children are more vulnerable to toxicants absorbed
through the skin.
• 1% BURN IS EQUAL TO 10 % BURN
• Death resulted even after 1% burn

33. Chronic Dermal Effect
• Chronic doses may result in onychronosis
(yellowing of the skin) and skin eruption .
• Death has been observed from repeated
application of small doses (Olson, 1994).
• "carbolic marasmus" characterized by
anorexia, headache, vertigo, salivation, dark
urine and increased skin and scleral
pigmentation

34. Facts of Phenol burn
• All forms of phenol cause irritation, and acute toxic
effects of phenol most often occur by skin contact.
• Even dilute solutions (1% to 2%) may cause severe
burns if contact is prolonged.
• Systemic toxicity can result from skin or eye exposures.
• Phenol vapor and liquid penetrate the skin with an
absorption efficiency approximately equal to the
absorption efficiency by inhalation.
• death occurred within 30 minutes after skin contact.

35. Ocular Effect
• Contact with concentrated phenol solutions
can cause
• severe eye damage including clouding of the
eye surface,
• inflammation of the eye, and
• eyelid burns

36. Metabolic effect
• Acid-base disturbances
• Metabolic acidosis
• Electrolyte imbalance

37. Reason for dark urine
• Phenol poisoning can lead to green or black
urine due to carboluria. Carboluria is due to
oxidation of phenol to hydroquinone and
pyrocatechol.

38. Mode of action
• Cellular uptake of phenol is due to its
lipophilic character. It denatures proteins .
• Phenol is known to disrupt disulphide bridges
in keratin in the skin (Brooks & Riviere, 1996).
• Covalent binding of phenol to tissues and
proteins produces coagulation necrosis.
• The acute lethality of phenol, associated with
exposure to high dose concentrations

39. Pharmacokinetic Mechanisms
• When it is absorbed through the lungs, gut, or
skin, phenol conjugated at the portal-of-entry
and free phenol enter the bloodstream where
it can then be distributed throughout the
body
• conjugation with glucuronic acid and
conjugation with sulfate are the main routes
of detoxification of phenol

40. Bio Transformation
• Conjugation with glucuronic acid to phenyl glucuronide and
sulphation to phenyl sulphate, have been shown to be
major metabolic pathways in several species.
• A shift from sulphation to glucuronidation was observed in
rats after increasing the phenol doses, which is thought to
be due to a saturation of the overall sulphation process, by
the limited availability of 3-phosphoadenosine-5-
phosphosulfate.
• The formation of sulphate and glucuronic metabolites
occurs in the hepatocytes, and then transported to the bile
or back into the blood (Ballinger et al, 1995)
• Covalent binding of phenol to tissue and plasma proteins,
some phenol metabolites also bind to proteins

41. Complications of phenol poisoning
• Cardiac arrhythmia
• Metabolic acidosis
• AKI
• Paralysis
• Respiratory failure
• Pulmonary oedema
• Intravascular haemolysis
• Intestinal perforation
• Coma
• Death
• Necrosis of skin
• Gangrene etc

42. Investigations
• Complete blood count
• ECG
• PFT
• Renal function test
• Cardiac Markers
• Serum Electrolytes
• X-ray chest
• ABG
• phenol in urine/Blood
• Urine R/M
• Liver function test
• plasma free hemoglobin and haptoglobin analyses
• Blood Sugar

43. Special Investigations
• Bronchoscopy
• Endoscopy
• EEG
• CT Scan

44. Antidote
• There is no specific antidote
• PEG –poly ethylene glycol molecular weight
300 ---is considered as an antidote for skin
burn .Mode of action --Unknown
• Note:Patients should be checked for
methemoglobinemia. Symptomatic patients
should be treated by slowly administering 1 to
2 mg/kg of 1% methylene blue intravenously.
Further doses may be required.

45. Fatal dose
• 10-15 ml
• Lethal dose-1 gram

46. Treatment Protocol
• First aid Treatment
• Emergency treatment
• Supportive treatment
• Surgical intervention

47. Aim of treatment
• Limit absorption
• Help the body to withstand the effect
• Help in elimination

48. First aid Management-Phenol burn
• Rescuers should wear protective clothing and gloves while treating patients whose
skin is contaminated with phenol.
• Remove contaminated clothing rapidly
• Irrigate or wipe exposed areas immediately and repeatedly with low-molecular-
weight polyethylene glycol (PEG 300 or PEG 400) which can be diluted to 50% for
easier application.
• Treatment should be continued until there is no detectable odor of phenol.
• If PEG is not available, a glycerine solution can be used instead.
• If neither of these are available, irrigation with a high-density shower will reduce
phenol uptake, but lesser amounts of water will merely dilute the phenol and
expand the area of exposure.
• After treatment with the high pressure shower, the skin should be washed with
soap and water for at least 15 minutes.
• Decontamination must begin as soon as possible to minimize phenol absorption.
• Use caution to avoid hypothermia when decontaminating children or the elderly.
Use blankets or warmers when appropriate.

49. Emergency and supportive
Management
• Make a proper assessment of airway, breathing, circulation and
neurological status.
• Maintain a clear airway.
• If unconscious give artificial respiration.
• If the patient has breathing difficulties, put them in a sitting
position.
• Monitor vital signs.
• Monitor blood pressure and ECG.
• Monitor fluid and electrolyte balance.
• Monitor acid-base balance.
• Control cardiac dysrhythmias with appropriate drug regimen.
• Control convulsions with appropriate drug regimen.
• Monitor ABG

50. Medicines May Required
• IV Fluids
• Correction of electrolyte imbalance
• Correction of acidosis
• Diuretics for pulmonary edema
• Antibiotics
• Inj Methylene Blue
• PEG
• Bronchodilators
• Activated charcoal etc
• Liquid paraffin
• Pain Management

51. Workplace standards
• OSHA PEL: TWA 5 ppm (skin)
• ACGIH TLV: TWA 5 ppm (skin)
• IDLN: 100 ppm
• DFG MAK: 5 ppm (19 mg/m3)
• NIOSH REL: TWA 20 mg/m3;
• CL 60 mg/m3/15 minutes

52. Specific preventive measures
• Phenol should be kept in a tightly closed container, in a
cool, dry place, away from heat, flame and oxidising agents.
• It is light sensitive and should be kept in the dark (WHO,
1994).
• Protective clothing should will be appropriate to the
amount and form of the phenol being handled.
• It should be handled wearing an approved respirator; viton,
butyl rubber or neoprene gloves (not nitrile or PVA gloves),
• safety goggles and other protective clothing. Safety
showers
• polyethylene glycol 300 should be near where phenol is
being

53. Figure-1