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27
Traditionally, the term hydrocarbons has been used to represent
compounds derived from petroleum distillation, and hence were
considered synonymous with petroleum distillates. But this is
incorrect since the term should (logically) cover all organic
compounds made of predominantly carbon and hydrogen
molecules. The number of carbon molecules can vary from
1 to 60. In general, compounds which contain 1 to 4 carbon
molecules are gaseous, while those which have 5 to 19 are
liquids, and compounds with more than 20 are solids.
1. Aliphatic Hydrocarbons (Paraffins)
These comprise compounds with saturated molecules
(containing no carbon-carbon double or triple bonds)
which have straight or branched-chain arrangements.
Common examples include butane, ethane, methane, and
propane (gaseous) ; benzine, gasoline or petrol, diesel oil,
kerosene, mineral seal oil, lubricating oil or mineral oil,
and turpentine or pine oil (liquids) ; paraffin wax, petro-
leum jelly or vaseline, grease, tar, and asphalt (semi-liquids
or solids).
2. Aromatic Hydrocarbons
They contain at least one benzene ring and are unsaturated
compounds. Common examples include benzene, toluene,
xylene, styrene and naphthalene.
3. Halogenated Hydrocarbons
Most of these are clear, colourless liquids which have a
chloroform-like odour. Common examples include carbon
tetrachloride, ethylene dibromide, ethylene dichloride,
dichloroethylene, trichloroethylene, methylene chloride,
propylene chloride, chloroform, methyl chloroform,
methyl bromide, fluorocarbons and organochlorine insec-
ticides.
4. Cycloparaffins (Naphthenes)
They are saturated hydrogen compounds which are arranged
in closed rings. Common examples include cyclohexane
and methylcyclopentane.
5. Alkenes (Olefins)
These compounds contain one carbon-carbon double bond
in the molecule. They are mostly used in the manufacture
of other hydrocarbon products such as halogenated hydro-
carbons.
Hydrocarbons
ALIPHATIC HYDROCARBONS
Uses
Listed in Table 27.1.
Mode of Action
Ingestion of aliphatic hydocarbons with high molecular
weight such as paraffin wax, vaseline, grease, etc. is
associated with little or no toxicity.
Liquid hydrocarbons are the most toxic, but symptoms gener-
ally are the result of aspiration into the airways rather than
absorption from the GI tract.
The aspiration potential of a hydrocarbon depends on
3 propertiesviscocity, surface tension, and volatility.
Viscocity is the tendency of a substance to resist flow
(the ability to resist stirring) which is measured in
Saybolt Seconds Universal (SSU). The lower the viscocity
(i.e. below 60 SSU), the higher the tendency for aspira-
tion. Surface tension refers to the adherence of a liquid
compound along its surface (the ability to creep). It is
the result of cohesive forces generated by the attraction
between molecules (van der Waals forces). The lower
the surface tension, the higher the tendency for aspira-
tion. Volatility refers to the ability of a liquid to become
a gas. The higher the volatility, the higher the tendency
for aspiration.
Aliphatic hydrocarbons possessing high aspiration potential
include gasoline, kerosene, mineral seal oil, and turpentine.
Clinical Features
1. RS: Respiratory distress from aspiration usually begins
within 30 minutes of exposure, and is manifested mainly
by gasping, coughing, and choking. There are 3 grades:
a. Mild : coughing, choking, tachypnoea, drowsiness,
rales, rhonchi.
b. Moderate : grunting, lethargy, flaccidity, bronchospasm.
c. Severe : cyanosis, coma, seizures.
Moderate fever is often present but does not correlate with
severity. Haemoptysis and pulmonary oedema may occur
after significant aspiration or inhalation.
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Table 27.1: Uses of Aliphatic Hydrocarbons d. Injection of kerosene, naphtha, turpentine, gasoline, or
376 hydrocarbon insecticides has resulted in febrile reac-
Compound Use
tions, local tissue inflammation and systemic effects,
I. Gases
including pulmonary oedema, pneumonia and mild
Butane, propane Fuel CNS depression. Injection of pressurised hydrocarbons
II. Liquids has caused severe tissue damage. Subcutaneous injec-
Benzine Solvent tion of paint, lacquer or other material via high pres-
Diesel oil Fuel sure spray guns is a surgical emergency. High-pressure
injection injuries can result in necrosis and thrombosis
Gasoline (Petrol)* Fuel
with amputation required in 60 to 80% of cases.
Kerosene Fuel, curing of tobacco, lighter fluid
e Exposure to hydrocarbons may result in the loss of
Mineral seal oil Furniture polish colour vision, with the risk of impaired colour vision
Turpentine (Pine oil)** Paint thinner, paint increasing with increasing exposure.
remover f. Poisoning due to inhalation of butane and other similar
Section 8 Hydrocarbons and Pesticides

III. Semiliquids, Solids gaseous hydrocarbons is dealt with under Glue

Paraffin wax Candles sniffing (page no 576).
Petroleum jelly (Vaseline) Lubricant Diagnosis
Tar, asphalt Road surfacing
1. X-RayChanges may be evident as early as 30 minutes
* May also contain small quantities of aromatic hydrocarbons such as
after exposure and peak at about 72 hours, after which there
xylene and benzene, as well as tetraethyl lead and cresyl phosphates.
** It is actually an aromatic hydrocarbon, but possesses properties of is gradual resolution. Common radiologic findings include
aliphatic hydrocarbons, and is not a petroleum distillate. It is derived by perihilar densities, bronchovascular markings, bibasilar
steam distillation of pine resin.
infiltrates, and pneumonic consolidation. Early upright
X-rays may reveal two liquid densities in the stomach
2. CNS: Lethargy with depressed sensorium. Coma and (double bubble sign) (Fig 27.1), which represents two
convulsions are rare. Aniline, heavy metals, camphor, pesti- interfaces: air-hydrocarbon, and hydrocarbon-fluid, since
cides and other additives or contaminants in hydrocarbon hydrocarbons are not miscible with water and are usually
preparations may produce additional CNS toxicity. For lighter. Two important points are to be noted in connection
instance, chronic cerebellar degeneration may be associated with radiographic changes in hydrocarbon ingestion
with lead additives of gasoline. a. They correlate poorly with clinical symptoms.
3. GIT: Burning of mouth, sore throat, nausea, and vomiting. b. They lag behind clinical improvement.
Haematemesis may occur. Diarrhoea is rare. 2. Arterial blood gasesThere is hypoxaemia.
4. CVS: Arrhythmias are seen in solvent abuse (page no 576), 3. BloodLeucocytosis is common during the first 48 hours.
but are rare in ingestions.
5. Skin: Acute exposure can cause dermatitis, and if this is
prolonged it may result in full thickness burns. Chronic
exposure to kerosene can cause severe acne. Contact with
liquefied petroleum gases (e.g. propane, butane, propylene,
isobutane, butenes, n-butane), ethane, etc. can result in
frostbite or effects resembling frostbite.
6. Haematologic: Disseminated intravascular coagulation,
haemolytic anaemia and pancytopenia have occasionally
been reported following vapour inhalation, aspiration, or
ingestion of hydrocarbons.
7. Other effects:
a. Elevated liver enzyme levels and hepatosplenomegaly
can occur with petroleum distillate ingestion.
b. Renal effects (acute renal tubular necrosis, proteinuria,
or haematuria) occur infrequently following acute expo-
sure to petroleum distillates and other unsubstituted
hydrocarbons.
c. Straight chain hydrocarbons with few carbon atoms
(e.g. methane, ethane, propane gases) can cause
asphyxiation if exposure occurs in poorly ventilated
Fig 27.1: Double bubble sign
spaces.
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Treatment
1. The following signs and symptoms present upon initial
examination of patients after hydrocarbon ingestion have
80% or better predictive value for pneumonitis:
a. Lethargy, rhonchi, rales, retractions, cyanosis, and the
development of leukocytosis and fever within 4 hours.
b. The only parameter with an 80% or greater predictive
value for NO toxicity was the absence of tachypnoea.
c. Early chest X-rays were not useful in predicting pneu-
monitis in symptomatic or asymptomatic patients.
2. The immediate concern is the threat of respiratory failure. A
chest X-ray should be taken after stabilisation to confirm or
rule out aspiration. The following measures are necessary
if respiration is compromised:
a. Endotracheal intubation.
b. Oxygen.
c. Continuous positive airway pressure or positive
end-expiratory pressure. A recent innovation is high
frequency jet ventilation (HFJV), utilising high
respiratory rates (220 to 260) with small tidal volumes.
Extracorporeal membrane oxygenaion (ECMO) is an
effective option in severe pulmonary toxicity when all
other meaures have failed.
d. Bronchodilatorspreferably inhaled cardioselective
drugs such as salbutamol.
3. Decontamination:
a. If there is suspicion of dermal exposure, all clothing
should be removed and the skin washed with copious
amounts of soap and water, since significant toxicity
can result from cutaneous absorption.
b. Induction of vomiting is not recommended.
c. Stomach wash may be done cautiously after intuba-
tion, especially in those cases where a large quantity
of hydrocarbon has been ingested. However, several
investigators are against this practice and assert that it
only enhances the risk of pulmonary toxicity.
d. Activated charcoal is generally considered to be inef-
fective in adsorbing petroleum distillates, though there
are experimental studies suggesting the opposite.
4. While prophylactic administration of corticosteroids was
advocated in the past, it is not advocated today, since studies
have not demonstrated any beneficial effects. On the other
hand it can increase the chances of bacterial superinfection.
5. Similarly, prophylactic administration of antibiotics which
was the norm in the past is also discouraged today, since
it can alter the bacterial flora and lead to subsequent
infection by resistant gram-negative bacteria. Pulmonary
cultures should be done to decide on antibiotic adminis-
tration, though this may not be practicable in critically
ill patients. In such cases, prophylactic antibiotic therapy
may be justified.
6. Crystalloid solutions must be administered judiciously.
Pulmonary artery monitoring may help. In general, the
pulmonary artery wedge pressure should be kept relatively
low while still maintaining adequate cardiac output, blood
pressure and urine output. 377
7. Treatment of frostbite:
a. Rewarming
Do not institute rewarming unless complete
rewarming can be assured; refreezing thawed tissue
increases tissue damage. Place affected area in a water
bath with a temperature of 40 to 420 Celsius for 15 to
30 minutes until thawing is complete. The bath should
be large enough to permit complete immersion of the
injured part, avoiding contact with the sides of the
bath. A whirlpool bath would be ideal. Some authors
suggest that an antibacterial (hexachlorophene or
povidone-iodine) be added to the bath water.
Correct systemic hypothermia.
Rewarming may be associated with increasing pain,
Chapter 27 Hydrocarbons
requiring narcotic analgesics.
b. Wound Care
Digits should be separated by sterile absorbent
cotton; no constrictive dressings should be used.
Protective dressings should be changed twice per
day.
Perform daily hydrotherapy for 30 to 45 minutes in
warm water 400 Celsius. This helps debride devital-
ised tissue and maintain range of motion.
The injured extremities should be elevated and
should not be allowed to bear weight.
Clear blisters should be debrided but haemorrhagic
blisters left intact.
Further surgical debridement should be delayed
until mummification demarcation has occurred (60
to 90 days). Spontaneous amputation may occur.
Analgesics may be required during the rewarming
phase; however, patients with severe pain should be
evaluated for vasospasm. Arteriography and nonin-
vasive vascular techniques (e.g. Doppler ultrasound,
digital plethysmography, isotope scanning), have
been useful in evaluating the extent of vasospasm
after thawing.
Tetanus prophylaxis as indicated.
Topical aloe vera may decrease tissue destruction
and should be applied every 6 hours.
Ibuprofen is a thromboxane inhibitor and may help
reduce tissue loss. Adult dose of 200400 mg every
12 hours is recommended.
8. The following treatment measures/drugs are contraindicated
in hydrocarbon poisoning:
a. Emetics
b. Activated charcoal
c. Olive oil/mineral oil
d. Cathartics
e. Catecholamines (dopamine, adrenaline, noradrenaline,
isoproterenol, etc.).
9. Tar and asphalt can cause distressing problems of a
different sort. These hot hydrocarbon mixtures can produce
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severe burns on dermal contact. The material hardens
378 quickly and becomes extremely difficult to remove.
Thermal injury can be minimised by immediate cooling
with cold water. Removal of hardened tar can be attempted
after application of mineral oil, petroleum jelly, or antibac-
terial ointment. Recent reports suggest that surface-acting
agents in combination withahydrocarbon ointment may
be more effective.
Autopsy Features
1. Pulmonary oedema and varying degree of lung pathology
(page no 376) are prominent features.
2. There may also be evidence of gastrointestinal congestion
and (rarely) corrosion.
Section 8 Hydrocarbons and Pesticides
3. There is often characteristic odour depending on the type
of hydrocarbon ingested.
Forensic Issues
Most cases of poisoning result from accidental exposure.
In India, accidental kerosene poisoning is quite common
in the paediatric age group, since it is a popular household
fuel and is often negligently left around in the kitchen in
bottles or cans.
Suicidal ingestion of hydrocarbon products is not
uncommon because of easy availability of many of these
agents.
Experimental animal studies and some studies on cancer
incidence and mortality in human occupational groups
suggest that hydrocarbon exposure is associated with renal
neoplasia.
AROMATIC HYDROCARBONS
Benzene
Synonyms
Benzol, Benzole, Benzolene, Coal naphtha, Phenyl hydride,
Annulene, Carbon oil, Cyclohexatriene, Mineral naphtha,
Motor benzol, Phene, Pyrobenzol, Pyrobenzole.
Physical Appearance
Colourless, volatile, inflammable liquid, with a strong, pleasant
odour.
Sources
Natural sources of benzene include volcanoes and forest
fires. Benzene is also a natural constituent of crude oil.
Benzene can be recovered from coal tar and produced
from the hydrodemethylation of toluene under catalytic or
thermal conditions.
A chief source of benzene is catalytic reformat, wherein
the naphthenes and paraffins contained in naphtha are
converted to aromatic hydrocarbons. Solvent extraction is
then used to recover the benzene.
Most of the benzene produced is generally derived from the
petrochemical and petroleum-refining industries.
Cigarette smoke also is said to contain benzene.
Uses
Benzene is extensively used in industry for the manufacture
of drugs, chemicals, insecticides, glues, varnishes, paints,
polishes, explosives, batteries, shoes, and rubber tyres.
It is also used in printing, photography, and dry cleaning.
It is a popular solvent in laboratories.
Petrol often has significant concentrations of benzene (as
an octane booster).
Clinical Features
1. Acute Exposure:
a. Benzene can be absorbed through all routes.
b. Most individuals can begin to smell benzene in air at
1.5 to 4.7 parts per million (ppm) and detect the odour
of benzene in water at 2 ppm.
c. Brief exposure (5 to 10 minutes) to very high benzene
air concentrations (10,000 to 20,000 ppm) can result in
death.
d. On inhalation (of lower concentrations), principal mani-
festations include vertigo, tinnitus, vomiting, dyspnoea,
convulsions, coma, and death. Cardiac arrhythmias are
possible.
e. On ingestion, symptoms include burning pain in the
mouth and pharynx, epigastric pain, vomiting, vertigo,
tachycardia, hypotension, dyspnoea, convulsions and
coma.
f. Aspiration produces similar manifestations as in the
case of aliphatic hydrocarbons.
g. Locally (on skin), benzene has a strong irritating effect,
producing erythema, burning and, in more severe cases,
oedema and blistering.
2. Chronic Exposure:
a. Benzene has been classified as a human carcinogen by
various international monitoring agencies. The causal
relationship between chronic exposure and a variety of
haematologic disorders has been known for the last 50
years or more. These include aplastic anaemia, acute
myeloblastic leukaemia, haemolytic anaemia, and
pancytopenia. Benzene exposure is associated with
translocations between chromosomes 8 and 21, and
hyperploidy of 8 and 21 in the circulating lymphocytes
of workers exposed to benzene. These aberrations may
be involved in benzene-induced leukaemia.
b. Headache, dizziness, irritability, nervousness, fatigue,
anorexia and epistaxis may also occur with chronic
benzene poisoning.
c. Paroxysmal nocturnal haemoglobinuria (PNH) has been
reported in patients occupationally exposed to benzene.
PNH is often associated with aplastic anaemia and
rarely with acute leukaemia.
d. Insulin-dependant diabetes mellitus has been reported
with benzene exposure.
e. An epidemiological study of pregnant women in a large
petrochemical industry showed a positive correlation
between reduced birth weight and exposure to benzene
and work stress.
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Diagnosis Toluene and Xylene produce similar (though milder) mani-
festations on acute exposure and are managed by supportive 379
1. Benzene is metabolised extensively in the liver and measures, with the same precautions in decontamination as for
excreted in the urine, with 51 to 87% excreted as phenol, other hydrocarbons.
6% as catechol, and 2% as hydroquinone. Other metabo-
lites include phenylmercapturic acid (0.5%), benzene Naphthalene
dihydrodiol (0.3%), and trans, trans-muconic acid (1.3%).
Monitoring benzene in expired air and urine phenol levels
Synonyms
may be useful for observing workers exposed to benzene. Moth flake, Tar camphor, White tar.
Urine phenol levels in unexposed individuals are less than
10 mg/L. Urine phenol levels after chronic exposure to Physical Appearance
airborne concentrations of 0.5 to 4 ppm are less than 30 White scaly powder which volatilises at room temperature.
mg/L. Urine phenol levels after exposure to 25 ppm average
200 mg/L. Sources
2. Analysis of urinary t, t-muconic acid appears to be a better Naphthalene occurs naturally in the essential oils of the
indicator than phenol for assessment of exposure to low roots of Radix and Herba ononidis, and crude oil.

Chapter 27 Hydrocarbons
levels of benzene. It can be manufactured by crystallising and separating the
3. Gas chromatography head-space analysis is the preferred naphthalene fraction.
method for determining benzene in blood or urine. The Naphthalene can also be produced by boiling coal tar oils
lower limit of detection is 0.64 nmol/L for benzene in blood at temperatures between 2002500 C, followed by crystal-
and 0.51 nmol/L in urine. lisation and distillation.
4. Obtain baseline CBC. It can also be derived from catalytic processing of petro-
5. Monitor ECG for cardiac arrhythmias. leum, or isolated from cracked petroleum.
Naphthalene is formed in cigarette smoke by pyrolysis,
Treatment and is also a photodecomposition product of carbaryl, an
Acute exposure is treated on the same lines as in the case of agricultural pesticide.
aliphatic hydrocarbons.
1. Ipecac-induced emesis is not recommended because of the Uses
potential for CNS depression and seizures. Moth repellent (in the form of moth balls) (Fig 27.2)*
2. Consider pre-hospital administration of activated charcoal Deodorant cakes
as an aqueous slurry in patients with a potentially toxic Scintillation counters.
ingestion who are awake and able to protect their airway.
3. Consider gastric lavage with a large-bore orogastric tube
after a potentially life-threatening ingestion if it can be
performed soon after ingestion (generally within 60
minutes).
4. Remove contaminated clothing and wash exposed area
extremely thoroughly with soap and water.
5. Administer 100% humidified supplemental oxygen,
perform endotracheal intubation and provide assisted
ventilation as required. Administer inhaled beta adrenergic
agonists if bronchospasm develops. Exposed skin and eyes
should be flushed with copious amounts of water.
6. Treat convulsions in the usual manner.
Autopsy Features
1. Marked congestion of brain.
2. Pulmonary oedema. On sectioning the lungs there is exuda-
tion of blackish, frothy liquid.
3. Multiorgan congestion.
Forensic Issues
Most cases of exposure (acute and chronic) are occupational
in nature. Fig 27.2: Moth balls

* While naphthalene is the commonest constituent of moth balls, other agents are also used as moth repellents, e.g. camphor, paradichlorobenzene, etc.
 www.PharmaDost.info
380 Toxicokinetics and Mode of Action
Naphthalene itself is not responsible for the toxic effects.
Its metabolites alpha and beta naphthol as well as naphtho-
quinone are powerful haemolytic agents. Individuals with
glucose-6-phosphate dehydrogenase (G-6-PD) deficiency
are especially vulnerable to the toxicity of these metabolites.
Naphthalene is first metabolised by hepatic mixed func-
tion oxidases to the epoxide, naphthalene-1,2-oxide. The
epoxide is enzymatically converted into the dihydrodiol,
1, 2-dihydroxy-1,2-dihydronaphthalene or conjugated with
glutathione. The dihydrodiol is then conjugated to form a polar
compound with glucuronic acid or sulfate, or further dehy-
drogenated to form highly reactive 1,2-dihydroxynaphthalene.
Section 8 Hydrocarbons and Pesticides

Dihydroxynaphthalene can be enzymatically conjugated with

sulfate or glucuronic acid or spontaneously oxidised to form
1,2-naphthoquinone. Naphthalene is also metabolised to
mercapturic acid derivatives.
Naphthalene metabolites (naphthols and naphthylglycuro-
nates) are excreted in the urine as 1-naphthylmercapturic acid
(15% of absorbed dose), as conjugates of 1,2-dihydronaphtha-
lene-1,2-diol (10% of absorbed dose), and as 1- and 2-naphthols
and 1,2-dihydroxynaphthalene. Conjugates of glutathione
(cysteinylglycine, and cysteine; intermediates in formation of
mercapturic acids) are excreted mainly in the bile as metabolites
of naphthalene.
Naphthalene can be absorbed via oral, inhalation, and
dermal routes.
Clinical Features
1. Non-haemolytic manifestations: Vomiting, abdominal pain,
diarrhoea, headache, diaphoresis, optic neuritis, restlessness,
lethargy, fever, convulsions, hepatomegaly, splenomegaly.
Hyperbilirubinaemia and fatal kernicterus may occur in
newborns with significant haemolysis. Centrilobular necrosis
occurred in one paediatric poisoning case. Coma and acute
lung injury may develop in severe toxicity. Naphthalene skin
exposure may cause hypersensitivity dermatitis. Repeated
exposure may cause corneal ulceration, lenticular opacities,
cataracts, headache, malaise and vomiting.
2. Haemolytic manifestations: Pallor, weakness, jaundice,
cyanosis, haemolysis, haemolytic anaemia, methaemoglo-
binaemia (Fig 27.3), hyperkalaemia, dysuria, haematuria,
and dark urine (haemoglobinuria), albuminuria, oliguria,
and acute renal failure. Cardiovascular shock can occur
in patients with severe haemolytic anaemia. Metabolic
acidosis may develop in patients with acute renal failure
secondary to haemolysis.
a. Haematological Findings: Increased WBC count,
fragmented RBC, anisocytosis, Heinz bodies, and
poikilocytosis.
b. Infants and patients with G6PD deficiency, sickle cell
anaemia, or sickle cell trait are more likely to develop
haemolysis and/or methaemoglobinaemia.
Fig 27.3: Methaemoglobinaemia
(Pic: Dr S Senthilkumaran)
3. Chronic exposure to naphthalene can result in aplastic
anaemia, hepatic necrosis, and jaundice. Naphthalene and
coal tar exposure have been associated with laryngeal and
intestinal carcinoma.
Diagnosis
1. Obtain baseline CBC, electrolytes, glucose-6-phosphate
dehydrogenase level, liver enzymes and renal function tests,
urinalysis and urine dipstick test for haemoglobinuria.
2. Measurement of urinary metabolites (1-naphthol or mercap-
turic acid) may help to confirm the diagnosis. Urinary naphthol
levels may be utilised to monitor industrial creosote exposure
(naphthalene is the most abundant compound found in creosote
vapour).
3. X-ray: Abdominal radiographs may help differentiate
between mothballs or other products which contain paradi-
chlorobenzene (densely radiopaque) from those which
contain naphthalene (radiolucent or faintly radiopaque).
Treatment
Acute exposure is treated on the same lines as in the case of
aliphatic hydrocarbons.
1. Ingestion of one mothball may produce toxicity; patients
with ingestion of more than this amount should be referred
to a health care facility for gastric decontamination and
observation. If laboratory findings are negative and the
patient is asymptomatic during a 4 to 6-hour observation
period, the patient may be discharged with instructions to
return for a follow-up CBC and urinalysis for up to 5 days
post-ingestion. Patients should be instructed to return if any
gastrointestinal symptoms, pallor, dark or diminished urine
output, or CNS symptoms develop.
 www.PharmaDost.info
2. Decontamination
a. Induced emesis is more useful for mothballs because
of their size. Do not induce vomiting if the patient has
any evidence of lethargy or CNS depression.
b. Gastric lavage may be useful for ingestion of flakes,
but its effectiveness may be limited by naphthalenes
poor water solubility. Mothballs dissolve slowly; gastric
decontamination should be considered even in patients
presenting late after ingestion.
c. Information on the benefit of activated charcoal is scant,
but adsorption is thought to occur. Consider adminis-
tration of activated charcoal after a potentially toxic
ingestion (up to 1 hour).
d. Dermal DecontaminationRemove contaminated
clothing and wash exposed area thoroughly with soap
and water. Consider discarding contaminated clothing,
as washing does not easily remove naphthalene.
3. Avoid oral administration of oil or fatty substances.
4. Control seizures.
5. Alkaline Diuresis
a. Should be performed if there is evidence of haemolysis.
This may prevent renal deposition of red blood cell
break down products in the renal tubules and resultant
renal failure.
b. Administer 1 to 2 mEq/kg of sodium bicarbonate as an
intravenous bolus. Add 132 mEq (3 ampoules) sodium
bicarbonate and 20 to 40 mEq potassium chloride (as
needed) to one litre of dextrose 5% in water and infuse
at approximately 1.5 times the maintenance fluid rate.
c. In patients with underlying dehydration additional
administration of 0.9% saline may be needed to main-
tain adequate urine output (1 to 2 ml/kg/hour).
d. Manipulate bicarbonate infusion to maintain a urine
pH of at least 7.5. Additional sodium bicarbonate (1 to
2 mEq/kg) and potassium chloride (20 to 40 mEq/L)
may be needed to achieve an alkaline urine. Do not
administer potassium to an oliguric or anuric patient.
e. Obtain hourly intake/output and urine pH. Assure
adequate hydration and renal function prior to alkalini-
sation. Monitor fluid and electrolyte balance carefully.
Monitor blood pH, especially in intubated patients, to
avoid severe alkalaemia. Administer furosemide as
needed to maintain urine output.
6. Treat haemolysis with blood transfusion, packed red cell
transfusions, or exchange transfusion.
7. Monitor methaemoglobin level and treat if symptomatic, or
if methaemoglobin levels are greater than 30%. Treat with
methylene blue 1 to 2 mg/kg/dose (0.1 to 0.2 ml/kg/dose)
IV over 5 minutes as needed every 4 hours. It is important
to remember that large doses of methylene blue may itself
cause methaemoglobinaemia or haemolysis. Also, meth-
ylene blue must not be administered if the patient has G6PD
deficiency.
8. Haemodialysis may help enhance elimination, though it is
not routinely recommended.
Forensic Issues
381
Most cases of exposure are accidental in nature.
A few are suicidal.
In the case of mothball ingestion (suicidal or accidental),
sometimes there is confusion as to whether the active
ingredient is naphthalene, camphor or paradichlorobenzene.
YY Differentiating between mothballs containing paradi-
chlorobenzene (PDB), naphthalene and camphor:
Physical appearanceNaphthalene is dry, while
PDB has a wet and oily appearance.
Specific gravityDistinguishing between camphor,
naphthalene, and PDB mothballs can be done by
testing whether they float or sink in a saturated solu-
tion of salt water (4 ounces of tepid water to which 3
heaping tablespoons of table salt has been added and
Chapter 27 Hydrocarbons
stirred vigorously until the salt will not dissolve any
more). Camphor mothballs float in both water and
salt solution. Naphthalene mothballs sink in water
but float in saturated salt solution. PDB mothballs
sink in both water and salt solution.
SolubilityPDB is more soluble in turpentine
than naphthalene. A mothball of PDB will usually
dissolve within 30 to 60 minutes whereas at least
one fourth of the naphthalene will be left.
HeatPDB produces a bright green colour in a
bunsen burner flame; Naphthalene does not.
Melting pointPDB: 530 C; Naphthalene: 800 C.
Placing a small piece of the mothball in a test tube
heated to 600 C in water bath may simplify the
melting point test. PDB will liquefy within several
minutes; naphthalene will remain intact.
Chemical testIf chloroform and ammonium chlo-
ride powder are added to PDB no colour change
occurs; naphthalene turns blue.
Polycyclic Aromatic Hydrocarbons
These compounds (also called polynuclear aromatic hydro-
carbons) contain three or more fused benzene rings in varying
arrangements that consist of carbon and hydrogen, e.g.
benzoanthracene, benzopyrene, anthracene, phenanthrene,
benzofluoranthene, chrysene, coronene, dibenzacridine,
dibenzanthracene, dibenzocarbazole, dimethylbenzanthracene,
3-methylcholanthrene and pyrene.
Sources
Polycyclic aromatic hydrocarbons (PAHs) are components of
most fossil fuels and are ubiquitous in the natural environment.
Forest fires.
Sea food and agricultural products.
Charring, barbecuing, smoking of foods; foodstuffs such as
coffee, roasted peanuts; refined vegetable oils, crude coconut
oil, heavily smoked ham.
Emissions sources:
YY Cigarette smoke
 www.PharmaDost.info
YY Coal tar pitch Routine monitoring and physical assessments (e.g.
382 YY Coke production complete blood count, hepatic and renal function tests, chest
YY Engine exhaust X-ray and pulmonary function tests, dermal assessments) of
YY Engine oil, used individuals with significant exposure is recommended, even
YY Fuel burning, and open burning of refuse in the absence of symptoms.
YY Restaurants and smokehouses
YY Roof tarring
HALOGENATED HYDROCARBONS
YY Sidewalk tarring
YY Wood-burning fireplaces. Examples
Clinical Features Listed in Table 27.2.
1. Acute poisoning is rare. Physical Appearance
2. Chronic exposure in the form of inhalation or dermal
contact can predispose to lung and skin cancer. Increased Most halogenated hydrocarbons are clear, colourless, non-
Section 8 Hydrocarbons and Pesticides

incidence of cancers of the skin, bladder, lung and gastroin-
testinal tract have been described in PAH-exposed workers.
Apart from such carcinogenic potential, PAHs are also
responsible for eye irritation and photosensitivity, skin
erythema, cough and bronchitis, and haematuria.
YY Chronic effects include:
Photosensitivity and irritation.
RespiratoryIrritation with cough and bronchitis.
MouthLeukoplakia.
DermalCoal tar warts (precancerous lesions
enhanced by UV light exposure), erythema, dermal
burns, photosensitivity, acneiform lesions, irritation.
Hepatic/RenalMild hepatotoxicity or mild
nephrotoxicity.
GenitourinaryHaematuria.
inflammable liquids with sweetish, chloroform-like odour.
Many of them also exist as gases. For instance, methyl bromide
is a toxic inhalant, and an intense vesicant, with dermal expo-
sures resulting in burns. It is a colourless, transparent, volatile
liquid or gas with a burning taste. It is nearly odourless, though
chloropicrin is typically added to commercial forms of methyl
bromide to give it an intense odour.
Toxicokinetics
The usual route of exposure is either inhalation or ingestion.
Many halogenated hydrocarbons can be absorbed through
skin, albeit slowly.
After absorption they are distributed mainly in the blood,
brain, and adipose tissue.
Metabolism occurs in the liver by cytochrome P450 oxida-
tion. There is partial glutathione conjugation.

Table 27.2: Halogenated Hydrocarbons

Compound Use
Acetylene tetrabromide Gauge fluid, solvent, refractive index liquid in microscopy
(Tetrabromoethane)
Carbon tetrachloride* Manufacture of fluorocarbon propellants (Freon), solvent, cleansing and degreasing agent,
(Tetrachloromethane) grain fumigant, dry cleaning, fire extinguisher
Chloroform Anaesthetic agent
Dichloroethylene (1,2-Dichloroethane) Degreaser, solvent, fumigant, manufacture of nylon, rayon, etc.
Ethylene dibromide (1,2-Dibromoethane) Soil fumigant
Ethylene dichloride (1,1-Dichloroethane) Cleansing and degreasing agent, solvent, grain fumigant
Fluorocarbon , Freon Solvent for cleaning electronic equipment, degreaser, refrigerant, fire extinguisher, dry
cleaning
Methyl bromide Fire extinguisher, fumigant insecticide, refrigerant
Methyl chloride Refrigerant (now obsolete)
Methylene chloride (Dichloromethane) Solvent, paint remover, degreaser, manufacture of aerosol propellants and urethane foam

Propylene dichloride (Dichloropropane) Degreaser, dry cleaning, stain remover, manufacture of cellulose plastics
Tetrachloroethane Feed stock, cleanser, degreaser
Tetrachloroethylene Solvent, dry cleaning, pesticide, metal cleaner
Trichloroethane Solvent, degreaser, pesticide
Trichloroethylene Solvent, degreaser, refrigerant, typewriter cleaning fluid, paint remover, adhesive,
anaesthetic
*Banned from most commercial uses in Western countries
 www.PharmaDost.info
Mode of Action
Most of these agents are powerful hepatorenal toxins,
producing centrilobular liver necrosis and renal tubular
degeneration.
In the case of carbon tetrachloride, the hepatic mixed-
function oxidase system metabolises it to the trichloro-
methyl radical (CCl3.). This initiates lipid peroxidation,
protein-lipid cross links, and trichloromethyl adducts with
DNA, protein and lipid. The trichloromethyl radical may
poison the cytochrome P 450. It may be released from
the cytochrome P 450 or may be converted to chloroform
via a one-electron reduction and abstraction of a proton.
Further reduction may release hydrochloric acid and carbon
monoxide. The trichloromethyl radical may alternatively
react with oxygen to form a trichloromethyl peroxy free
radical, which may react to form phosgene. This may
play a significant role in mediation of carbon tetrachloride
hepatotoxicity.
Recent studies have focused on intracellular calcium
homoeostasis. The metabolism of carbon tetrachloride
disrupts the hepatocyte ATP dependant Ca++ pump. This
results in a rise of intracellular cytoplasmic Ca++. The latter
may be a toxic second messenger that activates mechanisms
which destroy cellular membranes resulting in cell death.
Methyl bromide, and possibly some other hydrocarbons,
behave as alkylating agents and sulfhydryl enzyme
inhibitors in mammalian tissues. It has been speculated
that hexokinase and pyruvate oxidase may be especially
susceptible to inactivation by methylation of SH-groups
in the CNS. The similarity of neuropathological manifesta-
tions of methyl bromide toxicity to those seen in thiamine
deficiency may be related to effects of methyl bromide
interference with metabolism of pyruvate, where thiamine
acts as a co-factor.
Clinical Features
1. Acute Poisoning:
a. Vomiting, diarrhoea, abdominal pain, headache, leth-
argy, vertigo and stupor.
b. Headache, fatigue, confusion, altered mental status,
delirium, amnesia, incoherent speech, ataxia, inten-
tion tremor, and positive Rhomberg sign may occur.
Behavioural disturbances resembling psychosis may
be noted as an early manifestation of methyl bromide
toxicity.
Table 27.3: Hepatic Encephalopathy
Stage Mental Status Neuromuscular Changes
I Euphoria/depression, slowing of Slight tremor, ataxia
thought, slurred speech, restlessness
II Drowsiness, inappropriate behaviour, Tremor,asterixis,dysarthria, abnormal Generalised symmetric slowing, triphasic
lethargy, disorientation reflexes
III Somnolence, stupor, delirium, confu- Tremor, asterixis, muscle rigidity, abnormal Symmetric slowing, triphasic waves
sion reflexes, incontinence of urine, faeces
IV Coma Plantar extension, decerebrate
c. Liver damage results in hepatitis, jaundice, and hepatic
encephalopathy (Table 27.3). 383
d. Renal involvement is manifested by oliguria or anuria,
haematuria and renal failure.
e Additional features include acidosis, hypertension,
convulsions and respiratory failure. Hypotension,
ventricular arrhythmias, depressed cardiac muscles, fatty
degeneration, and a slowed or irregular pulse may occur.
f If alcohol has been consumed along with a halogenated
hydrocarbon, particularly carbon tetrachloride, there is
rapid onset and progression of symptoms.
g Methyl bromide intoxication is characterised by
myoclonic convulsions and permanent brain damage.
Signs and symptoms may include blurred or double
vision, nystagmus, hypotension, cough, tachypnoea,
cyanosis, lethargy, profound weakness, dizziness, slur-
Chapter 27 Hydrocarbons
ring of speech, hyperreflexia, albuminuria, haematuria,
oliguria, anuria, and impaired liver function.
h. Dermal exposure (especially by methyl bromide) may
result in second degree burns. Methyl bromide is an
intense vesicant with the capacity to penetrate protective
clothing. Skin blisters are produced, but are rarely deep
enough to destroy entire skin layer. Spillage of liquid
fumigant on the skin is likely to result in injury ranging
from erythema to vesiculation. The inflammation and
blistering can be delayed for 15 to 20 hours. Healing is
gradual, often taking several weeks. Skin contact with
many halogenated hydrocarbons, especially carbon
tetrachloride can lead to dermatitis through defatting
action. Erythema, hyperaemia, wheals, and vesicula-
tions may be seen. Gastrointestinal effects (abdominal
pain, nausea, vomiting, diarrhoea) and renal or hepatic
damage can occur even from dermal exposure.
2. Chronic Poisoning:
a. Trichloroethylene (together with ethanol) when used as
a degreaser results in intermittent skin contact producing
flushing (Degreasers flush) due to vasodilation of super-
ficial skin vessels.
b. Chronic exposure to halogenated hydrocarbon solvents
can cause Painters syndrome: headache, fatigue,
memory lapses, irritability, depression, and intolerance
to alcohol.
c. Occurrence of a protracted extrapyramidal syndrome
following low-level methyl bromide exposure has
been documented in several cases. Depression, slow
mentation, poor memory, neurosis, muscle paralysis,
EEG
Usually normal; sometimes slow (5 to 6
cycles/sec)
waves
Very slow (2 to 3 cycles/sec), delta activity
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and ataxia may be long-term or permanent disabilities
384 associated with methyl bromide poisoning. Other
long-term effects include myoclonus, difficult speech,
cognitive impairment, muscular atrophy, peripheral
neuropathy and seizure disorders.
d. Chronic exposure to carbon tetrachloride has been
possibly associated with myasthenic reaction, a defect
in neuromuscular transmission.
e. There are reports suggesting that some halogenated
hydrocarbons are carcinogenic and may cause renal
cancer (especially carbon tetrachloride, tetrachloro-
ethylene, and trichloromethane). Effects of chronic
exposure to carbon tetrachloride include liver cancer
in persons with acute poisoning, which might occur
Section 8 Hydrocarbons and Pesticides
with prior chronic exposure, even in the absence of
cirrhosis, and a possible association with brain tumours,
lymphatic leukaemias and lymphosarcomas.
Usual Fatal Dose
About 4 to 5 ml for most halogenated hydrocabons; 20 to 25 ml
for a few others. With reference to methyl bromide, airborne
concentrations as low as 100 ppm have been reported to be
harmful, while concentrations of 8,000 to 60,000 ppm may
be fatal.
Diagnosis
1. Characteristic odour in the breath.
2. Positive Fehlings test (for sugar in the urine).
3. Isonitrile Test: 10 ml of distillate or a small amount of the
suspected liquid in 10 ml of water is placed in a test tube.
To this, 1 ml of purified aniline and 2 ml of 20% sodium
hydroxide are added and gently heated. A positive result is
indicated by the development of a foul skunk-like odour
due to formation of phenyl isonitrile.
4. Gas chromatography can be used to quantitate halogenated
hydrocarbons in biological samples.
5. Carbon tetrachloride blood levels in acutely poisoned
patients ranged from 0.1 to 31.5 mg/L. 2 to 5 mg/dL are
generally considered toxic blood levels.
6. Serum inorganic bromide levels may be useful in
confirming exposure to methyl bromide and may correlate
with the clinical severity of poisoning. Values in excess of
5 mg/100 ml bromide are generally toxic. However, this is
not always the case.
7. Hepatorenal toxicity is indicated by elevated serum hepatic
aminotransferase, bilirubin, alkaline phosphatase, and
creatinine.
8. Individual serum bile acids appear to be very sensitive indi-
cators of liver damage and may be used as early indicators
of carbon tetrachloride-induced liver injury as measured
by high performance liquid chromatography. This appears
to be much more sensitive than measuring liver enzyme or
bilirubin levels.
9. A chest radiograph should be considered in patients with
respiratory symptoms. Carbon tetrachloride is radiopaque,
and some ingestions may be able to be confirmed with an
abdominal radiograph.
Treatment
1. Decontaminationdermal exposure should be treated
by stripping the patient and washing copiously with soap
and water. Eye involvement must be treated by irrigation
for at least 15 to 20 minutes. Consider administration
of activated charcoal after a potentially toxic ingestion.
Gastric lavage can also be done cautiously in potentially
lethal ingestions.
2. Administer oxygen if there is evidence of altered mental
status or respiratory failure.
3. Watch out for cardiac arrhythmias, aspiration pneumo-
nitis, and hepatorenal failure.
4. Carbon tetrachloride-induced liver cirrhosis results in bile
acids not being detoxified in the enterohepatic circulation.
In rat studies administration of cholestyramine, which has a
strong affinity for bile acids in the intestine, prevents their
enteral resorption and decreases the induction of cirrhosis.
5. N-acetylcysteine given within 8 to 10 hours after expo-
sure has been reported to prevent hepatic damage from
acute poisoning by CCl4 in humans. It is probably most
effective if given within 16 hours following ingestion of
carbon tetrachloride. Further studies are needed before
this therapy can be routinely recommended. Estimated
dose of NAC: Loading dose of 140 mg/kg orally as a 5%
solution in cola followed by a maintenance dose of 70
mg/kg orally every 4 hours for 17 doses. Alternatively,
the Prescott protocol can be followed: gastric lavage
followed by intravenous infusion of N-acetylcysteine at
150 mg/kg over 15 minutes, then 50 mg/kg over 4 hours,
followed by 100 mg/kg over 16 hours.
6. Intravenous administration of N-acetylcysteine has been
suggested as a treatment for methyl bromide poisoning
also, possibly based on the hypothesis that methyl
bromide preferentially reacts with dermal SH-groups.
N-acetylcysteine would serve as a source of SH-groups
to react with unbound methyl bromide. However, this
treatment cannot be recommended until further studies
are done to confirm efficacy.
7. Treat renal failure with dialysis and hepatic failure
with fresh frozen plasma, vitamin K, low-protein diet,
neomycin and lactulose.
8. Hyperbaric oxygen significantly improved survival and
decreased the degree of SGPT elevation in rats poisoned
with carbon tetrachloride. A review of subsequent litera-
ture suggests that hyperbaric oxygen treatment is appro-
priate treatment for carbon tetrachloride intoxication.
9. Haemodialysis is generally not effective, though an
anecdotal report suggests it may be useful in methyl
bromide poisoning. Haemodialysis or haemoperfusion
may be necessary to support patients in renal or hepatic
failure, respectively.
10. Treatment of dermal burns (methyl bromide):
 www.PharmaDost.info
a. After initial flushing with large volumes of water to
remove any residual chemical material, clean wounds
with a mild disinfectant soap and water.
b. Loose, nonviable tissue should be removed by gentle
cleansing with surgical soap or formal skin debride-
ment. Intravenous analgesia may be required.
c. Removal and debridement of closed blisters is contro-
versial. Current consensus is that intact blisters prevent
pain and dehydration, promote healing, and allow
motion; therefore, blisters should be left intact until
they rupture spontaneously or healing is well underway,
unless they are extremely large or inhibit motion.
d. Prophylactic topical antibiotic therapy with silver
sulfadiazine is recommended for all burns except
superficial partial thickness (first-degree) burns.
Systemic antibiotics are generally not indicated
unless infection is present or the burn involves the
hands, feet, or perineum.
e Depending on the site and area, the burn may be
treated open (face, ears, or perineum) or covered with
sterile nonstick porous gauze. The gauze dressing
should be fluffy and thick enough to absorb all
drainage. Alternatively, a petrolatum fine-mesh gauze
dressing may be used alone on partial-thickness burns.
f. Analgesics such as paracetamol with codeine may
be used for pain relief if needed.
g. Tetanus toxoid 0.5 ml intramuscularly (or other indi-
cated tetanus prophylaxis) should be administered if
required.
Autopsy Features
1. Characteristic odour.
2. Petechiae in the brain, airways, and lungs.
3 Pulmonary oedema.
4. Fatty degeneration, cardiomegaly
5. Renal and hepatic necrosis. Large foci of centrilobular
necrosis of the liver with normal portal vasculature was
reported at autopsy of a 36-year-old female following a
fatal methyl bromide exposure.
Forensic Issues
Most cases are accidental in nature arising out of occupa-
tional exposure. There have been cases of suicidal ingestion
involving one or other of these compounds.
FURTHER READING
385
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