Toxicity of aluminum signs

1. Toxicity of Aluminum
• Although aluminum is not a real heavy metal (specific
gravity of 2.55-2.80), it makes up about 8% of the surface
of the earth.
• It is readily available for human ingestion through the
use of food additives, antacids, buffered aspirin,
astringents, nasal sprays, and antiperspirants; from
drinking water; from automobile exhaust and tobacco
smoke; and from using aluminum foil, aluminum
cookware, cans, and ceramics .
• DFO is the recommended chelating agent in treatment of
acute toxicity of aluminum.

2. • Aluminium has no known function in living cells and presents
some toxicity if it is consumed in excessive amounts.
• Its toxicity can be traced to deposition in bone and the central
nervous system, which is particularly increased in patients with
reduced renal function.
• Because aluminium competes with calcium for absorption,
increased amounts of dietary aluminium may contribute to the
reduced skeletal mineralization and muscleoskeletal weakness.
• A small percentage of people are allergic to aluminium and
experience contact dermatitis, digestive disorders, vomiting or
other symptoms upon contact or ingestion of products
containing aluminium, such as deodorants or antacids.
• In very high doses, aluminium can cause neurotoxicity, and is
associated with altered function of the blood-brain barrier.
Many studies have suggested that aluminum might have a
possible connection with developing Alzheimer's disease.

3. Sulfur Dioxide (SO2)
• Sulfur dioxide is colorless, non-flammable gas heavier
than air. With strong, suffocating odor (rotting eggs) and
readily soluble in water. It is It extremely irritating to skin
and eyes and to the mucosa of respiratory tract.
• SO2 is a major air pollutant and has significant impacts
upon human health. It is produced naturally from the
decay of vegetation, volcanic eruption and in various
industrial processes like coal and petroleum combustion.
• SO2 combines easily with water vapor, forming aerosols
of H2SO3, a colorless, mildly corrosive liquid that may
then combine with oxygen in the air, forming the even
more irritating and corrosive H2SO4 (main constituent of
acid rain) that influence the environment suitability for
plant communities as well as animal life.

4. • The Major route of toxicity is inhalation (in
addition to eye and skin irritantion) . SO2 tends
to adhere to air particles and enter the inner
respiratory tract, where they are not effectively
removed.
• In the respiratory tract, SO2 combines readily
with water vapour to form sulfurous acid,
resulting in irritation of mucous membranes and
bronchial constriction.
• This irritation in turn increases the sensitivity of
the airway to other airborne toxicants and
cause pulmonary infection from destruction of
the ciliated epithelium
Sulfur Dioxide

5. Acute toxicity:
o Respiratory symptoms
– Upper respiratory tract irritation
– Rhinorrhea and expectoration
– Choking and coughing
– Nosebleeds and difficulty in swallowing
– Oropharyngeal erythema, glotic and pulmonary edema.
– Within 5 minutes temporary reflex bronchoconstriction
with Increased airway resistance.
– Asphyxiation from severe glottal edema and bronchiolar
constriction
– Loss of sensation of smell has been reported.
– Pulmonary infection and pulmonary pneumonia is a
common complication.
symptoms

6. SO2 symptoms of toxicity
o Eye symptoms:
– Severe irritation, lacrymation, photophobia and
conjunctival inflamation
– In sever forms of direct contact with liquefied sulfur
dioxide, corneal epithelium becomes grey and irregular, eye
lid becomes swollen, conjunctival epithelium appears white
and opaque.
– Blindness may occur.
o Other symptoms:
– Dermal Irritation, urticarea, and burns. More promenent
when contact with moist skin.
– Nausea, vomiting, and abdominal pain.
– Metabolic acidosis may occur and disorders in CHO and
protein metabolism

7. Treatment:
• No specific antidote is available. Care is only supportive
• Move patient to fresh air. Monitor for respiratory
distress. Treat bronchospasm with inhaled β2 agonist
and oral or parenteral corticosteroids.
• Administer 100% supplemental humidified oxygen with
assisted ventilation as required.
• Endotracheal intubation, may be needed if upper
airway obstruction occurs.
• Inhaled sympathomimetic bronchodilators (e.g.
albuterol) may be useful to treat bronchospasm.
• In acidotic patient, we anticipate seizures and treat with
anticonvulsants e.g. diazepam
Sulfur Dioxide

8. • For eye exposure: Irrigate exposed eyes with
copious amounts of room temperature water
for at least 16 minutes. If irritation, pain,
swelling, lacrymation, or photophobia persist,
the patient should be seen in a health care
facility.
• For dermal exposure: decontaminate and treat
skin irritation and burns topically, cover skin
burns with sterile dressings.
Treatment of SO2

9. Toxicity of hydrocarbons

10. • Hydrocarbons are a heterogenous group of organic
substances that are primarily composed of carbon and
hydrogen molecules. They are quite abundant in modern
society.
• Some of the most commonly ingested hydrocarbons
include gasoline, lubricating oil, motor oil, mineral spirits,
lighter fluid/naphtha, lamp oil, and kerosene.
• Other common sources of hydrocarbons include dry
cleaning solutions, paint, spot remover, rubber cement,
and solvents.
• In addition, many volatile substances that contain
hydrocarbons (eg, glue, propellants) are commonly
abused for their euphoric effects.

11. • Hydrocarbons can be classified as being
aliphatic, in which the carbon moieties are
arranged in a linear or branched chain, or
aromatic, in which the carbon moieties are
arranged in a ring.
• Halogenated hydrocarbons, in which one of the
hydrogen molecules is substituted by a halogen
group. The most important halogenated
hydrocarbons include carbon tetrachloride,
trichloroethylene, tetrachloroethylene,
trichloroethane, chloroform, and methylene
chloride.

13. • Toxicity from hydrocarbon ingestion can
affect many different organs, but the lungs
are the most commonly affected organ.
• The chemical properties of the individual
hydrocarbon determine the specific toxicity,
while the dose and route of ingestion affect
which organs are exposed to the toxicity.
• Unlike the aromatic or aliphatic
hydrocarbons, the halogenated
hydrocarbons tend to cause a wider range
of toxicity.

14. Pathophysiology
• The toxicity of hydrocarbons is directly related
to their physical properties, specifically the
viscosity, volatility, surface tension, and
chemical activity.
• lower viscosity is associated with a higher
chance of aspiration.
• the surface tension is also inversely related to
aspiration risk
• the degree of volatility is directly related with
the risk of aspiration.

16. Pulmonary
• Pulmonary complications, especially aspiration,
are the most frequently reported adverse
effect of hydrocarbon exposure.
• While most aliphatic hydrocarbons have little
GI absorption, aspiration frequently occurs,
either initially or in a delayed fashion as the
patient coughs or vomits, thereby resulting in
pulmonary effects.
• Once aspirated, the hydrocarbons can create a
severe pneumonitis.

17. • Cardiovascular
• Exposure to hydrocarbons can result in cardiotoxicity.
• Most importantly, the myocardium becomes
sensitized to the effects of catecholamines, which
can predispose the patient to tachydysrhythmias,
which can result in syncope or sudden death.
• Gastrointestinal
• Many of the hydrocarbons create a burning
sensation because they are irritating to the GI
mucosa.
• Vomiting has been reported in up to one third of all
hydrocarbon exposures.

18. Hepatic
• The chlorinated hydrocarbons, in particular carbon
tetrachloride, are hepatotoxic.
• Usually, the hepatotoxicity results after the
hydrocarbon undergoes phase I metabolism, thereby
inducing free radical formation.
• These free radicals subsequently bond with hepatic
macromolecules and ultimately cause lipid
peroxidation. This metabolite creates a covalent bond
with the hepatic macromolecules, thereby initiating
lipid peroxidation.
• The common histopathologic pattern is centrilobular
(zone III) necrosis.

19. • Renal chronic exposure to toluene, an
aromatic hydrocarbon, can result in a distal
renal tubular acidosis
• Hematologic
• Prolonged exposure to certain aromatic
hydrocarbons (especially benzene) can lead to
an increased risk of aplastic anemia, multiple
myeloma.
• In addition, hemolysis has been reported
following the acute ingestion of various types
of hydrocarbons.

20. Signs and symptoms
• Pulmonary toxicity most often occurs
following ingestion and subsequent aspiration
of hydrocarbon. Respiratory symptoms (eg,
coughing, gagging, choking) usually occur
within 30 minutes of exposure but often can
be delayed several hours.
• Lack of coughing does not exclude the
possibility of aspiration.
•

21. • The most common CNS symptoms include headache,
lethargy, and decreased mental status.
• in addition, because of sensitization of the myocardium to
catecholamines, a relatively young and previously healthy
patient can present in full cardiac arrest after being
suddenly startled or following strenuous athletic events.
• A common scenario for the cardiac arrest patient is the
teenager who is huffing, or bagging alone in a dark room,
who then gets startled when a parent opens the door.
This "sudden sniffing death syndrome" results in
ventricular fibrillation or ventricular tachycardia, following
a large catecholamine exposure to a myocardium that is
already sensitized to the effects of the catecholamines.

22. Work up
• 1- CBC
• 2- LIVER ENZYMES
• 3- CHEST RADIOGRAPHY
• All symptomatic patients should have a chest x-
ray performed.
• Patients who are asymptomatic (eg, no coughing
or signs/symptoms of respiratory distress) should
not have a chest radiograph obtained
immediately. Rather, asymptomatic patients
should have chest radiography performed at the
end of a 6-hour observation period.
• 4- ECG

23. Managment
1. remove any remaining hydrocarbon that might be on the
clothes or skin
2. Patients should be kept calm to prevent arrhythmia as a
result of myocardial sensitization.
3. All patients should have their airway, breathing, and
circulation managed per routine advanced life support
protocols.
4. Symptomatic patients should receive intravenous access
and cardiac monitoring.
5. The hydrocarbon agent should be transported with the
patient to the hospital, if this can be done in a safe manner.
Bringing the substance to the hospital can permit
identification.

24. • Management for hydrocarbon intoxication
is largely supportive.
• Asymptomatic patients should be observed
with continual pulse-oximetry for a period
of at least 6 hours. If the patient remains
asymptomatic (eg, no coughing, vomiting,
tachypnea, or other evidence of respiratory
difficulties), then a chest radiograph may
be obtained to evaluate for aspiration.

25. • Patients who show signs of impending respiratory failure
despite supplemental oxygen may require rapid sequence
intubation for definitive airway management. Intubation
and positive pressure ventilation may be required for
evidence of on-going respiratory distress.
• If arrhythmias occur, electrolytes, including magnesium
and potassium, should be replaced.
• If ventricular fibrillation occurs, and the thought is that the
arrhythmia is because of myocardial sensitization,
catecholamines, including epinephrine, should be avoided.
In this setting, lidocaine or beta-blockers can be used.
• Decontamination of the GI tract remains controversial.

26. • The use of ipecac-induced emesis is
contraindicated, and activated charcoal does
not absorb hydrocarbons well.
• Antibiotics are frequently given to patients
who develop a pneumonitis following
hydrocarbon aspiration. In animal models,
the empiric administration of antibiotics
altered the lung flora compared with
controls and did not yield any benefit.
Clinically, superinfection can definitely occur
• Steroids have not been proven to be
beneficial.

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