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Hair dye

What is hair dye?


Hair Dye or Hair Color: is
a chemical tool that is used
to change the color of a
person's hair.
used mostly to change
gray hair; a sign of an
advanced age.
Younger people that used
hair dye use it as a fashion
About our Hair:
Human hair is made of keratin, water and dead cells
Each strand of hair is made up of three layers;
Cuticle ,Cortex& Medulla
Cuticle is made up of scale-like, overlapping
protein cells which protect the
cortex
A healthy hair: when the cuticle lie flat
around the hair shaft.
A damaged hair is when the cuticle of the
hair is raised.
Natural black hair
color is due to melanin
clusters of dispersed
within the colorless
keratin-based cortex
of hair.
history of hair dye
French researchers have found that
Egyptians, Greek and Romans were using to
dye their hair several thousands years ago
Since the Greco-Roman period, organic
hair dyes obtained from plants such as
henna have been used, but other unusual
formulas based on lead compounds which
generated lead sulfide (PbS) nanocrystals
with a diameter of only 5
nanometers .
Pharaoh Ramesses II ,reddish-yellow
colour of the mummy's hair had been
brought about by its being dyed with a
dilute henna solution;
They found that the treated hair showed the
presence of galena nanocrystals(under 5 nm). but
these blackening PbS particles are much smaller than
melanin clusters by 4-5 orders of magnitude in
.volume
In 1907, Eugne
Schueller, a young
French chemist,
developed an innovative
hair-colour formula. He
called his improved hair
dye Aurole. Schueller
formulated and
manufactured his own
products, which he then
sold to Parisian
hairdressers.
?Who wants to dye too
Types of Hair color

most common classifications


Temporary
Semi-Permanent
Demi-Permanent:
Oxidative Deposit -Only
Permanent:
Non-Oxidative
Lift/Deposit
Oxidative
1.Temporary : Coating action(adsorbtion)
The pigment molecules
are large and cannot
penetrate the cuticle
layer. Instead, the color
particles remain
adsorbed (closely
adherent) to the hair
shaft and are easily
removed with a single
shampooing Dye molecules
:Temporary. 1
There is a physical action (coating) on the hair,
not chemical action (penetrating).
Does not lighten or change the structure of the
hair.
These are the least hazardous of all dyes. (food
grade dyes )
Spray-on temporary haircoloring that contain
metallic salts can build-up and can cause
adverse chemical reactions with future
chemical services.
These dyes are flammable
2.Permanent hair colors:
are the most popular hair dye
products
Permanent hair-coloring dyes consist
of three components. They are:
Primary intermediates & Couplers(the
color)
Oxidants (Hydrogen peroxide )
An alkali usually ammonia
The primary intermediates form color on
oxidation.
The modern permanent dyes consists of
solutions of paraphenylenediamine (PPD),
or similar para compounds.
Couplers will react with the oxidized
products of the primary intermediates and
form dyes which are then applied to hair.
Hydrogen peroxide is a major factor in
permanent hair coloring techniques
Hydrogen peroxide
diffuses the melanin,
and lightens the
natural color of hair
Ammonia causes
cuticle to swell and
separate
Both agents called the
developer
Dye
molecules
Semi-Permanent Hair Colors. 2

Also known as:


Oxidation Tints
Penetrating Tints
Peroxide Tints
Synthetic Organic Tints
Para-dyes
Tints
2-Semi-permanent hair
color:
Uses smaller molecules than
temporary dyes, and is
therefore able to partially
penetrate the hair shaft.
the color survives repeated
washing, 4-5 shampoos.
Semi-permanents contain no,
or very low levels of developer,
peroxide or ammonia.
:Semi-permanent hair color-2
Chemicals of Concern :
use Aniline Derivative Tints from Para-
Phenylediamines
Darker dyes have more phenylediamine
Health Affects
Skin, eye, respiratory sensitizer
Severe allergies e.g., facial and neck swelling
Dermatitis e.g., rashes
Mutagenic when mixed with peroxide
Semi-Permanent A.
- Traditional
Azo Colors
Derived from from
benzidine, a known
carcinogen.
Can revert back to
benzidine in the body.
Azo Direct Black 38 and
Direct Blue 6 are
carcinogenic in their own
right.
:Mechanism of hair dyeing
Uses a medium size molecule.
causes a slight alkaline reaction to swell the hair
shaft, causing the cuticle to rise.
This allows some color molecules to enter the
cortex, and some to coat the cuticle.
A neutral or slightly acid after-rinse is used to stop
the alkaline swelling reaction, allow the cuticle to
close, and trapthe color molecules inside.
Less damaging than permanent dyes since it does
not lighten.
Causes a mild chemical and physical change in the
hair shaft.
A. Semi-Permanent -. 2
Traditional Dye
molecules
Less damaging than
permanent
dyes since it does not
lighten.
Causes a mild
chemical and
physical change in the
hair shaft
B. Semi-Permanent - Polymer
different chemical
composition.
They combine many
molecules to form a
polymer. Polymers coat
the hair shaft rather
than penetrate. They
do not change the
melanin.
Heat is used to deepen
the color penetration
rather than the use of
the chemical oxidation
process
Demi-Permanent : . 3
(Oxidative Deposit-Only)

Process falls between the semi-permanent and


permanent dye process.
Uses a catalyst such as a 10% mild peroxide
developer with a non-ammonia alkali to swell
the cuticle, allow dye molecules to penetrate
into the cortex and deposit color inside the
hair shaft.
A neutral or slightly acid after-rinse is used to
stop the alkaline swelling reaction, allow the
cuticle to close, and trapthe color molecules
inside.
The mild chemical reaction does not lighten the
melanin and hardly changes the hair structure.
:Demi-Permanent. 3
Chemicals of Concern : Uses
mostly aniline derivative dyes.
The alkali (high pH) used to
swell the cuticle is from either
monoethanolylamine (MEA) or
amino methyl propanol (AMP).
MEA is a pH adjuster that can
release nitrosamines which
cause cancer in animals and can
cause severe eye irritation in
humans
dye
Demi-permanents : advantages over
permanent color:
no lifting (removal) of natural hair color
the final color is more natural looking.
safer, especially for damaged hair,
wash out over time (typically 20 to 28
shampoos), so root regrowth is less
noticeable ,
if a change of color is desired, it is easier
to achieve.
Permanent :. 4
Oxidative/Lift Deposit
These hair colors have the smallest molecule
which makes it easier for them to
penetrate the hair shaft and the scalp.
This process has the greatest impact on
the hair structure, which is permanently
changed, and the cuticle remains slightly
shifted
Formulas can have ranges of:
Phenylediamine .08% to 6%
Hydrogen Peroxide 3 10% 20 40%
Ammonia Resorcinol
Mechanism of hair dyeing
Oxidative/Lift Deposit
An alkaline reaction(most often ammonia )
causes the cuticle to swell, allowing
hydrogen peroxide and dye to enter.
The hydrogen peroxide oxidizes
(diffuses) the melanin, and lifts
(lightens) the color.
The hydrogen peroxide also causes the
dye to develop and deposit color.
A neutral or slightly acid after-rinse
stops the alkaline reaction, allows the
cuticle to
Close, and traps the color molecules inside
Dye deposited in
cortex
Permanent?
Permanent color is truly permanent and will
not wash out, although it may fade. New
hair regrowth will obviously be in the
hair's natural color. .
Permanent hair color is the only way to dye
dark hair into a lighter shade, and it must
be done in two parts: First, the hair is
lightened, then color is applied.
Permanent:. 5
Non-Oxidative
Vegetable Tints:
Made from plant
materials and henna
Builds up layers in hair
shaft
Problems with Vegetable
Tints:
Henna can trigger asthma
and other allergic reactions
Metallic Dyes:
Contain metallic salts from lead acetate, lead,
copper, cobalt, silver nitrate
Not used professionally .toys ,furs
Compound Dyes:
Mix of vegetative tints and metallic dyes
Not used professionally
Problems with Metallic Dyes
Can cause headaches, scalp irritation, facial
swelling, contact dermatitis, lead poisoning,
and hair breakage, toxic,.
Bottles of metallic dyes can explode
Hair dye poisoning
one of the important causes of
accidental or intentional self harm in
the developing world.
PPD is the most common constituent
of hair dye formulations. PPD is
commonly used in Africa, Middle East
and Indian subcontinent while it is
rarely used in the west,
Paraphenylene Diamine
(PPD)
paraphenylenediamine,
or
1,4-diaminobenzene,
or 1,4-phenylenediamine
PPD
This derivative of aniline,
aromatic amine, is a
colourless solid when
pure but are partially
oxidized and appear
yellowish.
Some misinformation has
led to PPD being
described as a black
mineral from the bank of
the River Nile. This gave
PPD an undeserved
distinction as being
natural. (PPD crystals)
Black stone dye
uses
PPD is a precursor to
aramid plastics and Kevlar (p-aramid fibre)
dyeings
fibers such as
Kevlar.
dyeing furs
Photochemical
measurements
azo-dye
manufacturing
as a hair dye
mixed with Henna to
color palms of hands and
soles of feet and to dye
hair a dark red shade .
it was also used to kill
wild animals when added
to food .
Toxicity of PPD
First case of PPD poisoning was reported in
a hairdresser in 1924 following exposure
due to PPD dye handling.
PPD is readily absorbed on dermal contact.
Six children in a series of 31 Sudanese
children with PPD poisoning were reported
not to have ingested hair dye. An Arab
lady developed acute life threatening
pulmonary edema after she had painted
one hand with a henna mixture.
PPD poisoning commonly by ingestion
PPD is metabolized by
cytochrome P450 oxidase to
form a reactive metabolite
Bondrawskis base ,a
compound reported to cause
anaphylaxis as well as being
strongly mutagenic and highly
toxic
Excreted by kidneys
Clinical manifestations
PPD intoxication is a life threatening
condition.
Clinical outcomes rely on early recognition,
prompt referral, and aggressive supportive
treatment in collaboration with different
specialties.
The toxicity of PPD is a multisystem
involvement.
The initial presentation may be confusing
and most deaths occur within hours of
admission. A typical case is illustrated by
the following account:
six-year old child presented with sore
throat, cough and anorexia followed by
severe dyspnoea caused by edema of the
tongue, pharynx and neck. He developed
AKI and metabolic acidosis. The initial
diagnosis was Ludwigs angina. Despite
initiation of vigorous supportive therapy,
the child developed irreversible
ventricular fibrillation and died eight
hours after admission. It was discovered
later that the child and his dog ingested a
hair dye containing PPD, and the dog died
few hours later
Another victim of PPD intoxication died
of cardiac complications, which
occurred 4 hours after admission
despite intensive supportive measures
Clinical scenarios are variable and
range from a local skin reaction to
multisystem involvement
. It is very important to obtain a
psychosocial history and evaluate the
home environment as many cases were
found to be precipitated by severe
psychiatric disturbances
Skin and eye manifestations
. Nowadays, it is well
known that PPD cause
skin irritation, kerato-
conjunctivitis,
conjunctival swelling and
eczema of the eyelids.
Allergic reactions
causing dermatitis,
urticaria and asthma
have also been reported
Respiratory system and upper airway
manifestations
One of the most severe
clinical manifestations
and the main cause of
death in PPD poisoning is
upper airway obstruction
(angio-edema)
manifesting with a hard
swollen protruding
tongue and edematous
bull neck.
required tracheostomy
for upper airway
obstruction
Kidney manifestations
The cardinal features of myoglobinuria
(dark-colored, chocolate-brown urine),
The extent of renal involvement varies
between transient proteinuria and oliguric
ARI. ARI commonly develops a few days
after PPD exposure.
The kidney injury :due to the direct toxic
effect of PPD, hypovolumia, hemolysis and
rhabdomyolysis with the deposition of
myoglobin casts within the renal tubules.
Neuromuscular toxicity
Rhabdomyolysis, which in turn
contributes to AKI and the increased
likelihood of sudden cardiac death .
skeletal and cardiac muscle necrosis
could be experimentally induced by
PPD. Scattered coagulative necrosis
of skeletal muscles was found in the
autopsy of a PPD victim .

Increased free radical formation in PPD


poisoning may be responsible for the
deleterious tissue damage observed in animal
studies .
Flaccid paraplegia, palato- pharyngeal and
laryngeal paralysis were also reported in
adults and children .
Neurotoxicity causing mental alteration and
coma was also observed and was possibly
related to brain anoxia and severe metabolic
acidosis associated with AKI
Other manifestations
Tender palpable liver with features of acute
hepatitis on liver biopsy was seen in many
patients.
Cardiac toxicity causing arrhythmia, heart
block and sudden death was also reported in
some studies.
It is commonly the direct cause of death in
children and adults with PPD poisoning.
Cardiac toxicity is mainly caused by the
direct toxic effect of PPD on the heart,
rhabdomyolsis of the cardiac muscle causing
severe damage and hyperkalemia
:Diagnosis
The symptoms are considered to be dose
related and patients with ingestion of
larger amounts of PPD have higher
morbidity and mortality.
Onset of symptoms after ingestion of the
dye is about 4-6 hours.

The major early challenge to life is


asphyxia and renal failure at later stages
Diagnosis :
The characteristic triad of
features encountered is early
angioneurotic edema with
stridor, rhabdomyolysis with
chocolate colored urine and
acute renal failure. When ever
this combination occurs in
poisoning, hair dye is a strong
suspect.
Other reported features are leukocytosis,
anaemia secondary to hemolysis,
haemoglobinaemia and haemoglobinuria.
Toxic features include methemoglobinaemia,
gastritis, hoarseness of voice, hepatitis,
convulsions, coma .
Hypotensive shock
markedly elevated creatinine phosphokinase
and lactate dehydrogenase, hyperkalemia,
hyperphosphatemia and hypocalcemia
Management
Hair dye ingestion is a medical emergency.
Emergency measures should include gastric
lavage. Patients should be monitored for
respiratory distress and endotracheal
intubation has to be performed early if
laryngeal edema develops.
Metabolic acidosis has to be corrected.
Early intervention with half normal saline
and soda bicarbonate infusion has been
shown to be beneficial in Rhabdomyolysis.
Management

All modalities of dialysis:


hemodialysis, peritoneal dialysis and
continuous renal replacement therapy
have been tried and have been found
to be useful in acute renal failure.
Antihistamines and steroids are
commonly used because of the
possibility of a hypersensitivity
reaction to PPD

Management
Alkaline diuresis using isotonic saline,
sodium bicarbonate and diuretics is
used in the management of
myoglobinuria
There is no specific antidote
available,
However, dialysis is an effective
supportive measure in case of oliguric
or anuric AKI .
Mortality rates vary between 0.03%
and 60%.
Thank you
Nashwa mostafa