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Hair dye presentation

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Hair dye uses and health implications

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Hair dye presentation

  1. 1. Hair dye
  2. 2. 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
  3. 3. 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
  4. 4. •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.
  5. 5. •Natural black hair color is due to melanin clusters of dispersed within the colorless keratin-based cortex of hair.
  6. 6. • 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 . history of hair dye
  7. 7. Pharaoh Ramesses II ,reddish-yellow colour of the mummy's hair had been brought about by its being dyed with a dilute henna solution;
  8. 8. 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.
  9. 9. • In 1907, Eugè ne Schueller, a young French chemist, developed an innovative hair-colour formula. He called his improved hair dye Auréole. Schueller formulated and manufactured his own products, which he then sold to Parisian hairdressers.
  10. 10. Who wants to dye too?
  11. 11. Types of Hair color most common classifications • Temporary • Semi-Permanent • Demi-Permanent: – Oxidative Deposit -Only • Permanent: – Non-Oxidative – Lift/Deposit – Oxidative
  12. 12. 1.Temporary : • 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 Coating action(adsorbtion)
  13. 13. 1.Temporary: • 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
  14. 14. 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
  15. 15. • 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
  16. 16. • 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
  17. 17. 2.Semi-Permanent Hair Colors Also known as: • Oxidation Tints • Penetrating Tints • Peroxide Tints • Synthetic Organic Tints • Para-dyes • “Tints”
  18. 18. 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.
  19. 19. 2-Semi-permanent hair color: 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
  20. 20. A.Semi-Permanent - 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.
  21. 21. 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.
  22. 22. 2.A. Semi-Permanent - Traditional • Less damaging than permanent dyes since it does not lighten. • Causes a mild chemical and physical change in the hair shaft Dye molecules
  23. 23. 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
  24. 24. 3.Demi-Permanent : (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.
  25. 25. 3.Demi-Permanent: • 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
  26. 26. 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.
  27. 27. 4.Permanent : 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
  28. 28. 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
  29. 29. Dye deposited in cortex
  30. 30. • 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?
  31. 31. 5.Permanent: 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
  32. 32. 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
  33. 33. 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,
  34. 34. Paraphenylene Diamine (PPD( paraphenylenediamine, or 1,4-diaminobenzene, or 1,4-phenylenediamine
  35. 35. 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(
  36. 36. Black stone dye
  37. 37. • PPD is a precursor to aramid plastics and fibers such as Kevlar. • dyeing furs • Photochemical measurements • azo-dye manufacturing Kevlar (p-aramid fibre) dyeings uses
  38. 38. • 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 .
  39. 39. 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
  40. 40. • PPD is metabolized by cytochrome P450 oxidase to form a reactive metabolite Bondrawski’s base ,a compound reported to cause anaphylaxis as well as being strongly mutagenic and highly toxic • Excreted by kidneys
  41. 41. 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:
  42. 42. • 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 Ludwig’s 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
  43. 43. • 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
  44. 44. 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
  45. 45. 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
  46. 46. 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.
  47. 47. 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 . •
  48. 48. • 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
  49. 49. 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
  50. 50. 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
  51. 51. 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.
  52. 52. • 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
  53. 53. 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.
  54. 54. 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 •
  55. 55. • 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%. Management
  56. 56. Thank you Nashwa mostafa

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