History

Fact Explanation
Nausea vomiting and abdominal pain Lead is a compound in most of cosmetic products. Gastrointestinal manifestations of lead poisoning include chronic or recurrent abdominal pain, nausea, vomiting, constipation, bloating, anorexia and weight loss.[4].
Fatigue , nervousness and/or irritability Mercury-containing compounds have historically been used in germicidal soap seething powders, medications for psoriasis and syphilis,Chinese patent medicines, and skin preparations including skin-lightening creams.Mercurial compounds can be absorbed through intact skin.Toxic renal, neurological, and dermal effects related to the use of topically applied products have been documented in the literature since the early 20th century.fatigue (67%), nervousness and/or irritability (63%),are common complains of mercury poisoning.[3].
Severe headache Beauty Cream users self-reported a high prevalence of symptoms associated with mercury poisoning. They are fatigue (67%), nervousness and/or irritability (63%),severe headaches (61%).[3].
Infertility Traditional remedies and eye cosmetics, and snooker chalks are source of lead. Lead causes testicular injury and infertility in men and interferes with implantation of fertilized ovum in the uterus in women.[1].
Damage to the fetus. Lead that contain in cosmetics, is stored in bones and it can be released in blood during pregnancy when there is calcium deficiency. Absorption of lead increases if there is concomitant iron or calcium deficiency. 95% of absorbed lead accumulates in bones or teeth. Half life of lead in soft tissue pool is 40 to 50 days whereas it is 10 to 20 years in skeletal pool.This is an important source of exposure to fetus as it freely crosses the placenta.[1].
Renal damage Also occurs due to lead poisoning which include in certain cosmetic products. Excretion of lead is 90% through kidney and 10% through bile. If intake exceeds 3.5 μg/kg/day accumulation in the body occurs.Clinical manifestations are diverse and involve multiple body systems. Glycosuria, aminoaciduria and phosphaturia occur due to reversible renal tubular dysfunction. Renal impairment secondary to renal interstitial fibrosis is irreversible.[1]
Acute lead encephalopathy Acute lead encephalopathy is most severe presentation of lead poisoning and has been reported to occur after use of lead containing eye cosmetic, kohl on the umbilical stump of newborns.[1].
lower IQ, cognitive deficits and growth retardation. Several studies carried out in the past two decades have proven that fetal and early childhood exposure to low doses of lead results in lower IQ, learning, reading and hearing deficits and physical growth retardation. A 2 to 4 point IQ deficit occurs for each microgram/deciliter increase in blood lead levels beyond the reference level (10 μg/dL.). Recent evidences indicate that blood levels between 5-10 μg/dL can also cause cognitive deficits in children, and thus no levels in blood are safe.[1].
Metallic taste in the mouth About 20% of people found to have metallic taste in the mouth due to mercury poisoning in beauty products.[3].
Insomnia and memory loss Also occurs due to mercury poisoning in cosmetic products. Insomnia reported among 51%, memory loss about 44% of people.[3].
Rhabdomyolysis with acute renal failure Hair dyes contain paraphenylene-diamine and a host of other chemicals that can cause rhabdomyolysis, laryngeal edema, severe metabolic acidosis and acute renal failure. Intervention at the right time has been shown to improve the outcome.PPD can bring about rhabdomyolysis by promoting calcium release and leakage of calcium ions from the smooth endoplasmic reticulum, followed by continuous contraction and irreversible change in the muscle's structure. Rhabdomyolysis is the main cause of acute renal failure and the morbidity and mortality are high once renal failure develops. Hypovolemia and the direct toxic effects of PPD or its metabolites on the kidneys also contribute.[2].
Asphyxia and respiratory failure Reported to be occurred due to hair dye poisoning.The respiratory syndrome following the ingestion of PPD is represented by asphyxia and respiratory failure secondary to inflammatory edema involving cricopharynx and larynx.[2].
Convulsion Can occur due to Paraphenylenediamin (PPD) poisoning which frequently contain in hair dye.[5].
Contact dermatitis Severe contact dermatitis is reported due to PPD poisoning.[5].
Bone changes Lead intoxication produces an array of effects on human skeletal system.These effects include perturbation of bone development, bone formation, and bone resorption.The developing skeleton seems more sensitive to lead than the adult skeleton.Lead readily crosses the placenta. Human congenital lead poisoning is associated with overt skeletal toxicity evidenced by dense cranial vault and delayed skeletal and deciduous dental development at birth.Postnatal growth of children also appears sensitive to chronic, low-level lead intoxication.Lead intoxication directly and indirectly alters many aspects of bone cell function. First, lead may indirectly alter bone cell function through changes in the circulating levels of those hormones, particularly 1,25-dihydroxyvitamin D3, which modulate bone cell function. Second, lead may directly alter bone cell function by perturbing the ability of bone cells to respond to hormonal regulation.Third, lead may impair the ability of cells to synthesize or secrete other components of the bone matrix, such as collagen or bone sialoproteins (osteopontin).Finally, lead may directly effect or substitute for calcium in the active sites of the calcium messenger system, resulting in loss of physiological regulation.[6].
Endothelial injury and hemorrhage The toxic metals like lead can target the vascular system in a variety of ways, ranging from hemorrhagic injury to subtle pathogenic remodeling and metabolic changes.The vascular endothelium consists of specialized epithelial-like cells that line the lumenal surface of all blood vessels and form the capillary networks that mediate the delivery of oxygen and nutrients to tissues of the body. Obviously, vascular endothelial cells would be exposed to any toxic metal(s) circulating in the blood stream and, if the metals are present at sufficiently high concentrations, the endothelial cells could be injured or killed. The resulting loss of endothelial barrier integrity would result in edema and hemorrhaging in various tissues. Indeed, acute exposure to high levels of many metals has been shown to cause hemorrhaging in tissues such as the lung. [7].
References
  1. MADHUSUDHANAN M, LALL SB. Acute Lead Poisoning In an Infant Oman Med J [online] 2007 Oct, 22(3):57-59 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294150
  2. SAMPATHKUMAR K, YESUDAS S. Hair dye poisoning and the developing world J Emerg Trauma Shock [online] 2009, 2(2):129-131 [viewed 01 September 2014] Available from: doi:10.4103/0974-2700.50749
  3. WELDON MM, SMOLINSKI MS, MAROUFI A, HASTY BW, GILLISS DL, BOULANGER LL, BALLUZ LS, DUTTON RJ. Mercury poisoning associated with a Mexican beauty cream West J Med [online] 2000 Jul, 173(1):15-18 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1070961
  4. BEGOVIC V, NOZIC D, KUPRESANIN S, TARABAR D. Extreme gastric dilation caused by chronic lead poisoning: A case report World J Gastroenterol [online] 2008 Apr 28, 14(16):2599-2601 [viewed 01 September 2014] Available from: doi:10.3748/wjg.14.2599
  5. GUDE D, BANSAL DP, AMBEGAONKAR R, PRAJAPATI J. Paraphenylenediamine: Blackening more than just hair J Res Med Sci [online] 2012 Jun, 17(6):584-586 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634302
  6. POUNDS JG, LONG GJ, ROSEN JF. Cellular and molecular toxicity of lead in bone. Environ Health Perspect [online] 1991 Feb:17-32 [viewed 03 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1519349
  7. PROZIALECK WC, EDWARDS JR, NEBERT DW, WOODS JM, BARCHOWSKY A, ATCHISON WD. The Vascular System as a Target of Metal Toxicity Toxicol Sci [online] 2008 Apr, 102(2):207-218 [viewed 03 September 2014] Available from: doi:10.1093/toxsci/kfm263

Examination

Fact Explanation
Anemia Lead is a compound of most of the cosmetics. Anemia in lead poisoning may be microcytic or normocytic hypochromic with red cells showing punctate basophilia. Haemolytic anemia is seen in severe lead poisoning.[1].
Lead lines in gums Lead lines in gums are due to blue colouration of the margins from lead sulphite deposits.[1]
Hypertension Also resulted due to lead poisoning in certain cosmetic use.[1].
Angioneurotic edema with stridor Hair dye poisoning has been emerging as one of the important causes of intentional self harm in the developing world.The characteristic triad of features encountered are early angioneurotic edema with stridor, rhabdomyolysis with chocolate colored urine and acute renal failure.[2].
Electrolytes imbalance and acidosis Found to be resulted due to hair dye poisoning.Rhabdomyolysis and metabolic acidosis were seen. hyperkalemia also a well recognized feature. In myoglobinuric ARF severe hypocalcemia and hyperuricemia during the oliguric phase and hypercalcemia during the diuretic phase are characteristic.[2].
Myocarditis and arrhythmias PPD contain in hair dye, has also been shown to produce myocarditis and arrhythmias leading to sudden death.[2].
Heamolysis Lead is commonly found in most of cosmetics,specially including eye cosmetics.The toxicity of lead is related to its multiple biochemical effects. It has high affinity for sulfhydryl groups and inhibits numerous enzymatic, receptor and structural proteins, including enzymes involved in heme biosynthesis. It competes with calcium ions and interferes with nerve transmission. It inhibits membrane associated enzymes and metabolic pathways leading to heamolysis.[1].
Tingling or burning sensations and tremors Mercury poisoning due to cosmetic creams also leads to loss of strength in legs (44%),tingling or burning sensations (39%), tremors or shaking of the hands (38%).[3]
References
  1. MADHUSUDHANAN M, LALL SB. Acute Lead Poisoning In an Infant Oman Med J [online] 2007 Oct, 22(3):57-59 [viewed 31 August 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294150
  2. SAMPATHKUMAR K, YESUDAS S. Hair dye poisoning and the developing world J Emerg Trauma Shock [online] 2009, 2(2):129-131 [viewed 01 September 2014] Available from: doi:10.4103/0974-2700.50749
  3. WELDON MM, SMOLINSKI MS, MAROUFI A, HASTY BW, GILLISS DL, BOULANGER LL, BALLUZ LS, DUTTON RJ. Mercury poisoning associated with a Mexican beauty cream West J Med [online] 2000 Jul, 173(1):15-18 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1070961

Differential Diagnoses

Fact Explanation
Mercury poisoning Symptoms of low-grade chronic elemental (Metallic) Mercury exposure are more subtle and nonspecific: weakness, fatigue, anorexia, weight loss, and gastrointestinal distress.At higher exposures, the mercurial fine tremor punctuated by coarse shaking occurs; erethism, gingivitis, and excessive salivation have also been described.Subtler clinical findings among dentists have been documented, including delayed reaction time, poor fine motor control, and deficits in mental concentration vocabulary, task switching, and the One Hole test, as well as mood lability.[1].
Lead poisoning Lead is a toxic metal that affects many organ systems and functions in humans.Inorganic lead is absorbed from the respiratory or gastrointestinal tract. Approximately 30%-40% of inhaled lead is absorbed into the blood stream.Gastrointestinal absorption varies depending on nutritional status and age. Iron is believed to impair lead uptake in the gut, while iron deficiency is associated with increased blood lead concentrations in children. The clinical manifestations can vary from individual to individual. Abdominal pain, nausea, vomiting and diarrhea can result.Even lower blood lead levels, previously considered normal, can cause cognitive dysfunction, neurobehavioral disorders, different neurological damages, hypertension and renal impairment.[2].
Paraphenylenediamine poisoning Paraphenylenediamine is an important constituent of hair dye toxicity of which one could herald fatal complications such as rhabdomyolysis, renal failure, angioneurotic edema, and respiratory failure.The angioedema of face and neck on initial presentation (probably from allergic or hypersensitive reaction associated with the increased permeability of mast cells) with chocolate colored urine is characteristic in most cases.Methemoglobinemia, hoarseness of voice, cardiac toxicity, hepatitis, hypotension, convulsions, coma, and sudden cardiac death are also reported.Rarely exophthalmos and blindness may also be seen.[3].
References
  1. BERNHOFT RA. Mercury Toxicity and Treatment: A Review of the Literature J Environ Public Health [online] 2012:460508 [viewed 01 September 2014] Available from: doi:10.1155/2012/460508
  2. BEGOVIC V, NOZIC D, KUPRESANIN S, TARABAR D. Extreme gastric dilation caused by chronic lead poisoning: A case report World J Gastroenterol [online] 2008 Apr 28, 14(16):2599-2601 [viewed 01 September 2014] Available from: doi:10.3748/wjg.14.2599
  3. GUDE D, BANSAL DP, AMBEGAONKAR R, PRAJAPATI J. Paraphenylenediamine: Blackening more than just hair J Res Med Sci [online] 2012 Jun, 17(6):584-586 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634302

Investigations - for Diagnosis

Fact Explanation
Full blood count Anemia and reticulocytosis can be identified if poisoning is due to lead.[1].
Blood film Basophilic stippling have been recognized in lead poisoning.[1].
Serum electrolytes Hyperkalemia can be identified.[4].
Renal function test The physiological effects on renal glomerular function were assessed by measuring creatinine clearance, urinary amino acids,phosphate and glucose.[1].
Blood lead levels Laboratory diagnosis includes increased blood lead levels; raised delta-amino levulinic acid in blood and urine, increased free red cell Zn protoporphyrin, and urinary corproporphyrinogen. However, whole blood lead estimation is definitive of diagnosis of lead poisoning. Two milliliters of blood must be collected in EDTA (1.8 mg/ml) and sent without separation to the laboratory for blood lead levels. The various methods of blood lead estimation include Anodic stripping voltammetry, Atomic absorption spectrophotometry and inductively coupled plasma mass spectrometry.[2].
Blood and urinary mercury level It is important to recall that blood, hair, and urine mercury levels reflect recent exposure and do not correlate with total body burden. Blood and urine levels correlate fairly well to each other, but not to total body burden . With half life of all mercury pools in the blood estimated to be in the range of three to five days , during which either excretion or deposition in solid organs occurs, more accurate means of estimating body burden have been required.[3].
Urine lead excretion It is measured in suspected cases of lead poisoning. elevated levels can be seen[1].
ECG Fatal ventricular arrhythmia can be identified.[5].
Liver function tests Elevated liver transaminases levels seen in 76% people with hair dye poisoning.[5].
References
  1. PAGLIUCA A, MUFTI GJ, BALDWIN D, LESTAS AN, WALLIS RM, BELLINGHAM AJ. Lead poisoning: clinical, biochemical, and haematological aspects of a recent outbreak. J Clin Pathol [online] 1990 Apr, 43(4):277-281 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC502353
  2. MADHUSUDHANAN M, LALL SB. Acute Lead Poisoning In an Infant Oman Med J [online] 2007 Oct, 22(3):57-59 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294150
  3. BERNHOFT RA. Mercury Toxicity and Treatment: A Review of the Literature J Environ Public Health [online] 2012:460508 [viewed 01 September 2014] Available from: doi:10.1155/2012/460508
  4. SAMPATHKUMAR K, YESUDAS S. Hair dye poisoning and the developing world J Emerg Trauma Shock [online] 2009, 2(2):129-131 [viewed 01 September 2014] Available from: doi:10.4103/0974-2700.50749
  5. GUDE D, BANSAL DP, AMBEGAONKAR R, PRAJAPATI J. Paraphenylenediamine: Blackening more than just hair J Res Med Sci [online] 2012 Jun, 17(6):584-586 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634302

Investigations - Followup

Fact Explanation
Blood lead and mercury level Blood lead and mercury levels are monitored several months after patient who underwent chelation therapy to assess the improvement.[1].
Renal function test The kidney is a organ that can damage by lead.Excessive exposure to lead may cause acute or chronic nephrotoxic effects. Two types of nephropathy, acute and chronic nephropathy, have been observed in humans.Chronic lead nephropathy is an irreversible renal disease that develops over months or years of excessive exposure. Various tests have been proposed for the early detection of the toxic effects at different sites on the nephron.Serum creatinine and urinary proteins are act as biomarkers used in Pb-induced nephrotoxicity.[2].
IQ test Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 μg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits.Intelligence test are carried out to assess the children's intellectual function.[3].
References
  1. BRODKIN E, COPES R, MATTMAN A, KENNEDY J, KLING R, YASSI A. Lead and mercury exposures: interpretation and action CMAJ [online] 2007 Jan 2, 176(1):59-63 [viewed 03 September 2014] Available from: doi:10.1503/cmaj.060790
  2. RASTOGI SK. Renal effects of environmental and occupational lead exposure Indian J Occup Environ Med [online] 2008 Dec, 12(3):103-106 [viewed 03 September 2014] Available from: doi:10.4103/0019-5278.44689
  3. LANPHEAR BP, HORNUNG R, KHOURY J, YOLTON K, BAGHURST P, BELLINGER DC, CANFIELD RL, DIETRICH KN, BORNSCHEIN R, GREENE T, ROTHENBERG SJ, NEEDLEMAN HL, SCHNAAS L, WASSERMAN G, GRAZIANO J, ROBERTS R. Low-Level Environmental Lead Exposure and Children's Intellectual Function: An International Pooled Analysis Environ Health Perspect [online] 2005 Jul, 113(7):894-899 [viewed 03 September 2014] Available from: doi:10.1289/ehp.7688

Management - General Measures

Fact Explanation
Assess airway,breathing and circulation The treatment of any kind of poisoning in the emergency department begins with stabilizing the patient and assessing the vital signs, starting with ABC (airway, breathing and circulation).[4].
Remove the source The first step in treating all cases of heavy metal toxicity is to reduce or remove the source of exposure.In most cases this is all that is required.Referral to the local public health unit can assist in identifying the source of an atypical exposure and may lead to additional case finding and removal of a source of exposure to the population.[2].
Frequent monitoring Patients should be frequently monitored for respiratory distress.[1].
Management of rhabdomyolysis and acute renal failure Early intervention with half normal saline and soda bicarbonate infusion has been shown to be beneficial in rhabdomyolysis. 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.[1].
Gastric lavage Hair dye ingestion is a medical emergency. Emergency measures should include gastric lavage.[1].
Endotracheal intubation In PPD poisoning endotracheal intubation has to be performed early if laryngeal edema develops.[1].
Steroids and antihistamine Used in Paraphenylenediamine poisoning. Early diagnosis, medical treatment with steroids and antihistamines are recommended. And if airway compromise is not improving, endotracheal intubation or tracheostomy can perform.[3].
References
  1. SAMPATHKUMAR K, YESUDAS S. Hair dye poisoning and the developing world J Emerg Trauma Shock [online] 2009, 2(2):129-131 [viewed 01 September 2014] Available from: doi:10.4103/0974-2700.50749
  2. BRODKIN E, COPES R, MATTMAN A, KENNEDY J, KLING R, YASSI A. Lead and mercury exposures: interpretation and action CMAJ [online] 2007 Jan 2, 176(1):59-63 [viewed 01 September 2014] Available from: doi:10.1503/cmaj.060790
  3. GUDE D, BANSAL DP, AMBEGAONKAR R, PRAJAPATI J. Paraphenylenediamine: Blackening more than just hair J Res Med Sci [online] 2012 Jun, 17(6):584-586 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634302
  4. ZYOUD SH, AL-JABI SW, BALI YI, AL-SAYED AM, SWEILEH WM, AWANG R. Availability of treatment resources for the management of acute toxic exposures and poisonings in emergency departments among various types of hospitals in Palestine: a cross-sectional study Scand J Trauma Resusc Emerg Med [online] :13 [viewed 03 September 2014] Available from: doi:10.1186/1757-7241-22-13

Management - Specific Treatments

Fact Explanation
Chelation therapy Chelation therapy has historically been used to reduce the body burden of heavy metals in patients with severe symptoms and highly elevated circulating levels of heavy metals.It is a process in which heavy metals are removed from the body with the use of a chelating agent, a charged molecule that binds metals in a stable complex known as a chelate. The chelate is subsequently excreted in the urine.The decision as to which patients should receive chelation therapy is a matter of clinical judgment.[1]. In lead poisoning the frequently using chelating agents are intravenous calcium disodium edetate (EDTA), oral dimercaptosuccinic acid (DMSA) and intramuscular dimercaprol (BAL). BAL is used only when there is severe toxicity as in lead encephalopathy.[2].
References
  1. BRODKIN E, COPES R, MATTMAN A, KENNEDY J, KLING R, YASSI A. Lead and mercury exposures: interpretation and action CMAJ [online] 2007 Jan 2, 176(1):59-63 [viewed 01 September 2014] Available from: doi:10.1503/cmaj.060790
  2. MADHUSUDHANAN M, LALL SB. Acute Lead Poisoning In an Infant Oman Med J [online] 2007 Oct, 22(3):57-59 [viewed 01 September 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3294150