Physical and Chemical Injuries of the Oral Mucosa V. Žampachová I. ÚP Introduction nThe oral mucosa - the first part of the digestive tract, exposed to various exogenous noxes nExposition of longer duration → reactive changes, ! diff. dg. x malignancies nMucosal lesions with an increased chance of turning into a malignancy - premalignant lesions nFrequently in areas of the oral cavity not obvious to the patient (sulcus glosso-alveolaris, dorsal and lateral tongue, oral vestibule, retromolar area) nTherefore thorough intraoral examination twice a year is necessary If mucosal lesions are evident: nTry to remove local factors that could have contributed to the lesion nAnti-inflammatory treatment for two weeks, if lesion remains: biopsy nDiagnosis based on clinical appearance alone usually not sufficient to determine the histological nature of the tissue Terminology nLesion – focus of abnormal finding (tissue) in the oral cavity: wounds, sores, any other tissue damage caused by injury or disease. nDetermining the type of lesion important for differential diagnosis. nAppearance: architecture •below or above the surface. •flat or even with the surface. nColor: white, red, white + red, pigmented Epithelial changes: terms nAcanthosis: excessively thickened intermediate cell layer with broad and long rete pegs nHyperkeratosis: excessively thickened keratin in stratum corneum nLeucoplakia: a white patch on the oral mucosa that cannot be scraped off and cannot be classified as any other disease psoriáza1, 100x.jpg Epithelial changes 1 2 3 1Acanthosis 2Papillomatosis, papillary oedema 3Hyperkeratosis, parakeratosis 4Chronic inflammation 4 Lesions extending below the surface nErosion: shallow defect in the mucosa, commonly caused by mechanical trauma, healing by regeneration. nUlcer: crater-like defect of the mucosa, deeper than erosion, healing by repair nAbscess: localized collection of pus in an area circumscribed by remaining tissue/granulation tissue. nCyst: pathological cavity lined with epithelium/endothelium/mesothelium; containing fluid or semisolid material. Lesions extending above the surface nBlisters: vesicles, bullae, lesions filled with watery fluid. Vesicobullous lesions. nPustule: similar in appearance to a blister, contains pus. nHematoma: similar to a blister, contains blood. nPlaque: any solid patch or flat area slightly raised above the surface. nPolyp: exophytic elevated lesion, superficial epithelium + fibrotic stroma Reactive fibroepithelial polyp Lesions above + below the surface nNodules – solid, commonly firm consistency, may be sharply demarcated, may be ulcerated Reactive nodule + ulceration on the tongue Etiology nPhysical injuries nChemical injuries nInfection nAllergies, immunologic diseases nHyperplasia, neoplasia nInborn lesions nCombination of multiple factors nIdiopathic n n Physical injuries ntrauma ndenture irritation leading to hyperplasia nburn nradiation injury namalgam tattoo Diseases caused by chemical agents nAspirin burn nNicotine stomatitis nSnuff lesion nHairy tongue nGingival hyperplasia 6-3-10 Oral lesions nWhite lesions: nLeucoplakia nLinea alba nLichen nLeucoedema nMorsicatio buccarum nWhite sponge nevus nFordyce’s granules nRed lesions: nErythroplakia nVaricosity nHemangioma nPurpura (petechiae, ecchymosis) - bleeding nHereditary hemorrhagic teleangiectasia Oral lesions nRed-white lesions: nSpeckled erythroplakia nSquamous cell carcinoma nLichen planus nLupus erythematodes nLichenoid drug reactions nCandidiasis (candidal leucoplakia, antibiotic sore mouth, denture stomatitis) nPigmented lesions: nMelanoplakia nEphelis (freckle) nPigmented naevus nMalignant melanoma nPeutz-Jeghers syndrome nAddisons’s disease nTobacco associated pigmentation (smokers melanosis) nAmalgam tattoo Etiology of white oral lesions nInborn nWhite sponge nevus (AD) nOral manifestation of other inborn/hereditary diseases nFordyce‘s granules (sebaceous glands heterotopy) - nTraumatic -reactive nmechanical-friction keratosis - hyperplasia due to chronic irritation nother physical – thermal burn, nicotinic stomatitis nchemical - burns, snuff lesion aj. n nInfections nCandidiasis (acute pseudomembranous, chronic hyperplastic) nDiphteria (pseudomembranous inflammation) nSyphilitic leucoplakia (glossitis) nOral hairy leucoplakia (EBV+HIV) n Etiology of white oral lesions nIdiopathic leucoplakias n nDermatologic nLichen planus nLupus erythematodes - nNeoplastic nCarcinoma in situ nSquamous cell carcinoma nothers n Common oral lesions in the primary care office nWhite lesions nCandida nOral leucoplakia nMorsicatio buccarum nHairy tongue nVesiculobullous lesions nPrimary herpetic gingivostomatitis nRecurrent herpes nHerpangina nHand-foot-and-mouth disease n Common oral lesions in the primary care office nUlcers nAphthous ulcers nBehçet’s syndrome (multiple/major oral aphthous ulcers + genital ulcers + ocular/skin lesions, multisystem immunologically mediated disorder) n White mucosal lesions nAppear white due to obscured visualization of the normal pink appearance (connective tissue vascularity). nPossible causes: nthe presence of a superficial material nepithelial thickening nsubmucosal alteration leading to a decrease in blood vessel density White mucosal lesions nFocal nphysiologic hyperkeratosis - homogenous appearance, sharp borders nidiopathic leucoplakia - heterogenous appearance, vague border nLarge or diffuse nnicotinic stomatitis, smokeless tobacco use, actinic keratosis, hairy tongue n n. White mucosal lesions nMultifocal nIrregular, commonly tongue: diminished host resistance to infection n Hyperplastic candidiasis – hairy leucoplakia n nChronic bilateral buccal mucosa: may be inborn, acquired dermatoses nleucoedema, white sponge nevus, lichen planus Submucosal change nWhite or pale lesions nCovered by normal epithelium nSurface smooth and translucent. nNo pain or burning. nCan not be rubbed off. nPatient history or the distribution of the lesions important for diagnosis. Clinical features of lesions caused by epithelial thickening nKeratin: rough or grainy surface texture when dried with air or a cotton gauze. nAdditional keratin (hyperkeratosis) → opaque appearance nAttached keratin only - wipe with gauze or scrape with a dull instrument. nEpithelium intact: no pain, burning, or tenderness Other superficial material n! food remnants, a dense accumulation of plaque: painless, mucosa appears normal. n nWhite material, soft or friable and rubbing → ! an ulcer or erythematous lesion nFrequent burning + discomfort sensation. nDiff. diagnosis: after removal of the white material (white surface coagulum) → defect - the ulcerative lesions category. Physiological hyperkeratosis nThickening due to recurrent friction (callus formation). nFocal keratosis, focal hyperkeratosis, frictional hyperkeratosis. Buccal hyperkeratosis Reactive white hyperkeratotic lesions nThey do NOT rub off nLinea alba nDenture acanthosis /papillary hyperplasia of the palate nNicotinic stomatitis nSnuff (Dipper’s lesion) nChemical burn nActinic cheilitis n Linea alba nA white line along the line of occlusion, usually bilateral nDue to increased formation of keratin as a result of frictional irritation (chronic cheek chewing, grinding), nSharp tooth surfaces, appliances, and masticatory function of edentulous ridges ngalvanic irritation Clinical features nOpaque, homogenous with sharply delineated borders. nUsually focal nLocation against the source of friction. nAsymptomatic, patient unaware. nIf irritation removed→ resolution within a few weeks, no other treatment needed nMultiple or diffuse - multiple or large sites fkerato Linea alba ncopy Cheek biting (morsicatio buccarum) nIrregular whitish focus on the buccal mucosa in the line of occlusion nMay be ulcerated nDue to chewing or biting the cheeks nMay also be seen on labial mucosa slide 10 copy Differential diagnosis nSource of friction to the location. nResolution. nVague borders, focal ulceration, variation of thickening, or heterogeneous color of the white area are more suspicious nEpithelial dysplasia and early carcinoma: unusual location for cheek biting (soft palate, floor of the mouth, facial vestibule) n n n Denture irritation nAn ill-fitting denture can cause small ulcers → continued irritation → mucosal hyperplasia in form of acanthosis Denture acanthosis nCaused by irritants nClinical appearance similar to hyperkeratosis nThickened intermediate cell layer nElongation of rete pegs nTreatment: avoid irritants, ie. ill-fitting dentures nIn chronic lesions hyperplasia ev. papillary possible, commonly + chronic candidiasis nDif. dg. x true tumors (papilloma, carcinoma) Papillary hyperplasia of the palate Nicotinic stomatitis nPhysical agent n„Smokers keratosis” „Smokers patches” nResponse of the palatal tissues to the recurring irritation from tobacco smoke usually from a pipe or cigar habit (heat). nHotter smoke of cigars or pipes → more prominent lesions (x cigarettes). nPossible influence of hot liquids n Nicotinic stomatitis nPalate initially diffusely erythematous, later grayish white (hyperkeratosis) stomatitisnicotina copy Nicotinic stomatitis nDiffuse, dull greyish-white, opaque on hard palate nGradually fades to a normal pink on soft palate nSevere - wrinkled or fissured surface texture nHomogeneous with erythematous spots (inflamed minor salivary glands orifices) nMaceration, ulceration and aphthae nTonsillar pillars are usually erythematous. nTobacco stains of the teeth, odor of tobacco, patient history confirms the cause of the lesion scan05a copy Nicotinic stomatitis Differential diagnosis nPipe or cigar + characteristic appearance. nIn long duration or non-healing ulceration, focal heterogeneous appearance and/or focal thickening: n CAVE CARCINOMA Smokeless tobacco lesions (STL’s) nChanges in color and texture of the oral mucosa nCommon oral soft tissue lesions among young people. Hyperkeratosis caused by smokeless tobacco n"snuff dipper's pouch." nprogression to carcinoma, (low grade squamous cell Ca, verrucous Ca). nWestern hemisphere (Sweden, US, Canada) lower carcinogenic rate nAsia higher rate due to added carcinogens n chewing tobacoo 5 copy Clinical features nHyperkeratotic lesion. nUniform, plaque-like thickening nHomogeneous white, greyish-white, or dark color. nGrainy rough surface with a uniform reticular pattern of wrinkles and folds (wrinkled, velvety). nLabial, buccal, and facial alveolar mucosa. nLarge focal lesions, multiple sites (habit). nFocal lesions - well delineated margins. Tobacco stains + residues. n Oral verrucous hyperplasia – possible precursor lesion Differential diagnosis nAppearance + history of habit: pathognomonic nTreatment: quit habit, switch site n ! x CA nnon- healing ulceration nexcessive verrucous thickening Actinic cheilitis nAlteration of the lower lip caused by chronic exposure to sunlight (UV). nUV portion of the spectrum → cellular damage of the epithelium + the underlying connective tissue . nPremalignant " + carcinoma cofactors (smoking). nBiopsy if thickened or ulcerated Clinical features. nFair skinned individuals. nUsually over 60 yrs. nExcessive sun exposure. nLower lip thinned + atrophic with indistinct demarcation of vermilion border. nPersists for years, unchanged over an observation period of several months. Actinic cheilitis nFocal, homogeneous, milky-white, thickened patches. nUlceration is rare unless SCC is present nActinic keratosis " skin. nFacial skin: nvariation in pigmentation. nscaly atrophic patches. nseborrheic keratosis (thick, dark plaque). nPossible skin cancers. Actinic cheilitis copy lip Lower lip thin + atrophic, indistinct demarcation of vermilion border. Actinic cheilitis copy Actinic cheilitis- atrophic epithelium, regressive changes in subepithelial elastic tissue - basophilic Actinic cheilitis akpath Superficial hyperkeratosis, dysplastic changes of squamous cell epithelium Invasive squamous cell carcinoma - lip Idiopathic or combined white hyperkeratotic lesions nGeographic tongue (erythema migrans, benign migratory glossitis) nHairy tongue Tongue papillae + bacteria Geographic tongue nMultiple areas of desquamation (loss) of the filiform papillae in several irregularly shaped but well-demarcated areas. nMay be on other parts of oral mucosa nThe smooth areas resemble a map → geographic tongue. nOver a period of days or weeks, the smooth areas and the whitish margins „migrate“ across the surface of the tongue by healing on one border and extending on another. Geographic tongue (Benign migratory glossitis) nCause unknown, possible hypersensitivity to external factor + other factors (genetic, hormonal, …) nWhite borders (+/-hyperkeratotic) nRed patches of denuded filiform papillae nCommon disorder (1 - 2%), females, young adults nPainfree usually nPainful if inflammation present nTreatment: none, or topical anesthetic Geographic tongue JG013.jpg (55669 bytes) copy geographicmunro's1 geographicpathlp1 Geographic tongue Histology: epidermal hyperkeratosis and marked transepidermal migration of neutrophils (Munro’s microabcess-like). Cannot be differentiated histologically from pustular psoriasis or Reiter’s syndrome. copy Hairy tongue nShaggy mat of filliform papillae nIn smokers, poor oral hygiene, antibiotics, … nHyperplasia may be stimulated by Candidiasis nCoffee, tea, tobacco, bacteria → black discoloration nTreatment: brush tongue, improve oral hygiene Hairy tongue copy Hairy tongue blackhairyhp1 Elongation + hyperkeratosis of filiform papillae, superficial bacterial colonies Dorsal localisation. Differential diagnosis x oral hairy leukoplakia (EBV in immunodeficiency, on the lateral border of the tongue) Hairy tongue - micro Hairy tongue – micro, G+ bacteria Fissured tongue nA variant of norm, cause unknown. nSome theories include a vitamin deficiency or chronic trauma over a long period. nThe dorsal surface (top) of the tongue appears to have deep fissures or grooves, irritation if food debris collects in them. Fissured tongue 17_011 nChemical burn § Different localization/size/appearance according to the type of chemical utilized, its concentration, the duration § Whitish surface ® desquamating ® painful erosion or ulcer ® bone damage § Healing within 1-2 weeks Chemical burn DSC_1139 copy Chemical burn nCommonly caused by aspirin nPainful nUsually in molar region nTreatment = discontinue aspirin use Aspirin burn copy Diff. dg. of white lesions Epithelial dysplasia and early squamous cell carcinoma nMost important diff. dg. nDysplasia: premalignant alteration in the differentiation, development, and maturation of lining epithelial cells. nSquamous cell carcinoma: malignant neoplastic proliferation of lining epithelial cells. nGross: focal epithelial thickening - leukoplakia RED LESIONS n Focal erythematous lesions nNonspecific mucositis nMucosal burn nMacular hemangioma (benign tumor) nErythroplakia (precancerosis) • RED LESIONS nDiffuse and/or multifocal red lesions •Geographic tongue (erythema migrans ) •Vitamin deficiency induced glossitis •Radiation mucositis •Xerostomic mucositis •Allergic mucositis •Lupus erythematosus (immunologic) • n Nonspecific mucositis (irritational): nAge, sex (different causes – piercing, denture…). nClinical features: nLocalized zones of redness correspond to the source of irritation. nRelated to a physical agent. Nonspecific mucositis (irritational): nDifferential diagnosis: n! precancerous erythroplakia nMay progress to ulcerative lesion nTreatment: nElimination of the irritating agent. nAnalgesia n Erythroplakia (precancerous) nBright red velvety plaque which cannot be characterized clinically or pathologically as being due to any other condition. Erythroplakia nErythroplakia of the buccal mucosa nErythroplakia of the buccal mucosa. Erythroplakia of the lateral margin of the tongue. copy Acute ulcerative lesion nCombined mucosal damage – acute necrosis, commonly in form of burn (aspirin burn) → nErosion → healing by epithelial regeneration, may become hyperkeratotic nUlcer → healing by granulation tissue n Etiology of ulcerations •Mechanical factors: a sharp or broken tooth, rough fillings, clumsy use of cutting dental instruments, hard foodstuffs, sharp foreign bodies, biting of the mucosa, denture irritation etc. •Physical factors – thermal, electrical burn •Chemical – caustic drug reactions, strong acid, strong base, (aspirin, hydrogen peroxide, silver nitrate, cleaning substances – acids, etc.) • • Tongue ulceration – central loss of epithelium, reactive inflammatory cells Scalloped tongue nIndentations along the lateral borders of the tongue nCorrespond to the teeth nThought to be habitual pushing of tongue against teeth nPossible progression to ulcers slide 20 copy Tongue jewellery nPierced tongue n nCan affect the teeth and/or gingiva nMultiple complications possible slide 21 copy Mucosal burn nClinical features: nChemical agents → caustic → coagulation necrosis of epithelium → whitish ( can be scraped off ) nDiluted chemicals → inflammation and redness without producing superficial necrosis (erythema of the superficial tissues) nThermal burns: hot foods, caustic drug or beverages → palatal erythema → painful. n Mucosal burn nDifferential diagnosis: nHistory. nHypersensitivity reaction. nBiopsy (cytological atypia). nTreatment: nStop the irritant. nTopical analgetics nAvoid spicy foods Hydrogen peroxide burn copy nThermal burn § Acute lesion (x stomatitis nicotinica) § very hot foods, liquid, or hot metal objects § palate, lips, floor of the mouth, tongue § initially painless, no bleeding; quick (hrs) edema evolution § painful, red, necrosis undergoing desquamation, leaving erosions or ulcers, ! complications – bleeding, infection § supportive treatment; self-healing in about a week Thermal burn nErosions on the dorsum of the tongue, caused by very hot food (microwave oven, …) Electrical burn nSimilar to thermal burn nCommonly significant tissue destruction incl. bone Other physical injury nTraumatic ulceration nmechanical nfactitious injury ntraumatic granuloma – eosinophilic ulcer nradiation nFactitious ulcer § Patients mentally handicapped, with serious emotional problems, incarcerated § Oral self-inflicted trauma by biting, fingernails, or by the use of a sharp object § Tongue, lower lip, gingiva § Slow to heal due to perpetuation of the injury by the patient § Local measures and psychiatric therapy Traumatic injury – factitious erosion → ulcer copy Toothbrush trauma - friction nDecubital ulcer - clinical features § mechanical irritating factors § the ulcer conforms in area and linearity to the source of the irritating factors § may affect mucosa, deep soft tissue, rarely progresses into the bone Chemo-22 Trauma – dentures – decubital ulceration HN21 copy PIC00001 Decubital ulcer copy Traumatic ulcer CX1018B1 copy Traumatic ulcer Traumatic bulla nFrequent, due to the constant motion of the masticatory mucosa over the teeth or the introduction of hard objects into the oral cavity. §buccal mucosa, soft palate, lips, tongue §self-healing in 4-6 days n Traumatic bulla H片-p18 copy Diagnosis nHistory nClinical features carcinoma, syphilis, tubercular ulcer, major aphthous ulcer thrombocytopenia, thrombasthenia, pemphigus, cicatricial pemphigoid Differential diagnosis Traumatic bulla Malignant ulcer V片-016 copy Soft tissue necrosis nTraumatic vs. spontaneous nIntraoral source RT nPossible late occurence nProlonged duration HN49 copy Cocaine induced necrosis copy Eosinophilic ulcer nUlcer with elevated borders usually covered by a pseudomembrane. nCommonly posterior aspect of tongue nRapid onset, spontaneously resolves in a few weeks. Benign, self-limited. nMicro: predominantly eosinophilic infiltrate with histiocytes and neutrophils nIf multifocal and recurrent, CD30 positive lymphoproliferative disease may be present. eosinophiliculcer1 eosinophiliculcer2 copy Healing of ulcers nMixed inflammatory infiltrate (neutrophils, lymphocytes, macrophages; eosinophils in eosinophilic ulcer) nGranulation tissue proliferation → possible elevated lesion (nodule) → maturation into connective tissue → fibroepitelial polyp („fibroma“, „epulis“) nDeep vascular connective tissue n Fibroepithelial polyp Epulis nBenign exophytic/polypous lesion situated on the gingiva. nReactive, inflammatory nPeripheral giant cell granuloma: solitary bluish- red, 10-20 mm tumor between or near bicuspids, incisors. Pyogenic granuloma (lobular capillary hemangioma) nExuberant overgrowth of granulation tissue nBleeds easily nRapidly growing nAsymptomatic pyogenicgranulomaclin2 pyogenicgranulomaclin1 pyogenicgranulomalp1 pyogenicgranulomahp1 well circumscribed nodule with lobules of dilated and congested capillaries myxoid stroma and bland endothelial cells Traumatic fibroma nFirm, smooth, pink nodule similar in color to surrounding mucosa nUsually present as late response to trauma nUsually present for long periods unchanged nPseudotumor, histologically fibroepithelial polyp (fibrotic stroma + superficial slightly hyperplastic epithelium) slide 11 copy Mucocele nDiff. dg. nDilatation of salivary gland duct – mucinous cyst +/- reaction nResult of trauma or obstruction of salivary ducts, usually on the lower lip nSoft rounded translucent cystic lesion often with a bluish tint. mucocele1 Noninfectious complications of antineoplastic therapy nRadiation therapy and/or chemotherapy nacute changes – oral mucositis, dermatitis n haemorrhage (thrombocytopenia) nchronic sequelae – xerostomia, loss of taste, osteoradionecrosis, chronic dermatitis, in children developmental abnormalities n Oral mucositis –collective consequence of a number of concurrent and sequential biological processes –Can be the most debilitating of side effects –oral and GI –Ranges from mild inflammation to ulceration Chemo-14 Chemo-23 * WHO Oral mucositis scale nGrade 0: No changes n nGrade 1: Soreness/erythema ■ Grade 2: Ulceration/solid foods n n n n n nGrade 3: Liquid diet ■ Grade 4: No alimentation mucositis RadiationInducedLesion18 copy * Oral mucositis – incidence nHigh dose chemoth. + Stem cell therapy nNear 100% for any grade n30-50% Grade 3/4 ? Chemotherapy stomatotoxicity Direct Indirect Bleeding Decreased nutrition Mucosal infection Cell renewal Thinning Mucositis and ulceration Thrombocytopenia Neutropenia Xerostomia Radiation mucositis nClinical features: nRadiation therapy in excess of 3500 to 4000 rad. nPainful diffuse erythema with telangiectasia of the mucosa. nInitially red zones → white pseudomembrane at areas of maximal radiation. (+candidiasis?) nUlcers - extremely painful nPossible xerostomia Radiation mucositis nDysphagia and oral soreness ( maximal 2-4 weeks after radiotherapy but usually subside in further 2-4 weeks ) nSlow/defective healing of the ulcers (inhibition of proliferation by radiation). n Erythema and erosions on the lower lip, caused by ionizing radiation copy Chemo-64 Mucosal sloughing Chemo-32 Diff. dg. x bullous oral lesions (pemphigus etc.) * Chemo-30 Atrophy and collagen degeneration Mucositis complications and sequelae nPain nOral infection nSystemic infection? nBacteremia/Sepsis nOral bleeding nXerostomia nTaste nHydration/Nutrition nFatigue nInterrupted cancer treatment Radiation effects on tissue nAcute (vasculitis, possibly „fibrinoid” necrosis) nChronic (obliterative vasculopathy, fibrosis) f009011 f009012 Delayed radiation injury nCarcinogenesis (atom bomb survivors) nmyeloid leukemias peak 5 to 7 years after exposure nbreast and thyroid cancers may show greater latency nno germline mutations noted in progeny of survivors nVascular effects nendothelial necrosis followed by intimal and medial fibrosis ncapillaries may become thrombosed and obliterated or ectatic nParenchymal atrophy and fibrosis Parotid atrophy post RT Attached gingiva nRecession of gingival margin nLoss of attachment nTooth abrasion nHyperkeratinized soft tissues Dental Recession Radiation mucositis nDifferential diagnosis: nHistory. nPersistence/increase in size → erythroplakia. nTreatment: nRegresses with time. nPersistence/ increase → cytological smears. nA soothing mouth rinse, soft diet. nAntifungal. Gingivitis associated with pharmacology nDrugs known to cause gingival inflammation: nDilantin (Phenytoin) nCalcium channel blockers nCyclosporin n Gingivitis associated with pharmacology nPhenytoin induced gingival hyperplasia nLeads to pseudopocketing → increased probing depth due to gingival hypertrophy, no due to bone loss nOccurs in 3 → 85% of those taking medication nMost likely due to increased platelet derived growth factor nCalcium channel blockers: nCauses gingival hypertrophy in 25-50% of those on it nCyclosporin: nCauses gingival hypertrophy in 30% Dilantin and cyclosporin induced gingival hypertrophy copy Localized exogenous pigmentations nAmalgam tattoo nIntentional intraoral tattoo nPigmentation due to systemic metallic intoxication – lead, silver (incl. colloidal), arsenic (drinking water), gold (medication) n Amalgam tatoo nA blue or black area usually on the gingival ridge adjacent to a large restoration nResult of impregnation of amalgam fragment into the tissue slide 12 slide 13 copy Metallic tatoo Lead nLead: commonly used heavy metal (others: mercury, arsenic, cadmium, …) n Source of exposure nlead paint nlead in plumbing (older houses) nlead-glazed ceramics nindustrial exposure nRoute of exposure ninhalation with industrial exposure ningestion with household exposure copy