a) Liquid paints can be categorized as water-, solvent-, or oil- based.

a) The use of powder-based paints for industrial applications is increasing. Powder-based paints require heat curing and do not contain any solvent. Formulations include polyester, acrylic, epoxy, epoxy-polyester hybrids, polytetraglycidal isocyanate (TGIC), and nylon (Reisch, 1990). Occupational exposures are usually from spraying applications.

a) Paints which are cured by electron beam or ultraviolet radiation may contain aliphatic isocyanates and polyisocyanates as the active ingredients and polyols as stabilizers. They may also contain photoinitiators, optical brighteners, and light stabilizers (Reisch, 1991).
b) Radiation-cured paints are used in industrial applications and contain acrylates of the following classes: mono-, di-, or trifunctional, epoxy, amine, urethane, or polyester. The acrylates used in radiation-cured coatings can cause skin and eye irritation and sensitization, and are possible skin carcinogens (Reisch, 1991).

a) In addition to the solvent and pigment, paints may contain a variety of additives including defoamers, deflocculants, biocides, (Reisch, 1990), surfactants, fillers, binders (alkyd resins, nitrocellulose), and catalysts.

a) Paints and lacquers contain a mixture of aromatic solvents (C9-C10) designated solveso 100 or shell soll A, xylene, light petroleum spirit, thinner (a mixture of light petroleum spirit, toluene, methyl ethylketone), ethanol, acetone, ethylbutyl acetate and isopropranol.
b) Varnishes contain mainly xylene and toluene but also small amounts of other solvents such as ethanol, isopropranol, ethyl acetate, and N-butanol. Many types of paints, varnishes and printing ink contain a mixture of alcohols (ethanol, propranol, butanol, etc.) and aliphatic and aromatic organic solvents.

a) Lead in paint is usually in the form of lead carbonate. It gains access to the body when paint chips are eaten, when paint is sucked, when the dust of the paint is picked up on the hands of toddlers, during house renovation, or when painted metal is cut with an acetylene torch.
b) Since 1977, household paint must contain no more than 0.06% (600 ppm) lead by dry weight. Overt lead poisoning usually occurs in housing built before World War II. A chip of old or industrial paint the size of a thumbnail may contain 50 to 200 mg of lead. For comparison, the average dietary intake of lead in children is only 20 to 80 micrograms per day (Anon, 1987).
c) HOME TEST KIT: A sodium sulfide-containing home lead paint test kit is available under the trade name Lead Detective, from Innovative Synthesis Corporation, 45 Lexington St, Ste 2, Newton, MA 02165.
d) Lead-containing pigments that have been used in paints include (Joly et al, 1987):
e) The solubility of lead-based pigments in gastric fluid determines the hazard after ingestion. Pigments with partial solubility include lead minium, basic lead carbonate, and metallic lead. Other pigments that are practically insoluble in gastric fluid include lead chromate, lead silicochromate, lead sulfochromate, and lead sulfochromomolybdate (Joly et al, 1987).
f) Alkyd paints may contain drying agents, such as lead naphthenate or lead octoate. Usual concentrations are 0.1 to 0.3% (Joly et al, 1987).
g) Blood lead levels in children living in homes undergoing refinishing of lead paints were elevated an average of 69 percent (Rabinowitz et al, 1985).

a) Indoor latex paint may contain up to 300 ppm of mercury as a preservative (CDC, 1990).
b) Exterior latex paints may contain mercury fungicides. "Mildew-Resistant" house paints usually have mercury compounds (phenylmercury oleate, phenylmercury acetate, or phenylmercury succinate). If there is less than 0.2% mercury compound, the special warning label is not required (Gosselin, 1984).
c) The use of mercury-based biocides in INTERIOR paints was canceled by the US EPA, effective August 20, 1990. Existing stocks of pesticides were allowed to be sold and used for manufacture of exterior products until June 27, 1991, provided they are properly labeled with language prohibiting use in interior paints and coatings (EPA, 1990).
d) Because current inventories were not affected, paints containing mercury-based biocides may still be available on the market.
e) Median level of airborne mercury detected in homes recently painted with latex paint containing phenylmercuric acetate was 10.0 nmol/m(3), and urinary mercury levels of persons living in these houses were also elevated when compared with unexposed persons (4.7 nmol/mmol creatinine versus 1.1 nmol/mmol). Urinary concentrations were in the range associated with symptomatic mercury poisoning (Agocs et al, 1990).

a) Marine paints often contain organotin polymers, usually tributyl tin oxide (TBTO), as antifouling agents to control growth of barnacles on hulls below the waterline (Reisch, 1990). TBTO is a strong irritant which can cause delayed pruritus, erythema, and vesiculation at the points of contact (Lewis & Emmett, 1987).
b) Tributyl tin has also been used in interior house paint (Wax & Dockstader, 1995).

a) Benzidine-derived azo dyes have been used in certain paints (Gregory, 1984). These have been speculated as a possible cause of increased risk of bladder cancer in painters (Myslak et al, 1991).

a) Automobile paints may contain isocyanates, which can be potent sensitizers (Reisch, 1991).
b) The airborne concentration of isocyanates during spraying operations can be high. In one study, levels of hexamethylene- diisocyanate monomer often exceeded 0.07 mg/m(3), the oligomer was at least ten-fold higher. Combined charcoal and particle filters on respirators were required to prevent significant exposure by the inhalation route (Rosenberg & Tuomi, 1984).

a) The distribution of the chemical components of a paint may vary with different sized aerosol fractions. Therefore, actual inhalation exposure may be different from the overall chemical composition of the paint (D'Arcy & Chan, 1990).

1) WATER BASED PAINTS: Include latex, tempera, and poster paints. These paints may be mildly irritating to skin and mucous membranes, but serious toxicity is not expected. Large doses (greater than 5 mL/kg) may cause nausea and vomiting without systemic toxicity. Some latex paints contain 5% to 10% glycols; potential glycol poisoning should be assessed in those patients who ingest large volumes.
2) SOLVENT BASED PAINTS: Contain relatively volatile organic solvents such as toluene, xylene, light petroleum spirit, methyl ethyl ketone, ethanol, acetone, ethyl butyl acetate, or isopropanol. Toxicity is primarily due to chronic inhalation as a consequence of recreational substance abuse (inhalant abuse or solvent abuse) and includes encephalopathy and metabolic acidosis if the solvent is toluene due to its metabolite hippuric acid. Acute exposure may cause CNS depression and there is potential for aspiration after ingestion. However the risk for this is not great because of the small amounts typically ingested and because of the viscous nature of these products.
3) OIL BASED PAINTS: Oil based paints use mineral oil as the solvent, which can cause GI upset and diarrhea. Risk is not great because of the small amounts typically ingested and because the viscous nature of these products makes aspiration unlikely. Lead, chromate, cadmium, arsenic, manganese, mercury, cobalt, and barium may be added as pigments. Toxicity is expected primarily with chronic exposure, but may result from acute ingestion of sufficient quantities.
4) SPECIALTY PAINTS: Active ingredients of some specialty paints can be significant sources of toxicity. Isocyanate-based automobile paints are potent pulmonary sensitizers.

1) Treatment is symptomatic and supportive.

1) Chelation may be necessary for patients with significant exposure to paints containing heavy metals. OBSERVE FOR ASPIRATION PNEUMONITIS and treat accordingly (see hydrocarbon management). Suspect aspiration if coughing or choking occurs following ingestion of oil-based paints. Aspiration pneumonitis should be treated with oxygen, inhaled beta agonists for bronchospasm, and in severe cases endotracheal intubation may be necessary.

1) PREHOSPITAL: GI decontamination is generally not indicated because of the low risk of acute toxicity and the possibility of aspiration. Activated charcoal can be considered after ingestion of lead based paint. Wash exposed skin with soap and water; mineral oil may help remove oil based paint. Irrigate exposed eyes.
2) HOSPITAL: GI decontamination is generally not indicated because of the low risk of acute toxicity and the possibility of aspiration. Activated charcoal and/or gastric lavage can be considered after substantial ingestion of lead based paint. Wash exposed skin with soap and water; mineral oil may help remove oil based paint. Irrigate exposed eyes.

1) Consider early chelation in patients with significant ingestion of paints containing heavy metals or symptoms of acute heavy metal poisoning. See monograph pertaining to the specific heavy metal for details.

1) Hemodialysis and hemoperfusion are not useful.

1) HOME CRITERIA: Patients with symptoms limited to minor irritation after inadvertent exposure to paints that do not contain heavy metals can be managed at home.
2) OBSERVATION CRITERIA: Patients with clinical evidence of aspiration (cough, increased work of breathing, wheezing) or ingestion of paints that contain heavy metals should be referred to a healthcare facility. Patients who deliberately inhale solvent based paint should be referred to a healthcare facility.
3) ADMISSION CRITERIA: Patients with persistent symptoms of aspiration or with acute symptoms of heavy metal poisoning should be admitted.
4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patients with significant ingestions of paints containing heavy metals. Refer patients who recreationally inhale solvent based paints for substance abuse counseling. Consult a pulmonologist for patients with severe aspiration.

1) Acute exposure is generally minimally toxic, avoid over treating. Patients with exposure to lead based paints require ongoing follow up of blood lead concentrations.

1) Unknown

1) Exposure to solvents, hydrocarbons.

1) DECONTAMINATION: Wash affected area twice with soap and water. Oil-based paints may be removed from the skin with mineral oil (baby oil). A physician may need to examine the exposed area if irritation or pain persists.

1) IRRITATION: Eye irritation was one of the most commonly reported symptoms among users of water-based paints (Hansen et al, 1987; Wieslander et al, 1994). However, eye irritation is more pronounced after exposure to solvent based paint as compared to water based paint (Wieslander et al, 1994).
2) KERATITIS: Superficial keratitis may develop after use of spray paints due to inadvertent impregnation of the cornea (MacLean, 1967).

1) RHINITIS: Nose irritation has been reported after occupational exposure to reactive dyes (Hagmar et al, 1986).

1) Aspiration pneumonitis is a potential consequence of paint ingestion. Although paints contain hydrocarbons in large concentrations, the likelihood of aspiration is usually reduced because of the viscosity of the finished product.

1) Pulmonary function abnormalities consistent with air flow obstruction (decreased FEV1, vital capacity and peak expiratory flow) have been found in spray paint abusers (Reyers de la Roche, 1987), construction painters (Schwartz & Baker, 1988), automobile painters exposed to hexamethylenediisocyanate who also smoked (Tornling et al, 1990), automobile painters exposed to toluene diisocyanate (Parker et al, 1991), painters exposed to epoxy paints (Rempel et al, 1991), and painters exposed to water-born paints (Ulfvarson et al, 1992).

1) Repeated or prolonged exposure to high concentrations of dusts of reactive dyes (fiber reactive dyes derived from azo, anthraquinone, and phthalocyanine classes) (Procion(R)), has resulted in pulmonary allergic sensitization with cough, chest tightness, and/or asthmatic wheezing (Alanko et al, 1978; Hagmar et al, 1986; Estlander, 1988). This is believed to be an IgE mediated (type I) reaction (Hagman et al, 1986).
2) A higher prevalence of respiratory symptoms was reported among automobile spray painters using isocyanate-based paints, than mechanics or industrial paint sprayers (Pisaniello & Muriale, 1989).
3) Painters exposed to epoxy paints had a higher incidence of lower respiratory symptoms such as cough, wheezing, chest tightness and shortness of breath compared with non-exposed control subjects (Rempel et al, 1991). In a study of house painters, Wieslander et al (1997) found that painters exposed only to water based paints had fewer self-reported symptoms related to airway obstruction or bronchial hyperresponsiveness as compared to solvent based painters, but noted that airway irritation can still occur among selected individuals.

1) Exposure to isocyanate-based acrylic paints may induce asthma in sensitive individuals (Selden et al, 1989). Pulmonary reactions to isocyanates in paints may be life-threatening (Belin et al, 1981).
2) Five patients exposed to a tributyltin containing interior paint complained of wheezing; mild expiratory wheezing was present on physical exam in the two youngest children (ages 35 and 28 months) only (Wax & Dockstader, 1995).
3) Two men developed fever and dyspnea with residual hyperreactive airways after electric arc welding steel painted with a chloro-containing polymer lacquer (Sjogren et al, 1991).
4) CASE REPORT: A 39-year-old man developed cough, dyspnea, severe airway obstruction, hypoxia, fever and leukocytosis after working in a factory where boards were painted with a paint containing an epoxy resin and a carboxylated polyester (Cartier et al, 1994).

1) CASE SERIES: In 8 textile printing factories in Spain, an outbreak of severe interstitial lung disease occurred, in which 6 deaths from pneumonia were reported (Moya et al, 1994). The outbreak was considered to be secondary to a change in products (Acramin FWR was substituted for Acramin FWN).
2) CASE SERIES: Five female workers who spray painted lace cloth developed respiratory distress, cough, fever, cyanosis, obstructive airway disease, hypoxia and bilateral alveolar-interstitial infiltrates on chest x-ray (Kadi et al, 1994). One patient died, and two others were left with permanent pulmonary disease. The responsible agent was believed to be Acramin FWN, an agent banned from Spain after causing similar pulmonary toxicity.

1) In one study, painters showed elevated risk of mortality from nonmalignant respiratory disease (Englund, 1980).

1) Headache, lightheadedness, and fatigue are commonly reported after acute exposure to paint fumes (Hansen et al, 1987; Atkinson et al, 1989). Severe exposure in poorly ventilated areas may cause ataxia, amnesia, confusion and lethargy (Atkinson et al, 1989).

1) Chronic exposure to paints and solvents due to recreational substance abuse is associated with a toxic encephalopathy characterized by memory impairment, difficulty concentrating, fatigue, headache, dizziness, apathy, depression, anxiety, and personality changes.
2) Decreased cerebral blood flow, cerebral atrophy, and vestibular dysfunction have been found in paint and solvent exposed workers with evidence of encephalopathy (Riusberg & Hegstadius, 1983; Orbaeck et al, 1985; Arlien-Soborg, 1984).
3) Neurologic effects do not appear to reverse with cessation of exposure (Arlien-Soborg, 1984; Brhun et al, 1981).

1) Workers in a paint manufacturing plant who were highly exposed to organic solvents had an increased incidence of loss of blue-yellow color vision compared with moderately exposed workers (Mergler & Blain, 1987).

1) Headache was one of the most commonly reported symptoms among users of water-based paints (Hansen et al, 1987).

1) NEUROPSYCHOLOGIAL PERFORMANCE: Several studies have suggested that people with chronic occupational exposure to paint and solvents perform more poorly on tests of learning, memory, visual perception, and attention (Colvin et al, 1993; Spurgeon et al, 1992; Daniell et al, 1993; Chen et al, 1999).
2) PAINTER'S SYNDROME - An irreversible deterioration of cognitive function, called painter's syndrome or ORGANIC SOLVENT DISEASE, has been described in painters after many years of exposure. Solvents are thought to be the causative agents; the possible additional effect of heavy metal pigments has not been explored. Structural changes on CT scans may be evident in the later stages. Psychiatric changes involve memory loss, personality change, depression, and anxiety (Linz et al, 1986).

1) Nausea and diarrhea may occur. Gamboge (from Garcinia hanburyi) is a cathartic and irritant.
2) CASE SERIES: Five patients exposed to interior paint containing tributyltin developed nausea and vomiting (Wax & Dockstader, 1995).

1) Painters showed elevated risk of mortality from nonmalignant disease of the upper gastrointestinal tract (Englund, 1980).

1) Stenosis, portal tract enlargement, and fibrosis which persisted for over a year has been reported in house painters following long-term occupational exposure to organic solvents (Dossing et al, 1983).

1) CHRONIC TOXICITY

1) Ingestion of a paint containing toluidine red may result in methemoglobinemia (McCann, 1979).

1) Transient bone marrow depression may be seen following heavy acute exposure to the fumes of polyurethane-based paint (Atkinson et al, 1989).

1) LEAD POISONING: Blood disorders characteristic of lead poisoning were seen in persons manufacturing paint under uncontrolled conditions (Tangredi et al, 1981).

1) CASE REPORT (ADULT): Leukocytosis was seen in a spray painter following application of a hexamethylene and toluene diisocyanate-based paint (Nielsen et al, 1985).

1) Allergic contact dermatitis is a common problem among workers exposed to paint, or in some case in individuals exposed to painted or lacquerware jewelry. Contact dermatitis has been associated with exposure to paints containing amino-substituted diacrylate, isothiazolinones, methyl ethyl ketone peroxide, triglycidyl isocyanurate, epoxy resins, lacquer, and other components.
2) Allergic contact dermatitis has been reported after the use of paints containing reactive dyes or triglycidyl isocyanurate (Estlander, 1988; Stern, 1985; Thoren et al, 1986; Mathias, 1988) Dooms-Goossens et al, 1989; (Foulds & Koh, 1992).
3) DELAYED pruritus, erythema, and vesiculation on the wrists and forearms, has occurred after exposure to antifouling paints containing tributyl tin oxide (Goh, 1985; Lewis & Emmett, 1987).

1) Irritant contact folliculitis was seen in a painter using a paint containing triphenyl tin fluoride (Andersen & Petri, 1982).

1) CASE REPORT: Second degree burn over 70 percent of the body surface area developed in a 22-year-old man who lost consciousness while painting a bathroom with a toluene-based sealer. It was estimated that he had skin contact with the spilled sealer for approximately five hours prior to receiving dermal decontamination. Shortly after arrival the patient developed asystole and was successfully resuscitated. However, coagulation necrosis of the burned skin, rhabdomyolysis, non-oliguric renal failure, and anoxic brain injury occurred and the patient died on the sixth hospital day (Shibata et al, 1994).

1) High-pressure injection injury of tissues is a hazard from the use of paint guns. Solvent-based paints injected into tissue can cause dissolution of fat and other tissues, resulting in necrosis of subcutaneous tissue and thrombosis of vessels, a 60 to 80 percent amputation rate, and possible systemic toxicity.
2) The majority of cases involve the hands (Scott, 1983; Neal & Burke, 1991). Of 14 injuries, 3 required digital amputation (Mrvos et al, 1987).
3) Paint solvents are most damaging because of their low viscosity and rapid spread through tissues (Schoo et al, 1980; Kaufman, 1968; Thacker et al, 1986; Herrick et al, 1980).
4) Systemic effects can occur within the first 48 hours; effects may persist for 4 to 6 days (Harter & Harter, 1986).
5) Factors which appear to correlate with worse prognosis include (Neal & Burke, 1991):

1) IgG ANTIBODIES: Titers for IgG antibodies against hexamethylene diisocyanate and its oligomers were detected in blood from automobile painters who had used polyisocyanate-containing paints (Welinder et al, 1988; (Selden et al, 1989).

1) PATERNAL EXPOSURE: Paternal occupation as a painter was associated with increased odds ratios for spina bifida, patent ductus arteriosus, and cleft palate among 14,415 live births in British Columbia between 1952 and 1973 (Olshan et al, 1991).
2) Solvent exposure has also been associated with birth defects and other reproductive disorders. In Finnish studies, the risk of CNS defects in the children of women working with solvents was increased (Holmberg, 1979; Holmberg & Nurminen, 1980). In a Danish study of female painters, there was an increased risk of spontaneous abortions that could not be attributed to a single chemical (Heidam, 1984).
3) Paint sniffing is a major form of solvent abuse. Three of 5 children born to women who sniffed paint were growth-retarded, and 2 had craniofacial abnormalities and hyperchloremic acidosis (Goodwin, 1988).

1) Chronic paint exposure has been associated with an increased risk of developing BLADDER (Myslak et al, 1991; Silverman et al, 1989; Matanoski et al, 1986), LARYNX (Englund, 1980; Brown et al, 1988), ESOPHAGUS (Englund, 1980), LUNG (Stockwell & Matanoski, 1985; Matanoski et al, 1986), BILE DUCT (Englund, 1980), and BOWEL AND RECTUM (Morgan et al, 1981) cancer, LEUKEMIA (Sandler, 1987; Matanoski et al, 1986), and MULTIPLE MYELOMA (Lundberg, 1986).
2) Scandinavian painters were at increased risk for developing cancers of the lung, oral cavity, esophagus, and liver, even after such confounders as cigarette smoking and ethanol drinking were considered (Skov et al, 1993). Persons chronically exposed to paint may be at increased risk for

1) Persons with past employment as painters had a 2.76-fold increased risk for bladder tumors when compared with a control group of persons with prostate disease (Myslak et al, 1991).
2) Painters were 1 of the occupational groups most at risk for bladder cancer in the National Bladder Cancer Study; the overall relative risk was 1.5 and ranged as high as 3.0 for older and longer exposures (Silverman et al, 1989).
3) US painters from 4 states were at increased risk for mortality from cancer of the bladder (Matanoski et al, 1986).

1) Workers potentially exposed to paint had elevated risk of laryngeal cancer (Englund, 1980; Brown et al, 1988). Esophageal cancers were also elevated (Englund, 1980).

1) Chronic exposure to paint has been associated with increased risk for acute myelogenous leukemia (Sandler, 1987). US painters from 4 states were at increased risk of mortality from leukemia, after correction for nonoccupational factors (Matanoski et al, 1986). Children of fathers who were exposed to spray paint during pregnancy or after birth were at 2-fold increased risk for leukemia (Lowengart et al, 1987).
2) Painting was identified as a risk factor for development of leukemias (acute myeloid, acute lymphocytic, various preleukemic states) in a large case-control study on Italian patients (Mele et al, 1994).

1) Painters who never wore a mask or respirator were at 5-fold excess risk for lung cancer when compared with random controls from a trade union population (Stockwell & Matanoski, 1985). An increased risk of mortality from lung cancer was still evident after correction for nonoccupational factors (Matanoski et al, 1986). Another study also found that painters had an increased risk of mortality from lung cancer (Skov et al, 1993).

1) Painters showed an excess of cancer of the intrahepatic bile ducts (Englund, 1980).

1) A group of Swedish workers in the paint manufacturing industry had a 5-fold greater than expected risk of mortality from multiple myeloma (Lundberg, 1986).

1) Increased mortality from bowel and rectal cancer was seen in a group of 16,243 men employed in the manufacture of paint and varnish; there was no major health hazard overall in this group, however (Morgan et al, 1981).

1) An increased risk of mortality from pharyngeal cancer was found in painters from Norway, Finland, and Denmark, and an increased risk of death from cancer of the mouth was found in painters from Sweden in 1 study involving painters from all Nordic countries (Skov et al, 1993).

1) Alcohol levels may be appropriate when indicated.
2) Levels of serum isocyanate-specific IgG have correlated better with exposure to isocyanates than with development of symptoms (Selden et al, 1989).
3) A specific heavy metal blood level (ie, blood lead) may be helpful, as may a chest X-ray for aspiration hazard. Obtain CBC, renal, and hepatic function studies as indicated. Individual hydrocarbon blood levels have only medicolegal value.

1) Monitor urinary excretion of heavy metals as indicated. Refer to documents on the specific metal involved for more information.

1) PULMONARY FUNCTION TESTS
2) MONITORING

A) Patients with persistent symptoms of aspiration or with acute symptoms of heavy metal poisoning should be admitted.

A) Patients with symptoms limited to minor irritation after inadvertent exposure to paints that do not contain heavy metals can be managed at home.

A) Consult a medical toxicologist or poison center for patients with significant ingestions of paints containing heavy metals. Refer patients who recreationally inhale solvent based paints for substance abuse counseling. Consult a pulmonologist for patients with severe aspiration.

A) Patients with clinical evidence of aspiration (cough, increased work of breathing, wheezing) or ingestion of paints that contain heavy metals should be referred to a healthcare facility. Patients who deliberately inhale solvent based paint should be referred to a healthcare facility.

1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) GI decontamination is generally not indicated because of the low risk of acute toxicity and the possibility of aspiration. Activated charcoal and/or gastric lavage can be considered after substantial ingestion of lead based paint. Wash exposed skin with soap and water; mineral oil may help remove oil based paint. Irrigate exposed eyes.

1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes).
2) PRECAUTIONS:
3) LAVAGE FLUID:
4) COMPLICATIONS:
5) CONTRAINDICATIONS:

1) CHARCOAL ADMINISTRATION
2) CHARCOAL DOSE

1) MANAGEMENT OF MILD TO MODERATE TOXICITY: Treatment is symptomatic and supportive.
2) MANAGEMENT OF SEVERE TOXICITY: Chelation may be necessary for patients with significant exposure to paints containing heavy metals. OBSERVE FOR ASPIRATION PNEUMONITIS and treat accordingly (see hydrocarbon management). Suspect aspiration if coughing or choking occurs following ingestion of oil-based paints. Aspiration pneumonitis should be treated with oxygen, inhaled beta agonists for bronchospasm, and in severe cases endotracheal intubation may be necessary.

1) No specific lab work is needed after exposure to most paints.
2) Obtain a serum lead concentration after acute ingestion or chronic exposure to lead based paint.
3) Obtain urinary (mercury, manganese, cobalt), blood (cadmium, manganese) concentrations of specific heavy metals after significant exposure to paints that contain them.
4) Obtain serum electrolytes after deliberate or prolonged inhalation of paint containing toluene or ingestion of paint containing barium.
5) Obtain CBC, renal function, and hepatic enzymes in symptomatic patients.
6) Chest radiographs as needed clinically for suspected aspiration.
7) An abdominal radiograph may be useful to assess the adequacy of decontamination after ingestion of paint containing lead or other heavy metals.

1) Chelation should be initiated for heavy metal poisoning as indicated. See specific heavy metal managements.

1) Patients exposed dermally should wash the exposed area twice with soap and water. Oil-based paint may be removed from the skin with mineral oil (baby oil). A physician may need to examine the exposed area if irritation or pain persists after the area is washed.
2) Dried paint will eventually wear off when the top layer of old skin sheds.

a) The use of mercury-based biocides in INTERIOR paints was canceled by the US EPA, effective August 20, 1990. Existing stocks of pesticides were allowed to be sold and used for manufacture of exterior products until June 27, 1991, provided they are properly labeled with language prohibiting use in interior paints and coatings (EPA, 1990).
b) Because current inventories were not affected, paints containing mercury-based biocides may still be available on the market.