HYDROCARBONS

Classification | Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

Specific Substances

1) Benzin
2) Petroleum ether
3) CAS 8030-30-6

1) CAS 8006-61-9

1) Petroleum naphtha
2) Charcoal lighter fluid
3) Lighter fluid

1) Varnish makers' naphtha
2) Painters' naphtha
3) Printers' naphtha
4) Dry cleaners' naptha
5) Spotting naptha
6) CAS 8030-30-6

1) Mineral spirits No. 10
2) High flash naphtha
3) White spirits
4) CAS 8052-41-3

1) Signal oil
2) Furniture polish

1) Kerosine
2) Range oil
3) Home heating oil no. 1
4) CAS 8008-20-6

1) Gas oil
2) Home heating oil no. 2

1) Motor oil
2) Grease
3) Petroleum lubricating oils

1) Petrolatum jelly
2) CAS 8009-03-8

1) CAS 8002-74-2

1) Mineral pitch
2) Bitumen
3) CAS 8052-42-4

1) CAS 106-99-0

1) CAS 106-97-8

1) CAS 74-84-0

1) n-hexane
2) CAS 110-54-3

1) CAS 74-82-8

1) CAS 74-98-6

1) CAS 71-43-2

1) CAS 108-88-3
2) Methyl benzene
3) Toluol

1) CAS 1330-20-7
2) o-xylene CAS 95-47-6
3) m-xylene CAS 108-38-3
4) p-xylene CAS 106-42-3
5) Mixed xylenes

1) Spirit of turpentine
2) Oil of turpentine
3) Wood turpentine
4) CAS 8006-64-2

1) Pine oil cleaner
2) CAS 8006-88-0

1) Tetrachloromethane
2) Perchloromethane
3) CAS 56-23-5

1) Trichloromethane
2) CAS 67-66-3

1) Monochloromethane
2) CAS 74-87-3

1) Dichloromethane
2) CAS 75-09-2

1) Ethylene tetrachloride
2) Perchloroethylene
3) CAS 127-18-4

1) 1,1,1-trichloroethane
2) alpha-Trichloroethane
3) Chlorothene
4) Methyl chloroform
5) CAS 71-55-6

1) Vinyl trichloride
2) Trichloroethane
3) 79-00-5

1) Chloroethylene
2) CAS 75-01-4

1) Trichloroethene
2) TCE
3) CAS 79-01-6

1) Automatic transmission fluid

1) Coal pitch

1) CTPV
2) Polycyclic aromatic hydrocarbons (PAH)
3) Polynuclear Aromatics (PNAS)
4) Particulate polycyclic organic matter (PPOM)
5) CAS 65996-93-2

1) Water-based cutting fluids

1) Dielectric fluids

1) Diesel fumes

1) Diesel oil

1) Liquid petroleum gas
2) LPG
3) Bottled gas
4) Compressed gas

1) Machining fluids

1) Pressurized paints

1) Thermoplastic roadpaint

1) Waste petroleum oils

1) Howard & Neal, 1992
2) Gosselin, 1984
3) Hathaway et al, 1996
4) Lewis, 1997

1) DIESEL FUEL
2) CYCLOHEXANE, METHYL-
3) COAL TAR NAPTHA
4) COAL TAR DISTILLATE
5) CASINGHEAD GASOLINE
6) DIESEL FUEL OIL
7) BENZINE (LIGHT PETROLEUM DISTILLATE)
8) JET FUEL: JP-1
9) RUBER SOLVENT (NAPHTHA)
10) OCTANE, NORMAL
11) PENTAN
12) PENTANEN
13) PENTANES, LIQUID
14) PENTANI
15) HYDROCARBON GASES, COMPRESSED
16) RESIDUAL (HEAVY) GUEL OILS
17) SKELLYSOLVE F
18) SKELLYSOLVE G
19) TOLUENE, HEXAHYDRO-
20) UN 1270 (DOT)
21) VM AND P NAPHTHA
22) BENZYNA DO LAKIEROW C
23) PETROLEUM SPIRIT
24) HYDROCARBON GAS MIXTURE, COMPRESSED
25) DISTILLATES (COAL TAR)
26) FUEL OIL NO.1 (KEROSENE)
27) GASOLENE
28) HI-FLASH NAPHTHAYETHYLEN
29) HYDROCARBON
30) NORMAL-HEPTANE
31) HYDROCARBON GAS, LIQUEFIED
32) NAPTHA
33) HYDROCARBON GAS MIXTURE, LIQUEFIED
34) HYDROREFINING
35) NAFTA (POLISH)
36) NAPHTHA
37) NAPHTHA DISTILLATE
38) DISTILLATE
39) HYDROGEN GAS, COMPRESSED, N.O.S.
40) COAL OIL (EXPORT SHIPMENT ONLY)
41) THINNER

Available Forms Sources

1) Available in numerous products and listed as "non-toxic" components of others. Many poisonings are due not to a product component but to the aspiration of the "non-toxic" hydrocarbon solvent.
2) Number 1 fuel oil refers to Kerosene.
3) Number 2 fuel oil refers to the general "fuel oil" category, e.g., gas oil or diesel oil. Number 2 fuel oil is slightly less volatile and more viscous than kerosene but shares the same toxic potential.
4) Retailers in South Africa sell paraffin in unmarked cooldrink bottles which may contribute to the high incidence of children being poisoned by paraffin in South Africa (Rainier-Pope, 1991; Violari & Levenstein, 1991).

1) Hydrocarbons are primarily derived from petroleum coal tar and plants.

Overview

Life Support

Clinical Effects

0.2.1)

A) USES: Hydrocarbons are a diverse group of organic compounds that are made up of primarily carbon and hydrogen atoms. Hydrocarbons are derived from petroleum, coal tar and natural gas, as well as from plants and animals. They may be classified as aliphatic (including the paraffins, olefins, acyclic terpenes, and acetylenes) and cyclic (including the alicyclics, aromatics and cyclic terpenes). Examples range from gasoline to essential oils to solvents. They are used as fuels and solvents, and are found in many household and commercial products.
B) PHARMACOLOGY: Pharmacology of hydrocarbons varies according to the specific substance. Some have sites of action in the CNS, namely increasing neurotransmitter binding and potentiating nicotinic blockade by interacting with acetylcholine receptors. Others stimulate GABA A activity. Glutamate release may be stimulated or transmission inhibited, depending on the specific agent. Glycine receptor activity may be augmented with certain hydrocarbons, and hydrocarbons are used as general anesthetics. In addition, alpha-2 adrenergic receptor activation can occur.
C) TOXICOLOGY: Hydrocarbons are a large and diverse group of substances with toxicity varying according to specific substance and route of exposure. Pneumonitis after aspiration is common and is the main route of injury from hydrocarbons. The exact mechanism of pulmonary toxicity is unclear but is likely due to direct toxicity to lung tissue as well as destruction of surfactant. Low viscosity, low surface tension and high volatility of a hydrocarbon (gasoline, for example, has all of these properties) increase the aspiration potential of that particular compound. Pulmonary toxicity can also occur after IV injection of hydrocarbons. Acute systemic toxicity is primarily due to CNS depression, reflecting the inhalational anesthetic effects of hydrocarbons. Inhalational abuse of hydrocarbons can cause simple asphyxiation. Chronic exposure in industrial settings or after long-term inhalational abuse can lead to chronic nervous system effects. Chlorinated hydrocarbons may cause cardiac sensitization to catecholamines, predisposing patients to cardiac dysrhythmias. Halogenated hydrocarbons may also cause hepatotoxicity, nephrotoxicity, and electrolyte disturbances. Hydrocarbons can destroy lipid bilayers and this can lead to "defatting" dermatitis following prolonged skin exposure. Capillary endothelium can be severely damaged in any organ system exposed to hydrocarbon. Hemolysis is rarely reported after hydrocarbon ingestion. Benzene is a bone marrow toxin.
D) EPIDEMIOLOGY: Poisoning is relatively common as these products are widely available in homes and industrial settings. Populations at highest risk include children with unintentional exposure (often ingesting pleasant-smelling oils), workers with occupational exposures, and those who intentionally abuse solvents via inhalation (often referred to as "sniffing" or "huffing"). Toxicity is primarily due to aspiration, but may occur via oral, parenteral, dermal or inhalational routes depending on the substance and nature of exposure.
E) WITH POISONING/EXPOSURE

1) ACUTE EFFECTS OF INGESTION by SIMPLE PETROLEUM DISTILLATES: Low viscosity, highly volatile hydrocarbons (eg, kerosene, gasoline, liquid furniture polish) are chiefly aspiration hazards. Pulmonary damage, transient CNS depression or excitement, and secondary effects of hypoxia, infection, pneumatocele formation, and chronic lung dysfunction can occur. Cardiac complications are rare. These hydrocarbons are poorly absorbed from the gastrointestinal tract and do not cause appreciable systemic toxicity by this route unless aspiration has occurred.
2) ACUTE EFFECTS OF INGESTION by CHLORINATED AND AROMATIC HYDROCARBONS: Many chlorinated, aromatic and other substituted hydrocarbons can produce systemic toxicity following ingestion. CNS, respiratory depression, dysrhythmias, gastrointestinal disturbances, and other effects may occur depending on the agent and amount ingested.
3) ACUTE EFFECTS OF INHALATION: Cardiac dysrhythmias and CNS depression are major concerns of acute exposure. Straight chain hydrocarbons with few carbon atoms (eg, methane, ethane, propane gases) can cause asphyxiation if exposure occurs in poorly ventilated spaces.

a) INHALATIONAL ABUSE ("sniffing") of some hydrocarbons can result in sudden death, encephalopathy, residual neurological impairment, nephrotoxicity, hepatotoxicity, acid-base disturbances, and rhabdomyolysis.

4) INJECTION of kerosene, naphtha, turpentine, gasoline, or hydrocarbon insecticides has resulted in febrile reactions, local tissue inflammation and systemic effects, including pulmonary edema, pneumonia, and mild CNS depression. Severe cases have resulted in multiorgan dysfunction syndrome. Injection of pressurized hydrocarbons has caused severe tissue damage.
5) DERMAL/EYE: Mild to moderate eye irritation and reversible ocular injury may occur after contact with most hydrocarbons. Acute but prolonged exposure to some hydrocarbons can result in dermal burns and occasionally, systemic effects. Frostbite can result from contact with some liquefied gases (eg, propane, methane, ethane).
6) TYPES OF HYDROCARBONS INCLUDE:

a) LOW VISCOSITY, UNSUBSTITUTED: Hydrocarbons with low viscosity (less than 100 S.U.S.), low surface tension, and high volatility are most likely to cause aspiration pneumonitis. Vapor inhalation can cause CNS depression or excitation and other effects. Examples: kerosene, mineral seal oil, gasoline, petroleum naphtha.
b) HIGH VISCOSITY, UNSUBSTITUTED ALIPHATIC: Hydrocarbons with high viscosity and low volatility are less likely to be aspirated after ingestion and are generally poorly absorbed from the gastrointestinal tract. Petroleum jelly may cause a mild laxative effect. Oil mist inhalation may cause lipoid pneumonia. Examples: motor oil, petroleum jelly.
c) TERPENES: In addition to aspiration, these tend to produce a mild CNS depression after ingestion. Examples: turpentine oil, pine oil. Pine oil cleaners may contain approximately 10% isopropyl alcohol and other additives which may contribute to the observed toxic effects.
d) AROMATICS: These have a high potential for CNS depression, a mild tendency to cause cardiac irritation, and little risk of aspiration. Adverse effects can result from vapor inhalation, ingestion, or skin exposure. Examples: benzene, xylene. Many polyaromatic hydrocarbons are potential carcinogens.
e) HALOGENATED-CHLORINATED: These can produce CNS effects, dysrhythmias, renal and hepatic effects. Aspiration is a small risk. Adverse effects can result from vapor inhalation, ingestion, or skin exposure. Examples: chloroform, carbon tetrachloride, trichloroethylene.
f) NOTE: Brominated hydrocarbons, fluorinated hydrocarbons, alcohols, esters, ethers, chlorinated hydrocarbon pesticides, and other hydrocarbons are covered in other managements.

7) MILD TO MODERATE POISONING: The primary effect seen in mild to moderate inhalational poisoning is euphoria and intoxication followed by CNS depression. This should resolve quickly with removal from the source of inhalational exposure. Patients with oral exposure usually have some gastrointestinal upset and then can develop systemic symptoms as the hydrocarbon is absorbed if a large quantity is ingested. Patients who have vomiting are at increased risk of aspiration. Aspiration may cause minimal respiratory symptoms (eg, an intermittent cough) initially but progress to severe respiratory injury.
8) SEVERE POISONING: Severe effects may include coma and dysrhythmias. Severe pneumonitis from aspiration may require prolonged intubation. Patients that aspirate will often display a systemic inflammatory response including fever. Chlorinated hydrocarbons can cause ventricular dysrhythmias, and can cause hepatic necrosis that may progress to liver failure. Injection can cause compartment syndrome and necrotizing fasciitis.
9) CHRONIC POISONING: Long-term or repeated exposure to certain aromatic and chlorinated hydrocarbons can result in hematologic (eg, benzene), hepatotoxic (eg, chlorinated hydrocarbons), renal (eg, chlorinated hydrocarbons), neuropsychiatric (eg, toluene), neurological (eg, n-hexane) and carcinogenic (eg, benzene, vinyl chloride) effects. Some effects have occurred primarily in chronic solvent abusers or glue sniffers (eg, neuropsychiatric, renal, and hepatic effects of toluene). Chronic or repeated exposure can result in skin irritation due to defatting of the skin. Greases, coal pitch, and cutting oils can produce acne and folliculitis. Chlorinated aromatic hydrocarbon exposure can result in chloracne.

0.2.20)

A) In a prospective study in Toronto, major congenital malformations were noted in 13 of 125 fetuses of mothers exposed to organic solvents during pregnancy. An analysis of data from the ongoing, case-control, National Birth Defects Prevention Study found that for women with occupational exposure to polycyclic aromatic hydrocarbons (PAH) in the month before through 3 months after conception had increased risk for having offspring with a neural tube defect (NTD), particularly spina bifida; however, after adjusting for confounders, the odds ratio for NTDs and spina bifida decreased and lost statistical significance.

Laboratory Monitoring

Treatment Overview

0.4.2)

A) MANAGEMENT OF MILD TO MODERATE TOXICITY

1) Remove the patient from the source of exposure. When a patient is removed from an inhalational exposure, the symptoms should quickly resolve. Adolescents may present without symptoms after responsible adults find them abusing hydrocarbons via inhalation. Provide oxygen and symptomatic and supportive care. After assuring that the patient is medically stable, remove contaminated clothing and wash exposed skin with soap and water.

B) MANAGEMENT OF SEVERE TOXICITY

1) Orotracheal intubation for airway protection should be performed early if a patient exhibits respiratory distress. Prophylactic antibiotics and steroids are of no proven benefit in hydrocarbon pneumonitis. Animal studies suggest that artificial surfactant via orotracheal tube may be of benefit. Monitor and treat for dysrhythmias.

C) DECONTAMINATION

1) PREHOSPITAL: GI decontamination is not recommended because of the risk of aspiration. Remove contaminated clothing and wash exposed skin with soap and water.
2) HOSPITAL: Studies fail to show if gastric emptying improves outcomes in patients with oral hydrocarbon ingestions. However, if a patient has ingested a large amount of a hydrocarbon that causes significant systemic toxicity shortly prior to presentation, it is reasonable to insert a small NG tube and aspirate gastric contents. Activated charcoal should NOT be used; it does not adsorb hydrocarbons well and increases the likelihood of vomiting and aspiration.

D) AIRWAY MANAGEMENT

1) Perform early in patients with severe intoxication (coma, dysrhythmias, respiratory distress).

E) ANTIDOTE

1) None.

F) HYPERTHERMIA

1) Consider antipyretics. Evaluate for secondary pneumonia and other infectious causes.

G) COMA

1) Treatment is symptomatic and supportive. Perform orotracheal intubation to protect airway. Assess oxygenation, evaluate for hypoglycemia, and consider naloxone if coingestants are possible.

H) TACHYCARDIA

1) Tachycardia may occur from a combination of agitation and catecholamine release. Treat with IV fluids and benzodiazepine sedation if agitation is prominent.

I) DYSRHYTHMIAS

1) Initiate ACLS protocols. Some solvents appear to sensitize the myocardium to catecholamines. Epinephrine and other sympathomimetics should be used with caution as ventricular dysrhythmias may be precipitated.

J) RESPIRATORY DISTRESS

1) Administer oxygen. Intubate early if patient has respiratory symptoms. Consider the use of a surfactant. Endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality in one study.

K) RESPIRATORY FAILURE

1) Partial liquid ventilation, high frequency jet ventilation, extracorporeal membrane oxygenation (ECMO) and high frequency chest wall oscillation have all been used with apparent success in cases of severe hydrocarbon pneumonitis.

L) ENHANCED ELIMINATION

1) Hemodialysis and hemoperfusion are not of value.

M) PATIENT DISPOSITION

1) HOME CRITERIA: Asymptomatic patients with inadvertent exposures may be monitored at home, with particular attention to the development of any respiratory symptoms. Patients who develop symptoms during home monitoring should be referred to a medical facility.
2) OBSERVATION CRITERIA: Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation for 6 to 8 hours. Although patients can develop a delayed pneumonitis, they are unlikely to do so if they have been completely asymptomatic during that time period.
3) ADMISSION CRITERIA: Patients with significant persistent central nervous system toxicity (somnolence, delirium), or respiratory symptoms of cough or tachypnea should be admitted. Patients with coma, dysrhythmias, or respiratory distress should be admitted to an intensive care setting.
4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (dysrhythmias, coma or respiratory distress), or in whom the diagnosis is not clear.

N) PITFALLS

1) Failure to aggressively manage the airway can result in death. Patients with minimal respiratory symptoms may progress to severe toxicity over several hours. Patients with altered mentation should be ruled out for intracranial hemorrhage, infection, metabolic disturbance and other toxicologic causes.

O) DIFFERENTIAL DIAGNOSIS

1) Hypoglycemia, central nervous system infection, pulmonary infection, rheumatologic or endocrine etiology, other sedative poisoning (ethanol/benzodiazepine/barbiturate for example), mental illness.

0.4.3)

A) INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.

0.4.4)

A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

0.4.5)

A) OVERVIEW

1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
2) Some chemicals can produce systemic poisoning by absorption through intact skin. Carefully observe patients with dermal exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.

Range Of Toxicity

Clinical Effects

Summary Of Exposure

Heent

3.4.3)

A) WITH POISONING/EXPOSURE

1) KEROSENE: In small amounts, low viscosity compounds such as kerosene usually cause little or no injury even when the eye is directly exposed to the liquid (Grant & Schuman, 1993).
2) GASOLINE: The more volatile petroleum derivatives (e.g., gasoline) may cause pain on contact with the eye but usually result in only slight, transient corneal irritation. Vapor concentrations of 270 or greater ppm produce a sensation of eye irritation (Grant & Schuman, 1993).
3) COLOR VISION IMPAIRMENT: Exposure to hydrocarbons may result in the loss of color vision, with the risk of impaired color vision increasing with increasing exposure (Semple et al, 2000).

3.4.5)

A) WITH POISONING/EXPOSURE

1) OLFACTORY FUNCTION: Occupational exposure to low or moderate concentrations of organic solvent vapors in 54 painters did NOT alter olfactory function (smell) when compared to 42 unexposed referents (Sandmark et al, 1989).

Cardiovascular

3.5.2)

A) CONDUCTION DISORDER OF THE HEART

1) WITH POISONING/EXPOSURE

a) INGESTION: Cardiac dysrhythmias, including ventricular fibrillation, have been reported only rarely following ingestion, but are most likely due to hypoxia or acidosis, rather than the hydrocarbon (Kulig & Rumack, 1981).

1) MYOCARDIAL DEPRESSION: CASE REPORT: A 19 month-old-girl developed severe myocardial depression with a cardiac index of 2.9 L/min/m(2), central venous pressure of 19 mm Hg and clinical evidence of hypoperfusion (tachycardia, delayed capillary refill and decreased urine output) 72 hours after ingesting paint thinner (Anene & Castello, 1994). She also developed severe aspiration pneumonitis requiring 18 days of ventilator support. Cardiac indices improved with dobutamine and amrinone and the follow up echocardiogram was normal.

b) INTRAVENOUS INJECTION: Atrial fibrillation with a rapid ventricular response occurred following IV injection of gasoline (Greenberg et al, 1993; Domej et al, 2007).

B) DEAD - SUDDEN DEATH

1) WITH POISONING/EXPOSURE

a) INHALATION of hydrocarbons may cause arrhythmias. The fatal ventricular arrhythmias, popularly labelled "sudden sniffing death" syndrome, may result from sensitization of the myocardium to circulating catecholamines (Kulig & Rumack, 1981).

1) The most commonly implicated hydrocarbons have been the halogenated hydrocarbons, trichloroethane and trichloroethylene (Bass, 1970). Freons, butane, methane, propane, and ethane have also been associated with sudden death in inhalant abusers (Anderson et al, 1985; Anderson et al, 1986; Garriott & Petty, 1980). Death was assumed to be due to cardiac arrhythmias and/or asphyxiation.
2) CASE REPORT: Prolonged exposure to concentrated vapors from mineral spirits was associated with the development of ventricular fibrillation and cardiopulmonary arrest in a 42-year-old female (Nierenberg et al, 1991).

b) INHALATION: CARBOXYHEMOGLOBINEMIA: Some methylene chloride (dichloromethane) is metabolized to carbon monoxide (Stewart et al, 1972). The contribution of carbon monoxide to the toxicity of dichloromethane is unknown. Theoretically, smokers and persons with cardiovascular diseases who are exposed to dichloromethane may be at increased risk of adverse effects which can result from elevated carboxyhemoglobin levels (US DHHS, 1992).

1) Two occupational studies did not find significantly increased incidence of fatal ischemic heart disease or ECG abnormalities in workers exposed to methylene chloride (Ott et al, 1983; Ott et al, 1983a).

Respiratory

3.6.2)

A) PULMONARY ASPIRATION

1) WITH POISONING/EXPOSURE

a) Aspiration resulting in significant pulmonary effects is most frequently associated with low viscosity (<100 SUS) hydrocarbons, such as kerosene, gasoline and lighter fluid. Aspiration of automatic transmission oil has been reported in one fatal pediatric case (Perrot & Palmer, 1992).
b) Initial signs and symptoms of aspiration most frequently occur during the act of swallowing and may include coughing, choking, and gagging (Beamon et al, 1976). If persistent coughing occurs immediately following ingestion, aspiration should be suspected.
c) Later signs and symptoms of aspiration pneumonitis include fever, dyspnea, tachypnea, cyanosis, rales, rhonchi, and decreased breath sounds. Fever and leukocytosis occur secondary to the aspiration and do not necessarily indicate a bacterial infection.
d) PINE OIL CLEANER (PEDIATRIC CASES): Chemical pneumonitis developed in 3 out of 5 pediatric cases of pine oil cleaner ingestion. Two of the 3 cases had almost immediate emesis after being given milk. Spontaneous vomiting occurred in all 5 cases within 10 to 90 minutes of ingesting the pine oil cleaner (Brook et al, 1989).
e) PINE OIL CLEANER (ADULT CASES): Nine out of 17 adults had spontaneous emesis after pine oil cleaner ingestion. Three cases who had gastrointestinal decontamination and who were comatose developed chemical pneumonitis (Brook et al, 1989).
f) LAMP OIL: Coughing, throat irritation, and pulmonary infiltrates have been reported following lamp oil ingestions of 10 mL or less (Burda et al, 1997; Martins et al, 1999). Lamp oil has a low viscosity of approximately 30 saybolt seconds universal units and primarily consists of aliphatic hydrocarbons (Martins et al, 1999).
g) CASE REPORT (INFANT): Aspiration pneumonitis was reported in an 11-month-old infant following ingestion of a high viscosity hydrocarbon-containing hair and body oil (safflower oil 50% to 80%, mineral oil 30% to 50%, and castor, avocado, sesame and jojoba oils <2% each). Approximately 15 minutes after ingestion, the patient presented with fever, tachycardia, tachypnea, persistent coughing, hypoxia, and wheezing. Over the next 24 hours, the patient developed bilateral pneumothoraces and pneumomediastinum necessitating tube thoracostomies and ECMO. Following the development of further barotrauma, hemorrhage from the chest tube sites, and inability to be weaned from ECMO, the patient eventually died 30 days post-ingestion (White et al, 2000).
h) CASE REPORT: A 30-year-old man was diagnosed with chemical pneumonia that progressed to necrotizing pneumonia after aspirating 10 mL of liquid hydrocarbon fuel during a fire-eating performance. Complications included large pleural effusions, pneumatoceles, and spontaneous pneumothorax. The patient made a full recovery 2 weeks after the exposure (Guandalini & Steinke, 2007).

B) PNEUMONITIS

1) WITH POISONING/EXPOSURE

a) TRIAGE CRITERIA: Wason & Katona (1987) reported that the following signs and symptoms present upon initial examination of patients after hydrocarbon ingestion have 80% or better predictive value for pneumonitis:

1) Lethargy, rhonchi, rales, retractions, cyanosis, and the development of leukocytosis and fever within 4 hours.
2) The only parameter with an 80% or greater predictive value for NO toxicity was the absence of tachypnea.
3) Early chest x-rays were not useful in predicting pneumonitis in symptomatic or asymptomatic patients (Wason & Katona, 1987).

b) IV INJECTION: CASE REPORT: A patient developed severe hemorrhagic pneumonitis after IV injection of 3 mL of charcoal lighter fluid (Vaziri et al, 1980).
c) IV INJECTION: CASE REPORT: A 26-year-old man injected 10 mL of gasoline in a suicide attempt and presented with a chemical pneumonitis. The patient's status deteriorated and he developed multi-organ dysfunction syndrome. The patient made a full recovery within 12 days of admission with aggressive, intensive care management (Domej et al, 2007).
d) CASE REPORTS: After ingesting naphtha, two 3-year-old boys developed chemical pneumonia with severe symptoms (dyspnea, suppressed breath sounds, crackles, hypoxemia, and cyanosis) unresponsive to supportive measures. On the first day of hospitalization, radiographic exam revealed pneumonic infiltration; severe pulmonary symptoms developed on the second and fourth days, respectively. Despite supportive care, their symptoms worsened; chest radiographs revealed localized consolidation and bilateral diffuse reticulonodular infiltration. Both patients were successfully treated with nebulized budesonside (0.5 mg every 12 hours for 4 days). They were discharged after a week of hospitalization (Gurkan & Bosnak, 2005).
e) CASE REPORT: A 45-year-old man developed lightheadedness, dyspnea, near-syncope, cough, chest tightness, vomiting, diarrhea, chills, and tremor after a 15-minute exposure to a canvas waterproofing spray (Meguiar's Marine Canvas Protectant) containing liquefied petroleum gas (1% to 10% w/v), ethylene glycol monobutyl ether (1% to 3% w/v), and isopropranol (1% to 3% w/v). He presented with respiratory distress (respiratory rate, 30 breaths/min) and tachycardia (HR, 140 beats/min) 2 hours after exposure. An initial chest x-ray was normal; however, a left sided infiltrate was observed on a repeat x-ray 12 hours post-exposure. Following supportive care, his dyspnea improved (respiratory rate, 20 to 24 breaths/min), but he remained tachycardic (HR, 120's beats/min). His condition gradually resolved following treatment with IV methylprednisolone and nebulized albuterol in the ICU and oral prednisone (Weibrecht & Rhyee, 2011).

C) ACUTE LUNG INJURY

1) WITH POISONING/EXPOSURE

a) Hemoptysis and pulmonary edema may occur after significant aspiration or inhalation (Shirkey, 1971; Janssen et al, 1988; Nierenberg et al, 1991; Segev et al, 1999).
b) IV INJECTION: CASE REPORT: Pulmonary edema and hypoxia immediately developed in 1 case after IV injection of pure gum turpentine (Wason & Greiner, 1986).

D) AIR CYST

1) WITH POISONING/EXPOSURE

a) PNEUMATOCELES developed 8 to 10 days after hydrocarbon ingestion in 3 children who developed severe pneumonitis (Bergeson et al, 1975). Six other published pediatric case reports indicated that the pneumatoceles developed within 5 to 15 days of hydrocarbon ingestion (Bergeson et al, 1975).

1) Pneumatoceles generally resolve within days or months of hydrocarbon ingestion (Bergeson et al, 1975), although pneumatoceles were still present in 1 patient at 230 days following ingestion (Stones et al, 1987).

b) CASE REPORT: A 20-year-old man presented with fever and dyspnea following aspiration of white spirit ingested in a suicide attempt. Bibasilar rales were detected following auscultation of the lungs and a chest x-ray revealed bilateral basal alveolar opacities. A high-resolution (HR) CT scan of the lungs showed patchy opacities, with well-defined walls, of the middle lobe, lingula, and lower lobes. After receiving symptomatic treatment and antibiotics for 14 days, a follow-up HRCT showed regression of the opacities; however, pneumatoceles in the left lobe had developed as well as a right asymptomatic pneumothorax. The patient continued to improve and he was discharged 20 days post-exposure. A follow-up CT scan, performed 23 months later, was normal (Facon et al, 2005).
c) LIPOID PNEUMONIA

1) CASE REPORT: An elderly woman developed lipoid pneumonia after using a lightweight aerosol cutting oil (WD-40(R)) for relief of arthritis for 2 years, with increased frequency of use several months prior to admission (Glenn & Gale, 1990).
2) CASE REPORT: Lipoid pneumonia was confirmed on autopsy in a 50-year-old woman following kerosene exposure in an unusual drowning accident (Segev et al, 1999).
3) CASE REPORT (PEDIATRIC): A 14-month-old child developed fatal pneumonitis, fibrosis and lipoid pneumonia after ingesting approximately 5 to 10 mL of automatic transmission fluid (Perrot & Palmer, 1992).

E) SINGLE LUNG ABSCESS

1) WITH POISONING/EXPOSURE

a) CASE REPORT (PEDIATRIC): A 5-year-old boy accidentally ingested kerosene oil, and presented with vomiting and tachypnea. Approximately 12 hours after admission, he became progressively more tachypneic and febrile to 39 degrees Celsius. Chest x-ray showed pneumonitis of the left lung, and antibiotics were initiated. A follow-up chest x-ray 1 week later showed a thick walled cavity, consistent with lung abscess. The patient completed 4 more weeks of antibiotics, and a chest x-ray at 5 months showed the cavity to be completely resolved (Aziz et al, 2007).

F) INJURY DUE TO ASPHYXIATION

1) WITH POISONING/EXPOSURE

a) Respiratory arrest, pneumonitis, or CNS depression can occur following hydrocarbon aspiration or vapor inhalation (Andrews & Snyder, 1991; Rodriguez et al, 1991; Goldfrank et al, 1998).
b) Methane, propane, butane, ethane, ethylene, and other gases can cause loss of consciousness and asphyxiation if their concentrations in the air are high and ventilation is poor (Klaassen, 1990; NIOSH, 1986) Compressed Gas Association, Inc, 1990).

G) PNEUMOTHORAX

1) WITH POISONING/EXPOSURE

a) CASE REPORT (PEDIATRIC): Pneumothoraces developed in a 14-month-old 2 days after ingesting about 5 to 10 mL of automatic transmission fluid (Perrot & Palmer, 1992).

H) BRONCHOSPASM

1) WITH POISONING/EXPOSURE

a) Human and animal data suggest kerosene may induce or aggravate asthma in susceptible individuals (Rodriguez de la Vega et al, 1990).
b) The environmental concentrations of selected volatile organic compounds were correlated with reported chronic lower respiratory symptoms and physician diagnosed asthma in a study of children who attended schools near chemical manufacturing industries (Ware et al, 1993). The study limitations have been addressed by Ware et al (1993) and DasSarma (1995).
c) CASE REPORT: Increasing dyspnea and cough were reported in an 18-year-old man, with a history of asthma, following unintentional inhalation of a toluene-containing solvent. On physical examination, the patient exhibited shallow breathing and nasal flaring. Breath sounds were diminished and O2 saturation was 82%. Chest x-ray revealed pulmonary hyperinflation. Suspecting mucus plugging, high-frequency chest wall oscillation (HFCWO) was initiated. Because of increased agitation and severe fatigue, non-invasive positive-pressure ventilation (NPPV) via nasal mask was added, in order to reduce the work of breathing and to avoid endotracheal intubation. Within minutes of initiating HFCWO-NPPV, the patient began to expectorate bronchial casts and his O2 saturation increased to 93% (Koga et al, 2004).

I) EPIGLOTTITIS

1) WITH POISONING/EXPOSURE

a) AIRFLOW OBSTRUCTION: Kennedy et al (1989) report an association of airflow obstruction with exposures to aerosols of various machining fluids (0.16 to 2.03 mg/m(3)) (Kennedy et al, 1989).

J) APNEA

1) WITH POISONING/EXPOSURE

a) Respiratory failure was reported in 4 patients following near-drowning in a river contaminated with kerosene. Two of the four patients died, with one autopsy revealing lipoid pneumonia (Segev et al, 1999).

Neurologic

3.7.2)

A) CENTRAL NERVOUS SYSTEM DEFICIT

1) WITH POISONING/EXPOSURE

a) INGESTION: ALIPHATIC HYDROCARBONS: Transient, mild CNS depression or excitement can occur after ingestion (Kulig & Rumack, 1981) of petroleum distillates and other aliphatic hydrocarbons. Profound CNS depression may represent hypoxia secondary to hydrocarbon pneumonitis (Eade et al, 1974).

1) Results of animal studies suggest that systemic effects of kerosene or naphtha are not likely to be due to gastrointestinal absorption (Bratton & Haddow, 1975; Capel & Gardner, 1960; Mann et al, 1977; Wolfe et al, 1970). CNS effects of these chemicals may be due to vapor inhalation or aspiration. Aliphatic hydrocarbons which have a large number of carbons are more likely to cause CNS depression (Sandmeyer, 1982).
2) TERPENES: CASE SERIES (PINE OIL CLEANER INGESTION): Five out of 5 pediatric cases and 3 out of 17 adult cases developed coma. An additional 5 adults were lethargic (Brook et al, 1989).
3) HALOGENATED & AROMATIC HYDROCARBONS such as carbon tetrachloride, and aromatic hydrocarbons (e.g., benzene) can produce CNS depression following ingestion (Klaassen, 1990).
4) ADDITIVES/CONTAMINANTS: Aniline, heavy metals, camphor, pesticides and other additives or contaminants in hydrocarbon preparations may produce CNS toxicity. Exposure to these substances should be ruled out in cases who exhibit significant CNS effects.

a) Aniline and nitrobenzene can cause methemoglobinemia (Harrison, 1977; Harvey & Keitt, 1983; Kearney et al, 1984). CNS effects may result from methemoglobinemia-associated hypoxia.

b) INHALATION: Vapors of halogenated, aromatic, other higher molecular weight hydrocarbons, and volatile petroleum distillates can cause CNS depression. High vapor concentrations of gasoline can cause CNS depression and death due to respiratory failure (Klaassen, 1990; Goldfrank, 1994).

1) TOLUENE CASE SERIES: Headache, dizziness and a sense of intoxication was reported by about 8 out of 16 subjects exposed for 6 hours to 100 ppm (Andersen et al, 1983). No CNS effects were reported following toluene exposures of 0, 10, or 40 ppm.
2) Methane, ethane, propane, butane, ethylene and other straight-chain hydrocarbons with few carbon atoms can indirectly cause CNS effects secondary to simple asphyxiation (Klaassen, 1990; NIOSH, 1986) Compressed Gas Association, Inc.).
3) Lightheadeness and tremor were reported in a patient who developed respiratory distress after exposure to a canvas waterproofing spray containing liquefied petroleum gas (1% to 10% w/v), ethylene glycol monobutyl ether (1% to 3% w/v), and isopropranol (1% to 3% w/v) (Weibrecht & Rhyee, 2011).

c) PERCUTANEOUS: Aromatic and halogenated hydrocarbons can be absorbed through the skin. Extensive or prolonged dermal exposure may contribute to systemic effects. Some contaminants or additives (e.g., aniline) may produce toxicity following skin absorption (Phillips et al, 1990).

1) CASE REPORT: A 12-year-old was disoriented, semicomatose and developed seizures after a 1 hour immersion in leaded gasoline. Renal failure also occurred. Cerebral edema was present at autopsy (Walsh et al, 1974).

B) CEREBELLAR DISORDER

1) WITH POISONING/EXPOSURE

a) GASOLINE: Chronic cerebellar degeneration may be associated with lead additives of gasoline, based on a case involving an adolescent who chronically sniffed gasoline (Young et al, 1977).
b) TOLUENE: Cerebellar abnormalities including ataxia, nystagmus and dysarthria have been reported in chronic toluene sniffers (Streicher et al, 1981; Malm & Lying-Tunell, 1980) and in a worker regularly exposed to toluene in a poorly ventilated room (Boor & Hurtig, 1977).

C) TOXIC ENCEPHALOPATHY

1) WITH POISONING/EXPOSURE

a) GASOLINE: Acute or subacute encephalopathic syndrome may result from gasoline sniffing (Burbacher, 1993).
b) TOLUENE: Ataxia, nystagmus, slurred speech, and impaired concentration and memory were reported in an optician who regularly used a 99% toluene cleaning fluid in a poorly ventilated room. Discontinuation of exposure resulted in complete recovery (Boor & Hurtig, 1977).
c) CASE REPORT: Depression, concentration and short-term memory impairment, decreased appetite, headaches, fatigue, decreased libido, and sleep disturbances were reported in seven male boilermakers following occupational exposure to varying amounts of benzene, toluene, and tetraethylene glycol (Leikin et al, 2000).
d) CASE REPORT: Three welders developed confusion, dizziness, loss of balance, headache, nystagmus, weakness and nausea while working in a storage container for waste oil. Vestibular dysfunction persisted for 3 to 18 months after the incident (Hodgson et al, 1989).

D) AMNESIA

1) WITH POISONING/EXPOSURE

a) MINERAL SPIRIT VAPORS: A 42-year-old female lacked recollection of any events of the day of admission following prolonged exposure to concentrated mineral spirit vapors (Nierenberg et al, 1991). The woman also had a cardiopulmonary arrest and metabolic abnormalities.

E) DISTURBANCE IN THINKING

1) WITH POISONING/EXPOSURE

a) SOLVENTS: El Massioui et al (1990) found evoked potential changes suggestive of minor peripheral and central nervous system dysfunction and mild cognitive impairment in 13 workers occupationally exposed to a mixture of solvents(El Massioui et al, 1990).
b) Memory deficits and decreased concentration were associated with (5 year or greater) occupational exposure to organic solvents (Hein et al, 1990).
c) Painters exposed to organic solvents reported more somatic and psychological symptoms than persons in occupations which were not believed to involve organic solvent exposure (Hooisma et al, 1994).
d) Cognitive impairment has been reported in chronic toluene sniffers (Malm & Lying-Tunell, 1980; Knox & Nelson, 1966; Streicher et al, 1981) and in a worker regularly exposed to toluene in a poorly ventilated room (Boor & Hurtig, 1977).

F) SEIZURE

1) WITH POISONING/EXPOSURE

a) RARE EFFECT: Seizures may occur, but are a rare effect.
b) CASE REPORT: Generalized grand mal seizures repeatedly occurred in an adolescent after the use of a xylene-based model airplane glue (Arthur & Curnock, 1982). Seizures did not occur when other glue was used. The boy had a history of seizure disorder.
c) CASE REPORT: One case of precipitated latent epilepsy was attributed to heavy exposure to xylene (80%) and methylglycolacetate (20%) vapors (Goldie, 1960).
d) CASE REPORT: Jacobsen et al (1994) report a case who was exposed during age 24 to age 52 to cyclohexanone, white spirit, isopropanol, and other organic solvents. Seizures were experienced weekly to monthly, but ceased when the man discontinued work with organic solvents. Exposure to cyclohexanone 4 years later resulted in seizures (Jacobsen et al, 1994).

G) SECONDARY PERIPHERAL NEUROPATHY

1) WITH POISONING/EXPOSURE

a) N-hexane and methyl n-butyl ketone produce sensory and motor neuropathy (Klaassen, 1990; Bos et al, 1991). Bilateral sensory dysfunction of the distal areas of the extremities, progressive muscle weakness, decreased nerve conduction velocity and decreased or lost deep sensory reflexes may occur. Gradual recovery usually occurs except in extreme cases of exposure.
b) Motor-neuron disease has been associated with occupational exposure to solvents and glues (Hawkes et al, 1989; Chio et al, 1989). N-hexane, methyl n-butyl ketone and toluene have been proposed as causative agents in the glues used by leather workers (Hawkes et al, 1989).
c) Peripheral neuropathy following inhalational abuse of naphtha has been reported in 2 cases (Tenenbein et al, 1984). The neurotoxic effects were attributed to n-hexane in the naphtha. Peripheral neuropathy in a 4-year-old petrol sniffer was also attributed to n-hexane (Hall et al, 1986).
d) Other studies suggest a possible association between solvent exposure and amyotrophic lateral sclerosis (Gunnarsson & Lindberg, 1989) or multiple sclerosis (Flodin et al, 1988).
e) CASE REPORT: Axonal polyneuropathy was reported in a 14-year-old male following ingestion of a thinner containing toluene, n-hexane, and xylene. Despite two months of hospitalization and supportive care, the patient continued to have severe polyneuropathy (Akisu et al, 1996).

H) PARALYSIS

1) WITH POISONING/EXPOSURE

a) BELL'S PALSY: RARE EFFECT: A case of Bell's palsy associated with acute on chronic occupational exposure to toluene has been reported (Aleguas et al, 1991).
b) PROGRESSIVE SUPRANUCLEAR PALSY: McCrank & Rabheru (1989) report four cases of progressive supranuclear palsy associated with exposure to organic solvents (McCrank & Rabheru, 1989).
c) CASE REPORT: Flaccid quadriplegia was reported in a 14-year-old male following ingestion of a thinner containing toluene, n-hexane, and xylene. The patient recovered following supportive care (Akisu et al, 1996).

I) EXTRAPYRAMIDAL DISEASE

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 20-year-old man developed signs of Parkinsonism 8 days after ingesting about 120 mL of a petroleum waste mixture. Three months after exposure a 6-fluorodopa, PET scan showed decreased striatal dopamine uptake. Follow-up studies at 24 and 29 months post-exposure were normal although the patient's symptoms were worsening (Tetrud et al, 1994).
b) Parkinsonism has also been reported in a lacquer thinner abuser (Uitti et al, 1994).
c) CASE REPORT: A 45-year-old female developed signs of Parkinsonism following long- term occupational exposure to hydrocarbon vapors. Despite short-term improvement with medication and neurosurgical implantation of the adrenal medulla in the caudate nucleus, the patient required total care with frequent choking episodes and died of aspiration pneumonia almost 6 years after diagnosis. An autopsy of the brain revealed dopaminergic neuronal loss and severe depigmentation of the substantia nigra and locus ceruleus (Pezzoli et al, 1996).
d) CASE SERIES: A cohort study, involving patients with Parkinson's disease who have a positive history of hydrocarbon solvent occupational exposure, determined that occupational exposure of hydrocarbon solvents is directly correlated to disease severity and inversely correlated to latency period. Therefore, according to this study, occupational exposure to hydrocarbon solvents is a risk factor for earlier onset of symptoms of Parkinson's disease and for a more severe disease throughout its course (Pezzoli et al, 2000).

Gastrointestinal

3.8.2)

A) VOMITING

1) WITH POISONING/EXPOSURE

a) A burning sensation in the mouth, nausea, and vomiting may occur.
b) Vomiting was reported in a patient who developed respiratory distress after exposure to a canvas waterproofing spray containing liquefied petroleum gas (1% to 10% w/v), ethylene glycol monobutyl ether (1% to 3% w/v), and isopropranol (1% to 3% w/v) (Weibrecht & Rhyee, 2011).
c) PETROLEUM DISTILLATES: Spontaneous vomiting was reported in 39% (59 of 150) of pediatric cases hospitalized for ingestion of products which contained petroleum distillates (Anas et al, 1981).
d) PINE OIL CLEANER: A study of 22 cases of pine oil cleaner ingestion reported that spontaneous emesis usually occurred within 10 to 90 minutes of ingestion (Brook et al, 1989).

B) DIARRHEA

1) WITH POISONING/EXPOSURE

a) Hydrocarbon gastroenteritis is frequent but usually self-limited (Kulig & Rumack, 1981).
b) Diarrhea was reported in a patient who developed respiratory distress after exposure to a canvas waterproofing spray containing liquefied petroleum gas (1% to 10% w/v), ethylene glycol monobutyl ether (1% to 3% w/v), and isopropranol (1% to 3% w/v) (Weibrecht & Rhyee, 2011).
c) CASE SERIES: Three patients developed diarrhea and perianal injury with burns, blistering, redness, broken skin and severe excoriation after ingesting 350 mL to 2 L of white spirit (Cassidy et al, 2014).

C) PANCREATITIS

1) WITH POISONING/EXPOSURE

a) The relationship between occupational hydrocarbon exposure and pancreatitis is controversial. Positive and negative results have been reported.
b) A case-comparison group study by McNamee et al (1994) reported an increased risk of chronic pancreatitis associated with diesel exhaust fumes (odds ratio 2.66), petrochemicals (odds ratio 1.82), and chlorinated solvents (odds ratio 1.49). The odds ratios were adjusted for alcohol, smoking, diet and social class, but not for other occupational exposures (McNamee et al, 1994).
c) Pancreatitis was not associated with hydrocarbon exposure in a study by Hotz et al (1990) (Hotz et al, 1990).

Hepatic

3.9.2)

A) LIVER DAMAGE

1) WITH POISONING/EXPOSURE

a) NON-HALOGENATED, ALIPHATIC HYDROCARBONS - Hepatic injury may occur following acute ingestion of petroleum distillates, but is uncommon (Janssen et al, 1988). Elevated liver enzyme levels and hepatosplenomegaly can occur with petroleum distillate ingestion (Garcia et al, 1995; Shirkey, 1971). Hepatic damage may also rarely follow hydrocarbon vapor inhalation (Gosselin et al, 1976).

1) XYLENE CASE REPORT - Two survivors of exposure to estimated xylene vapors of 10,000 ppm in the tank of a ship had transiently elevated serum transaminase levels (Morley et al, 1970). Hypoxia and exposure to toluene may have contributed to these effects. Studies reviewed by the National Toxicology Program did not find published evidence of irreversible liver damage from xylene exposure (NIOSH, 1986).
2) TOLUENE CASE REPORT - Hepatomegaly was identified through post-mortem examination of one case who died from toluene ingestion (Ameno et al, 1989).
3) TOLUENE CASE REPORT - Hepatorenal dysfunction developed in a 19-year-old after inhalational abuse of a toluene-containing cleaning fluid. The case had a prior history of ethanol use and glue sniffing (O'Brien et al, 1971).

b) HALOGENATED HYDROCARBONS - Carbon tetrachloride, chloroform, 1,1,2-trichloroethane (vinyl trichloride), are examples of halogenated hydrocarbons which are considered significantly hepatotoxic. Trichloroethylene, tetrachloroethylene, and 1,1,1-trichloroethane are examples of halogenated hydrocarbons which are considered less hepatotoxic (Meredith et al, 1989; Torkelson, 1994).

1) Many of the reports of hepatotoxicity are historical, involving medications or other products which are no longer in use, have involved exposure to extremely high vapor concentrations sufficient to produced anesthesia, or have resulted from volatile solvent abuse. Some reports regarding the less hepatotoxic chemicals often lack clear exposure and response data, or have otherwise been flawed.
2) Hepatotoxicity has usually been defined as elevated hepatic enzymes and/or hepatomegaly. Reversible hepatic enzyme elevation usually occurs with cessation of exposure except in extreme exposure situations, such as involving carbon tetrachloride or resulting in prolonged anesthesia.
3) Ranking of selected hydrocarbons from most to least hepatotoxic in animals: carbon tetrachloride > benzene or trichloroethylene > pentane (Wirtschafter & Cronyn, 1964).
4) CARBON TETRACHLORIDE: Although reports of poisoning are rare in recent years, carbon tetrachloride can produce potentially fatal hepatic effects, including centrilobular necrosis. Inhalation, ingestion, or dermal exposure to small amounts of carbon tetrachloride can be fatal (Meredith et al, 1989).
5) CARBON TETRACHLORIDE CASE REPORT: Two cases developed elevated alanine aminotransferase levels within 48 hours of topical application of a product which contained carbon tetrachloride (Perez et al, 1987).
6) CARBON TETRACHLORIDE CASE REPORT: Inhalational abuse of carbon tetrachloride resulted in significantly elevated SGOT levels (2660 units) in a case who had a 14 year history of sniffing toluene (Knox & Nelson, 1966). No prior report of hepatotoxicity was reported in previous medical evaluations of this case.
7) TRICHLOROETHYLENE CASE REPORT: Baerg & Kimberg (1970) report the development of acute toxic hepatitis in 3 teenagers after inhalational abuse of a cleaning fluid which contained trichloroethylene and petroleum distillates. All of the patients had a history of multiple drug abuse. Liver enzymes were significantly, but temporarily, elevated in 3 patients and hepatocentrilobular necrosis was determined by biopsy in 2 cases (Baerg & Kimberg, 1970).
8) 1,1,1-TRICHLOROETHANE CASE REPORT: Mildly elevated liver enzymes were present in a 4-year-old child following inhalation of 1,1,1-trichloroethane vapors (Gerace, 1981). Liver enzymes were normal 48 hours later. Hypoxia may have contributed to the hepatic effects.

c) IV INJECTION: CASE REPORT: A 26-year-old man injected 10 mL of gasoline in a suicide attempt and presented with a chemical pneumonitis. The patient's status deteriorated, and he developed multi-organ dysfunction syndrome that manifested in part as a transient elevation of liver enzymes (AST 2.208 Units/L, ALT 3.099 Units/L). The patient made a full recovery within 12 days of admission with aggressive, intensive care management (Domej et al, 2007).

3.9.3)

A) ANIMAL STUDIES

1) HEPATOCELLULAR DAMAGE

a) TOLUENE ANIMAL STUDIES: Either increased liver weight or no hepatic effects following toluene ingestion have been reported (ATSDR, 1994).

Genitourinary

3.10.2)

A) ACUTE RENAL FAILURE SYNDROME

1) WITH POISONING/EXPOSURE

a) PETROLEUM DISTILLATES/DIESEL FUELS: Acute tubular necrosis has been rarely reported following inhalation and dermal exposure to diesel oil and petroleum naphtha (Crisp et al, 1979; Landry & Langlois, 1998) and ingestion of refined petrol (Janssen et al, 1988). Acute renal failure has also been reported following pediatric ingestion and aspiration of mineral spirits (Coffman et al, 1994), the use of diesel fuel to cleanse the hair of an adult (Barrientos et al, 1977), and in a fatal case involving a 12-year-old who was immersed for 1 hour in leaded gasoline (Walsh et al, 1974).
b) CHLORINATED HYDROCARBONS: Carbon tetrachloride produces glomerular damage and necrosis of the proximal tubule and loop of Henle. Acute tubular necrosis and renal failure can also result from tetrachloroethylene. Tubular necrosis has primarily occurred with inhalational abuse of trichloroethylene (Feinfield, 1994).

1) CARBON TETRACHLORIDE CASE REPORT: Acute renal failure developed in 3 cases within days of topical application of a product which contained carbon tetrachloride. Symptoms onset was within 2 to 48 hours of exposure (Perez et al, 1987).
2) CARBON TETRACHLORIDE CASE REPORT: Acute inhalational abuse of carbon tetrachloride resulted in acute renal failure in a case who had a 14 year history of sniffing toluene (Knox & Nelson, 1966). No prior report of nephrotoxicity was found in previous medical evaluations of this case.

c) TOLUENE: Acute renal failure and distal renal tubular acidosis have been reported in some painters and chronic inhalational abusers (Kaysen, 1990). Renal tubular acidosis and myoglobinuria may occur (Goldfrank et al, 1998) Feinfield, 1994; (Taher et al, 1974). The Agency for Toxic Substances and Disease Registry (ATSDR) has reported that many human studies have been confounded by other exposures and study limitations, and the renal effects reported in many animal studies conflict (1994).

1) TOLUENE INHALATION CASE REPORT: Hematuria, oliguria or anuria, moderate proteinuria, and elevated blood urea and serum creatinine were present in 1 case (O'Brien et al, 1971).
2) TOLUENE INGESTION CASE REPORT: Acute tubular necrosis was present in a fatal case involving ingestion of approximately 60 mL of a toluene-containing liquid (Ameno et al, 1989).

d) IV INJECTION: CASE REPORT: A 26-year-old man injected 10 mL of gasoline in a suicide attempt and presented with a chemical pneumonitis. The patient's status deteriorated, and he developed multi-organ dysfunction syndrome that manifested in part as acute oligoanuric renal failure. This was further aggravated by rhabdomyolysis (CK peak 3.29 Units/L). Continuous veno-venous hemofiltration was required for several days. The patient made a full recovery within 12 days of admission with aggressive, intensive care management (Domej et al, 2007).

B) GLOMERULONEPHRITIS

1) WITH POISONING/EXPOSURE

a) Biopsy confirmed glomerulonephritis and nephrotic syndrome has been reported following long term inhalation or dermal exposure to various hydrocarbons (Cagnoli et al, 1980; Beirne & Brennan, 1972; Ehrenreich, 1977; Ravnskov, 1979; Roy et al, 1991).
b) Daniell et al (1988) report that the risk of glomerulonephritis may be increased 2.8 to 8.9 times in solvent-exposed individuals, based on analysis of data from several published studies (Daniell et al, 1988).
c) A case referent study, however, found no relation between occupational exposure to organic solvents and glomerulonephritis or renal cancer (Harrington et al, 1989).
d) GOODPASTURE'S SYNDROME: Hydrocarbon-associated anti-glomerular basement membrane disease has been reported (Roy et al, 1991).

1) ONSET: In a review of 23 cases of individuals in which the duration of exposure was known, 18 developed anti-glomerular basement membrane disease within 1 year of exposure (Bombassei & Kaplan, 1992).

C) RENAL INTERSTITIAL FIBROSIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 30-year-old man was reported to develop progressive tubulointerstitial nephritis, documented by biopsy, following inhalation and dermal occupational exposure to mineral spirits and helicopter fuel. Only mild glomerular sclerotic changes were present (Narvarte et al, 1989).

D) ABNORMAL SEXUAL FUNCTION

1) WITH POISONING/EXPOSURE

a) Sexual dysfunction, including erectile abnormalities, decreased libido, and Peyronie's disease, has been reported following occupational exposure to varying amounts of benzene and toluene, and may not occur until several months post-exposure (Leikin et al, 2000).

Hematologic

3.13.2)

A) DISSEMINATED INTRAVASCULAR COAGULATION

1) WITH POISONING/EXPOSURE

a) Four cases of disseminated intravascular coagulation (DIC) which developed after hydrocarbon aspiration have been reported (Banner & Walson, 1983; Janssen et al, 1988; Algren & Rodgers, 1992). Matsumoto et al (1992) report 1 case of DIC following gasoline vapor inhalation and skin exposure (Matsumoto et al, 1992). Extensive dermal exposure to a toluene-containing sealer has resulted in DIC (Shibata et al, 1994).

B) HEMOLYTIC ANEMIA

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Hemolytic anemia developed in a 42-year-old female who sustained a cardiopulmonary arrest after prolonged exposure to concentrated mineral spirits vapors (Nierenberg et al, 1991). Screening for DIC was negative.
b) ONSET: The onset of hemolysis is rapid, with signs and symptoms present on admission or within 8 hours in 2 out of 3 cases (Algren & Rodgers, 1992).

C) LEUKOCYTOSIS

1) WITH POISONING/EXPOSURE

a) CASE SERIES: In a case series involving patients with a hydrocarbon self-injection to an upper extremity, leukocytosis occurred in 18 of the 21 patients (Farahvash et al, 2009).

D) PANCYTOPENIA

1) WITH POISONING/EXPOSURE

a) ADULT: CASE REPORT: A 58-year-old man developed pancytopenia and fatal multiorgan failure secondary to a two week history of drinking gasoline mixed with carbonated cola. On day 1 of hospital stay, his hemogram was as follows: WBC 3.0 x 10(9)/L, Hemoglobin 14.5, Hematocrit 44.0 and platelets 128. By end of hospital day 4, his condition deteriorated and a repeat hemogram revealed the following: WBC 0.3 x 10(9)/L Hemoglobin 12.7, Hematocrit 41.7, and platelets 13/mm(3) (Rahman et al, 2009).
b) PEDIATRIC: CASE REPORT:A 9-year-old girl developed pancytopenia (WBC 500/mm(3), platelets 3,000/mm(3), hematocrit 27.8) without evidence of DIC one day after ingesting 4 oz of mineral spirits (Coffman et al, 1994).

E) PROTHROMBIN TIME LOW

1) WITH POISONING/EXPOSURE

a) CASE SERIES - Hypoprothrombinemia was reported in children following acute kerosene poisoning. In approximately 83% of the patients with abnormal prothrombin times, liver enzyme levels were also increased. The authors speculated that hypoprothrombinemia may be an early indicator of kerosene-induced transient hepatotoxicity (Garcia et al, 1995).

Dermatologic

3.14.2)

A) ERUPTION

1) WITH POISONING/EXPOSURE

a) Transient discomfort and erythema may develop following brief or prolonged contact, due to the defatting effects of hydrocarbons.
b) CASE REPORT: A 34-year-old male injected approximately 1.5 mL of dripless oil into his left antecubital fossa in a suicide attempt and developed a painfully indurated, tender, erythematous area at the injection site. The patient gradually recovered with complete resolution of the pain, induration, and erythema (Shusterman et al, 1999).

B) CHEMICAL BURN

1) WITH POISONING/EXPOSURE

a) Second (partial thickness) or third degree burns from gasoline, kerosene, toluene, and paint thinner have been reported and most commonly occur if a person remains in prolonged contact with the hydrocarbon (Hansbrough et al, 1985; Mosconi et al, 1988; Mozingo et al, 1988; Shibata et al, 1994). Second degree, partial-thickness burns have also resulted from exposure to highly concentrated trichloroethylene fumes (Balakrishnan et al, 1993).
b) CASE SERIES: Three patients developed diarrhea and perianal injury with burns, blistering, redness, broken skin and severe excoriation after ingesting 350 mL to 2 L of white spirit (Cassidy et al, 2014).

1) One man presented with vomiting, abdominal pain, and diarrhea 1 hour after ingesting 350 mL of white spirits and 500 mL of plant fertilizer. Laboratory results revealed hyperkalemia (potassium= 5.3 mmol/L, possibly caused by the plant fertilizer) which was treated with insulin/dextrose. Blistering, redness, broken skin and excoriation were observed around his anus 2 days postingestion. He was treated with prophylactic IV pantoprazole, IV penicillin and oral acetaminophen for 3 days, followed by oral antibiotics. Another man developed perianal burns and diarrhea after ingesting 2 L of white spirits. On presentation, he required intubation via tracheostomy. Two days postingestion, a computed tomography contrast scan and an esophago-gastroduodenoscopy revealed corrosion on the tongue and hypopharynx, mild esophagitis and gastritis. He received prophylactic amoxicillin, clarithromycin and pantoprazole. A woman developed diarrhea and presented 7 hours after ingesting 1 L of white spirit. She received IV omeprazole for dyspepsia. She had watery rectal fluid, inflammation, and severe excoriation to the inner thighs and perianal area 16 hours postingestion. She received acetaminophen/codeine sulfate for pain, prophylactic oral antibiotics (penicillin, metronidazole) and topical silver sulfadiazine (1% w/w) (Cassidy et al, 2014).

c) CASE REPORT (TOLUENE): Extensive chemical burns, which progressed in severity and became necrotic despite cessation of exposure, were reported in a 22-year-old man. The man had lost consciousness and spilled a 65% toluene-based sealer on his clothes while working in a poorly ventilated space. He was in cardiac arrest upon arrival at the emergency department and developed rhabdomyolysis, acute renal failure, DIC, and permanent brain damage. Death was due to uncal herniation (Shibata et al, 1994).
d) THERMAL BURNS: Thermal burns have been reported from direct contact with hot tar, bitumen, and thermoplastic road paint (Riley et al, 1991).

C) SYSTEMIC DISEASE

1) WITH POISONING/EXPOSURE

a) DERMAL ABSORPTION: Severe dermal exposures may rarely be associated with marked toxicity and death (Hansbrough et al, 1985; Sayjari et al, 1986).
b) Tetraethyl lead in leaded gasoline can be dermally absorbed, possibly resulting in systemic toxicity (Mozingo et al, 1988). Some aromatic hydrocarbons, additives or contaminants (e.g. polychlorinated biphenyls, aniline, nitrobenzene) are readily absorbed and can produce systemic toxicity (Emmett, 1991; Phillips et al, 1990).
c) CASE REPORT: Walsh et al (1974) report a fatal case involving a 12-year-old who was immersed for 1 hour in leaded gasoline. Renal failure and severe CNS depression developed. Cerebral edema, pneumonia, and hepatorenal toxicity were present at autopsy (Walsh et al, 1974).

D) DERMATITIS

1) WITH POISONING/EXPOSURE

a) Repeated or prolonged contact can cause drying, itching, and cracking of the skin. Blistering may occur from some hydrocarbons, particularly if exposure to the concentrated hydrocarbon is prolonged and the exposed area of skin is occluded (ILO, 1998).

E) ACNE

1) WITH POISONING/EXPOSURE

a) Cutting fluids, diesel oils, coal tar pitch, and pitch fumes can cause acne-like lesions and folliculitis (Emmett, 1991). Oil acne and folliculitis are the most common skin conditions of workers exposed to straight oils (Mackerer, 1989).

F) CHLORINE ACNE

1) WITH POISONING/EXPOSURE

a) Halogenated aromatic compounds cause a unique kind of acneiform lesion characterized by straw-colored cysts and comedones, ranging from pinhead size to the size of a pea (Emmett, 1991; Mathias, 1988). The lesions develop initially on the face on the skin lateral to the eyes, and progress to other areas of the face, neck, trunk, scrotum and buttocks.

G) FROSTBITE

1) WITH POISONING/EXPOSURE

a) Contact with liquefied petroleum gases (e.g. propane, butane, propylene, isobutane, butenes, n-butane), ethane, vinyl chloride, or methyl chloride (liquid or a stream of concentrated vapor) can result in frostbite or effects resembling frostbite (Compressed Gas Association, Inc, 1990).

H) SKIN NECROSIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: A 33-year-old male subcutaneously injected approximately 4 mL of charcoal lighter fluid (containing 99.4% naphtha) into the left antecubital fossa and several hours later developed necrosis of the left forearm skin extending from the mid-humerus to the fingers, and cellulitis at the injection site. The patient gradually recovered following extensive surgical debridement and closure and subsequent grafting (Rush et al, 1998).

I) NECROTIZING FASCIITIS

1) WITH POISONING/EXPOSURE

a) CASE SERIES: In a case series involving patients with a hydrocarbon self-injection to an upper extremity, necrotizing fasciitis occurred in 5 of the 21 patients. Two of those patients had myonecrosis predominantly (Farahvash et al, 2009).

J) CELLULITIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Cellulitis was reported in a 24-year-old male after injecting a total amount of 0.5 mL of a lubricating agent containing petroleum distillates and oils. The patient recovered following treatment with IV antibiotics and analgesics (Kleinschmidt et al, 1999).

K) SYSTEMIC SCLEROSIS

1) WITH POISONING/EXPOSURE

a) A study conducted by Nietert et al (1998) showed that in men, occupational exposure to organic solvents, including trichloroethylene, benzene, carbon tetrachloride, and trichloroethane, was associated with the development of systemic sclerosis and may be considered a risk factor. However, in women, occupational exposure to organic solvent did not appear to be a risk factor for the development of systemic sclerosis (Nietert et al, 1998).

L) INJECTION SITE REACTION

1) WITH POISONING/EXPOSURE

a) CASE SERIES: In a case series involving 21 patients with self-injections to the upper extremities, pain and swelling, erythema, indurations, and localized tenderness appeared to be the most commonly occurring signs and symptoms at the injection site. Five of the 21 patients developed necrotizing fasciitis, and 13 developed compartments syndrome requiring fasciotomy and debridement (Farahvash et al, 2009).

Musculoskeletal

3.15.2)

A) INJECTION SITE REACTION

1) WITH POISONING/EXPOSURE

a) 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% amputation rate, and possible systemic toxicity.
b) The majority of cases involve the hands (Scott, 1983; Neal & Burke, 1991). Of 14 injuries, 3 required digital amputation (Mrvos et al, 1987).
c) 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).
d) Systemic effects can occur within the first 48 hours; effects may persist for 4 to 6 days (Harter & Harter, 1986).
e) Factors which appear to correlate with worse prognosis include (Neal & Burke, 1991):

1) Greater time from injury to decompression
2) More irritant types of material injected
3) Greater quantity of material injected
4) Greater injection pressure of appliance
5) Secondary infection
6) More distal site of injection

B) NECROSIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Deep intramuscular injection of lamp oil into the pronator teres muscle of the upper left arm by a 21-year-old male attempting suicide produced severe muscle necrosis requiring debridement. There was no evidence of pulmonary sequelae (Kresel et al, 1987).

C) RHABDOMYOLYSIS

1) WITH POISONING/EXPOSURE

a) CASE REPORT: Rhabdomyolysis developed in a 42-year-old female who had a cardiopulmonary arrest following prolonged exposure to concentrated vapors from mineral spirits (Nierenberg et al, 1991). Rhabdomyolysis has also resulted from sniffing toluene-containing substances (Streicher et al, 1981).
b) CASE REPORT: Anetseder et al (1994) report an unusual case of rhabdomyolysis associated with accidental gasoline vapor inhalation while driving. The patient consumed excessive amounts of ethanol 2 days prior to symptom onset.

1) Key signs and symptoms were CK >8,000 Units/L, muscle pain, muscle weakness, and decreased deep tendon reflexes. A diagnosis of malignant hyperthermia susceptibility possibly induced by gasoline vapors, with or without ethanol, was based on muscle bundle tests and the patient's history.
2) Muscle bundle test results included: abnormal contracture to caffeine and halothane; dose-dependent increasing contracture to very low (0.01% to 0.05%) concentrations of the hydrocarbon, benzine; contracture only with ethanol concentrations of 2%.

c) CASE REPORT: Muscle weakness, muscle pain, elevated creatine kinase (CK 219,600 Units/L), and occasional myoglobinuria repeatedly occurred after gasoline sniffing in 1 case (Kovanen et al, 1983). Blood and urinary lead levels were elevated, indicating that the gasoline probably contained tetraethyl lead.
d) CASE REPORT: Rhabdomyolysis was reported in a fatal case involving a 22-year-old adult who lost consciousness while using a toluene-based sealer and had his clothing contaminated with the sealer. Extensive chemical burns with massive loss of fluid and cardiac arrest also occurred (Shibata et al, 1994).
e) A study examining blood lead and creatine kinase levels in patients following sniffing of leaded and unleaded gasoline showed that creatine kinase levels were elevated after inhaling both types of gasoline. Blood lead and creatine kinase levels also appeared to be directly proportional to each other, however it is speculated that it is not a causal relationship (Burns et al, 1994).
f) CASE REPORT: A 14-year-old male developed rhabdomyolysis with a creatine kinase of 168 units/liter and a myocardial CPK of 1,860 units/liter after ingesting 200 mL of thinner containing 60% toluene, 25% n-hexane, and 5% xylene. The patient recovered following supportive care (Akisu et al, 1996).
g) IV INJECTION: CASE REPORT: A 26-year-old man injected 10 mL of gasoline in a suicide attempt and presented with a chemical pneumonitis. The patient's status deteriorated, and he developed multi-organ dysfunction syndrome that manifested in part as acute oligoanuric renal failure. This was further aggravated by rhabdomyolysis (CK peak 3.29 Units/L). Continuous veno-venous hemofiltration was required for several days. The patient made a full recovery within 12 days of admission with aggressive, intensive care management (Domej et al, 2007).

D) COMPARTMENT SYNDROME

1) WITH POISONING/EXPOSURE

a) INJECTION INJURIES may result in a compartment syndrome.

1) CASE REPORT: Compartment syndrome, erythema, local tenderness, and fever developed in an adult who subcutaneously injected gasoline into the chest and forearm (Blindlish, 1993).
2) CASE REPORT: A 17-year-old woman developed compartment syndrome of both hands with 8 necrosis of fat and interosseus muscles bilaterally after injecting the dorsum of both hands with an insecticide containing kerosene and aromatic hydrocarbons (Larsen et al, 1992).
3) Paint and grease guns have produced high-velocity injection injuries requiring immediate surgical decompression (Mann, 1975; Anon, 1972).

b) CASE SERIES: In a case series involving patients with a hydrocarbon self-injection to an upper extremity, compartment syndrome occurred in 13 of the 21 patients (Farahvash et al, 2009).
c) STERILE ABSCESS may result at injection sites of hydrocarbons.

1) CASE REPORT: Intravenous injection of pure gum turpentine initially resulted in burning, erythema, swelling and tenderness, followed by the development of a sterile abscess at the injection site (Wason & Greiner, 1986).

E) NECROTIZING FASCIITIS

1) WITH POISONING/EXPOSURE

Reproductive

3.20.1)

3.20.2)

A) GROWTH RETARDED

1) A retrospective study of birth records reported that there was an increased risk of growth retardation associated with paternal employment in some, but not all, solvent related occupations (Daniell & Vaughan, 1988). Due to the study limitations, these results need to be confirmed by additional research.

a) In utero low-level occupational solvent exposure did not appear to cause neurobehavioral deficits in children (Eskenazi et al, 1988).

B) CONGENITAL ANOMALY

1) An analysis of data from the ongoing, case-control, National Birth Defects Prevention Study found that for women with occupational exposure to polycyclic aromatic hydrocarbons (PAH) in the month before through 3 months after conception had increased risk for having offspring with a neural tube defect (NTD), particularly spina bifida; however, after adjusting for confounders, the odds ratio for NTDs and spina bifida decreased and lost statistical significance. The crude odds ratio (OR) for any NTD was 1.43 (95% CI, 0.92 to 2.22); however, after adjusting for BMI, secondhand smoke at home, and study center, the OR was reduced and not statistically significant (adjusted OR, 1.01; 95% CI, 0.61 to 1.66). The crude OR for spina bifida was 1.71 (95% CI, 1.03 to 2.83), which also was attenuated and not statistically significant after adjusting for BMI and education (adjusted OR, 1.21; 95% CI, 0.69 to 2.11). Stratification by BMI resulted in a crude OR for spina bifida in children of normal and underweight mothers (OR, 3.13; 95% CI, 1.63 to 6.03) that was significantly higher than that for overweight or obese mothers (OR, 0.63; 95% CI, 0.23 to 1.59). After adjusting for education, the OR for normal and underweight mothers was slightly attenuated but still statistically significant (adjusted OR, 2.59; 95% CI, 1.32 to 5.07). A statistically significant dose-response trend was observed for spina bifida, where the highest exposure category had a crude OR of 2.43 (95% CI, 1.31 to 4.53); however, after adjustment for BMI and education, the trend lost significance and the risk was attenuated (adjusted OR, 1.73; 95% CI, 0.87 to 3.42) (Langlois et al, 2012).
2) A retrospective, case-control study of 1951 female laboratory workers found no significantly increased risk of major congenital malformations related to laboratory work in general. There was an excess risk with organic solvents, particularly benzene, for major congenital malformations and for neural crest malformations for women who worked with benzene before the end of the second trimester of pregnancy (Wennborg et al, 2005).
3) In a prospective study in Toronto, major congenital malformations were noted in 13 of 125 fetuses of mothers exposed to organic solvents during pregnancy. The malformations varied but included cardiac anomalies, spina bifida, deafness, hernias, clubfoot requiring correction, and congenital hydronephrosis requiring nephrectomy. The most common solvents involved were aliphatic and aromatic hydrocarbons, phenols, trichloroethylene, vinyl chloride, xylene, acetone, and related compounds (Khattak et al, 1999).

3.20.3)

A) ABORTION

1) A study of women biologically monitored for solvent exposure suggested an increased risk of spontaneous abortion with exposure during pregnancy to aliphatic hydrocarbons and other organic solvents (Lindbohm et al, 1990).
2) One study reported no significantly increased risk of spontaneous abortion associated with paternal exposure to benzene, after adjusting the odds ratio for tobacco use, maternal age and pregnancy order (Stucker et al, 1994).

3.20.5)

A) FERTILITY DECREASED MALE

1) In one study, semen abnormalities, including low sperm count, a decrease in sperm motility, and morphologically abnormal sperm, were associated with men occupationally exposed to hydrocarbons as compared with unexposed workers. There appeared to be a correlation between some of the semen abnormalities and the duration of exposure to the hydrocarbons (De Celis et al, 2000).

B) FERTILITY DECREASED FEMALE

1) One study reported daily or high exposure to organic solvents significantly decreased the fertility in women (Sallmen et al, 1995).

Carcinogenicity

3.21.3)

A) CARCINOMA

1) NATIONAL TOXICOLOGY PROGRAM SUMMARY - A partial list of known carcinogens or processes known to be carcinogenic, reported by the US DHHS (1994) National Toxicology Program includes:

a) benzene; benzidine; bis(chloromethyl) ether and technical-grade chloromethyl methyl ether; vinyl chloride; coke oven emissions; soots, tars and mineral oils (untreated and mildly treated)

2) A partial list of substances anticipated to be carcinogens reported by the US DHHS (1994) National Toxicology Program includes:

a) bromodichloromethane; 1,3-butadiene; carbon tetrachloride; chlorinated paraffins (C12, 60 percent chlorine); chloroform; 1,4-dichlorobenzene; dichloromethane (methylene chloride); formaldehyde gas; hexachlorobenzene; polybrominated biphenyls; polychlorinated biphenyls; polycyclic aromatic hydrocarbons (15 listed); 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); tetrachloroethylene (perchloroethylene); o-toluidine and o-toluidine hydrochloride

3) The cancer risk was evaluated from 5 cohort studies of 6,500 carbon electrode workers exposed to polycyclic aromatic hydrocarbons. Two studies, involving 2203 workers, provided data on incidence; 52 cases of all neoplasms were reported versus 56.28 that were expected. There were 9 cases of lung cancer versus 9.93 expected cases and 3 cases of urinary cancer versus an expected 3.69 cases. Four studies, involving 5241 workers, reported data on mortality. There were 269 deaths reported from all neoplasms versus an expected 292.1 deaths. There were 82 deaths from respiratory cancer versus an expected 95.8 deaths and 15 deaths from urinary cancer versus an expected 12.7 deaths (LaVecchia & Bosetti, 2003).
4) BONE, BRAIN, BLADDER CANCER - Excess deaths from cancer of the bone, brain, and bladder were seen in 10- to 19-year-old children living in the proximity of petrochemical plants in Taiwan for the period 1971 to 1990 (Pan et al, 1994).

B) LEUKEMIA

1) Numerous studies have reported that exposure to benzene is associated with a high incidence of leukemia (US DHHS, 1994; (Rinsky et al, 1987).

C) RENAL CARCINOMA

1) Experimental animal studies and some studies on cancer incidence and mortality in human occupational groups suggest that hydrocarbon exposure is associated with renal neoplasia (Nelson et al, 1990).
2) Moderate levels of hydrocarbon exposure produced the highest risk (odds ratio = 1.6) of renal cell carcinoma in a population-based case-control study (Kadamani et al, 1989).
3) A retrospective study on 365 persons with renal-cell carcinoma identified exposure to gasoline and other hydrocarbons as risk factors (Mellemgaard et al, 1994).

D) GASTRIC CARCINOMA

1) A retrospective, cohort study showed a higher rate of lung, stomach, and colon-rectum cancers in a group of over 4,000 workers in a coke gas plant which the authors attribute to coal carbonization fumes (Berger & Manz, 1992).

E) SKIN CARCINOMA

1) Squamous cell carcinoma has been reported in skin exposed to cutting oil over a 15-year period (Tsuji et al, 1992).

F) SPECIFIC AGENT

1) GASOLINE - The majority of the used gasoline engine oils tested were carcinogenic in the dermal carcinogenesis bioassay (McKee & Plutnick, 1989). Fresh gasoline engine oil was not carcinogenic.
2) GASOLINE - The Tranguch Gasoline Spill leaked 50,000 to 900,000 gallons of gasoline from underground storage tanks. A retrospective cohort study of 663 residents was undertaken to determine the incidence of cancer among those potentially exposed to the spill. Cancers recorded included 2 with acute myeloid leukemia, 1 with chronic myeloid leukemia, and 1 with chronic lymphocytic leukemia. The 2 residents with acute myeloid leukemia lived on the border of the projected gasoline plume which was within the affected area. The standard incidence ratio for leukemia was 4.40 (95% CI 1.09 to 10.24) for the gasoline-affected area (Patel et al, 2004).
3) DIESEL - Fresh and used diesel engine oils were not carcinogenic in the dermal carcinogenesis bioassay (McKee & Plutnick, 1989).
4) The carcinogenicity of the used gasoline engine oils may have been due to the high concentration of polyaromatic hydrocarbons in the used oil. Fresh gasoline oils and fresh or used diesel oils had low levels of polyaromatic hydrocarbons (McKee & Plutnick, 1989).

Laboratory Monitoring

Monitoring Parameters Levels

4.1.1)

A) Monitor vital signs and mental status.
B) Blood concentrations are not readily available or useful to guide management.
C) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity or chlorinated hydrocarbon exposure.
D) Obtain CBC, basic chemistry panel, serum creatinine and liver enzymes in severe overdoses or in patients with chronic exposures.
E) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests and obtain chest radiograph in patients with any respiratory symptoms. NOTE: The chest radiograph may be normal early in the clinical course.
F) Standard urine toxicology screen does not detect hydrocarbons.
G) Monitor fluid and electrolyte status in patients with significant diarrhea and vomiting.
H) Head CT should be obtained in patients with altered mental status.
I) Monitor for methemoglobinemia in cyanotic patients who do not respond to supplemental oxygen, and who may have been exposed to hydrocarbons which contain nitrobenzene or aniline.

4.1.2)

A) ACID/BASE

1) Obtain arterial blood gases in symptomatic patients.

B) HEMATOLOGIC

1) Monitor CBC and blood chemistry panel.
2) Monitor for methemoglobinemia in cyanotic patients who do not respond to supplemental oxygen, and who may have been exposed to hydrocarbons which contain nitrobenzene or aniline.

C) BLOOD/SERUM CHEMISTRY

1) Monitor BUN, creatinine, serum CPK, and liver enzymes in patients exposed to chlorinated hydrocarbons, in cases of significant inhalational abuse, if prolonged unconsciousness and hypoxia has occurred, in cases of extensive, prolonged dermal exposure to liquid hydrocarbon, or in cases of hydrocarbon injection.

4.1.3)

A) URINALYSIS

1) Standard urine toxicology screen does not detect hydrocarbons.
2) Monitor urine for evidence of hemoglobin in patients with aspiration pneumonitis or in cases of suspected rhabdomyolysis. Monitor urinary output.
3) URINARY CELLULAR SEDIMENT: The presence of urinary cellular sediment was associated with increasing frequency of use of organic solvent in study of 284 newspaper press workers (Hashimoto et al, 1991).

a) Occasional use of analgesics was associated with a decreased incidence of urinary cellular sediment in newspaper press workers exposed to solvents (Hashimoto et al, 1991).

4) ALBUMINURIA: Detectable albuminuria occurred more frequently in workers with urinary cellular sediment (Hashimoto et al, 1991).

B) OTHER

1) FRACTIONAL ALBUMIN CLEARANCE: This was a better marker of hydrocarbon exposure in workers when compared to glycosaminoglycans (Hotz et al, 1991).

4.1.4)

A) OTHER

1) MONITORING

a) Pulmonary function tests, pulse oximetry, and chest x-ray may be indicated in symptomatic patients.
b) COMPARTMENTAL PRESSURE MONITORING: Monitor patients with injection injury for evidence of compartment syndrome.

2) NEUROPSYCHOLOGICAL TESTING

a) Lower performance in associative learning, digit span, and block design were present in exposed individuals when compared to their unexposed monozygotic twin (Hanninen et al, 1991).

3) CEREBROSPINAL FLUID

a) It has been found the concentrations of albumin, IgG, and total protein were significantly higher in cerebrospinal fluid from 19 patients (11 were painters) with organic solvent-associated chronic encephalopathy than found in 16 patients with myalgia and/or backache. The concentration of taurine in cerebrospinal fluid was found to decrease with increasing solvent exposure (Moen et al, 1990).

Radiographic Studies

1) Obtain chest x-ray in symptomatic patients. Early chest x-rays prior to development of symptoms were not predictive of aspiration pneumonitis in one study (Wason & Katona, 1987).

1) Chlorinated hydrocarbons may be radio-opaque (Dally et al, 1987).

1) Computed tomography (CT) can assist in identifying atelectasis, consolidation, necrosis, cavitating lesions, and pleural effusions which may develop with severe hydrocarbon aspiration (Guandalini & Steinke, 2007).
2) High-resolution computerized tomography (HRCT) was used to detect alveolar opacities, pneumatoceles, and pneumothorax, as complications of hydrocarbon pneumonia, following aspiration of white spirit ingested in a suicide attempt (Facon et al, 2005).

1) One study found cerebral magnetic resonance imaging (MRI) superior to computerized tomography (CT) in the diagnosis of solvent-induced encephalopathy (Leira et al, 1992).

Methods

1) NMR SPECTROSCOPY - Yamaguchi et al (1992) report a method for analyzing gastric contents for kerosene using nuclear magnetic resonance (NMR) spectroscopy (Yamaguchi et al, 1992).

1) GC/MS - Broncho-alveolar lavage and pleural fluid were analyzed for evidence of cutting oil-induced lipoid pneumonia using direct hexane extraction, followed by gas chromatography/mass spectrometry (Penes et al, 1990).
2) Various chromatographic methods, including thin-layer chromatography, high-performance liquid chromatography, and gas chromatography, have been used to determine the metabolites of aromatic hydrocarbons in human blood and urine. For determination of unchanged aromatic hydrocarbons in the blood, gas chromatography with head-space analysis may be the preferred method (Angerer & Horsch, 1992).
3) Gas chromatography was used for determining blood concentrations of various volatile organic compounds, including benzene, xylene, styrene, and toluene, following non-occupational exposure. The detection limits, using this method, ranged from 0.019 to 0.092 parts per billion (Ashley et al, 1994).

Treatment

Life Support

Patient Disposition

6.3.1)

6.3.1.1) ADMISSION CRITERIA/ORAL

A) Patients with significant persistent central nervous system toxicity (somnolence, delirium), or respiratory symptoms of cough or tachypnea should be admitted. Patients with coma, dysrhythmias, or respiratory distress should be admitted to an intensive care setting.
B) Admit asymptomatic patients with abnormal chest x-rays suggestive of aspiration if sufficient home follow-up cannot be provided (Goldfrank et al, 1998).

1) In a series of 184 cases of accidental hydrocarbon ingestions none of the 120 patients with no initial symptoms developed later complications (Machado et al, 1988).

C) Admit patients who have the potential for delayed systemic toxicity (Goldfrank et al, 1998). Examples include exposure to highly toxic halogenated hydrocarbons or exposure to hydrocarbons which have large amounts of aniline or nitrobenzene.
D) Admit cases of attempted suicide or cases involving ingestion of large amounts of hydrocarbon (Goldfrank et al, 1998). Obtain psychiatric evaluation when appropriate (e.g., suicide attempt). This will help determine need for admission. Not all suicide "gestures" require admission if medically cleared and appropriate follow-up is possible.

6.3.1.2) HOME CRITERIA/ORAL

A) Asymptomatic patients with inadvertent exposures may be monitored at home, with particular attention to the development of any respiratory symptoms. Patients who develop symptoms during home monitoring should be referred to a medical facility.
B) Results of a study of Poison Center calls involving hydrocarbon ingestions (types not specified; believed to be petroleum distillates) indicated that accidental ingestions of small quantities of hydrocarbons can be safely handled at home with Poison Center monitoring, provided that the patient is asymptomatic, there is access to a follow-up mechanism, and there are no indications of child abuse or attempted suicide (Machado et al, 1988).

6.3.1.3) CONSULT CRITERIA/ORAL

A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity (dysrhythmias, coma or respiratory distress), or in whom the diagnosis is not clear.

6.3.1.5) OBSERVATION CRITERIA/ORAL

A) Patients with deliberate ingestions and symptomatic patients should be sent to a health care facility for observation for 6 to 8 hours. Although patients can develop a delayed pneumonitis, they are unlikely to do so if they have been completely asymptomatic during that time period.

Monitoring

Oral Exposure

6.5.1)

A) PREHOSPITAL: GI decontamination is not recommended because of the risk of aspiration. Remove contaminated clothing and wash exposed skin with soap and water.

6.5.2)

A) SUMMARY: Studies fail to show if gastric emptying improves outcomes in patients with oral hydrocarbon ingestions. However, if a patient has ingested a large amount of a hydrocarbon that causes significant systemic toxicity shortly prior to presentation, it is reasonable to insert a small nasogastric tube and aspirate gastric contents. Activated charcoal should NOT be used; it does not adsorb hydrocarbons well and increases the likelihood of vomiting and aspiration.
B) EMESIS/NOT RECOMMENDED

1) Emesis is not recommended because of the risk or aspiration (Goldfrank et al, 1998; Gossel & Bricker, 1994).

C) ASPIRATION

1) Gastric aspiration after endotracheal intubation should only be considered in rare patients who ingest large doses of highly toxic hydrocarbons (e.g., halogenated hydrocarbons, carbon tetrachloride) or hydrocarbons which contain very toxic additives (e.g., heavy metals, pesticides) It should be performed one hour of exposure. Questionable efficacy thereafter.
2) Use a small flexible nasogastric tube to aspirate gastric contents, instillation of water to lavage the stomach is probably not worthwhile.

D) ACTIVATED CHARCOAL

1) Activated charcoal is generally not indicated, as it may cause vomiting and subsequent aspiration. It may be considered in rare patients with ingestions of highly toxic hydrocarbons (e.g., halogenated hydrocarbons, carbon tetrachloride) and for hydrocarbons which contain very toxic additives (e.g., heavy metals, pesticides). Should be given within 1 to 2 hours of ingestion. Questionable efficacy thereafter.
2) Activated charcoal adsorbs kerosene, turpentine, and benzene in vitro and in animal models (Chin et al, 1969; Laass, 1974; Laass, 1980) Raush, 1935; (Decker et al, 1981).
3) CHARCOAL ADMINISTRATION

a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.

4) CHARCOAL DOSE

a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).

1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).

b) ADVERSE EFFECTS/CONTRAINDICATIONS

1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).

6.5.3)

A) MONITORING OF PATIENT

1) Monitor vital signs and mental status.
2) Blood concentrations are not readily available or useful to guide management.
3) Obtain an ECG and institute continuous cardiac monitoring in patients with moderate to severe toxicity or chlorinated hydrocarbon exposure.
4) Obtain CBC, basic chemistry panel, serum creatinine and liver enzymes in severe overdoses or in patients with chronic exposures.
5) Monitor arterial blood gases, pulse oximetry, and pulmonary function tests and obtain chest radiograph in patients with any respiratory symptoms. NOTE: The chest radiograph may be normal early in the clinical course.
6) Standard urine toxicology screen does not detect hydrocarbons.
7) Monitor fluid and electrolyte status in patients with significant diarrhea and vomiting.
8) Head CT should be obtained in patients with altered mental status.
9) Monitor for methemoglobinemia in cyanotic patients who do not respond to supplemental oxygen, and who may have been exposed to hydrocarbons which contain nitrobenzene or aniline.

B) ACUTE LUNG INJURY

1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases.
2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011).

a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)

3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011).
4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998).
5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995).
6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005).
7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015).
8) Steroids have not been shown to be of benefit in treating the early phase of hydrocarbon pneumonitis, however pulse steroid therapy may be useful in the late phase of adult respiratory distress syndrome following hydrocarbon ingestion. Two children with naphtha-induced chemical pneumonia were successfully treated with nebulized budesonide.

a) CASE REPORT - A 23-year-old woman developed severe respiratory distress, requiring mechanical ventilation, after ingesting 1000 milliliters of petroleum naphtha. Chest x-ray showed progressively worsening of infiltrates and diffuse interstitial consolidation of both lungs with a large pneumatocele in the right upper lobe. Pulse steroid therapy was initiated, on hospital day 17, with hydrocortisone 1000 milligrams/day IV for the first three days, followed by gradually decreasing prednisolone doses over 7 weeks, and concurrent administration of piperacillin sodium 2 grams IV every 12 hours. A follow-up chest x-ray showed rapid improvement of interstitial consolidation 3 days after beginning therapy, and, despite an enlargement of the pneumatocele, as well as, the appearance of several smaller pneumatoceles, the patient was successfully extubated six days later (Kamijo et al, 2000).

1) The patient's enlarging pneumatocele; however, became infected and subsequently ruptured, leading to recurrent respiratory distress. The patient gradually recovered following a protracted illness (hospitalized for 67 days) with no permanent sequelae after administration of antibiotics and open thoracic surgery for a bronchopleural fistula repair.

b) After ingesting naphtha, two 3-year-old boys developed chemical pneumonia with severe symptoms (dyspnea, suppressed breath sounds, crackles, hypoxemia, and cyanosis) unresponsive to supportive measures (Gurkan & Bosnak, 2005).

1) On the first day of hospitalization, radiographic exam revealed pneumonic infiltration; severe pulmonary symptoms developed on the second and fourth days, respectively. Despite supportive care, their symptoms worsened; chest radiographs showed localized consolidation and bilateral diffuse reticulonodular infiltration. Both patients were successfully treated with nebulized budesonide (0.5 mg every 12 hours for 4 days). A response (improvement in oxygen saturation and decrease in symptoms) was noted within 6 hours of budesonide administration. They were discharged after a week of hospitalization (Gurkan & Bosnak, 2005).

9) PARTIAL LIQUID VENTILATION - In a rat model of kerosene aspiration and subsequent pneumonitis, mortality was significantly greater in the rats who received partial liquid ventilation (PLV) with perfluorocarbon as compared to the rats who did not receive PLV (Burns et al, 1999).
10) EXTRACORPOREAL MEMBRANE OXYGENATION

a) Extracorporeal membrane oxygenation (ECMO) has been reported to be successful therapy in pediatric aspiration involving hydrocarbons. These children received standard therapy for hydrocarbon aspiration without success prior to the institution of extracorporeal membrane oxygenation (Jaeger et al, 1987; Hart et al, 1991; Weber et al, 1992).

11) HIGH FREQUENCY JET VENTILATION

a) A 13-month-old boy with severe hydrocarbon pneumonitis required high PEEP to maintain oxygenation and developed high peak inspiratory pressures and barotrauma (pneumomediastinum and subcutaneous emphysema) (Bysani et al, 1994). Changing the patient from a conventional ventilator to a high frequency jet ventilator allowed adequate oxygenation with lower peak inspiratory pressures and eventual recovery from the pneumonitis.

12) HIGH FREQUENCY CHEST WALL OSCILLATION

a) High frequency chest wall oscillation (HFCWO) was used in an 18-year-old man, with a history of asthma, who developed severe respiratory distress (dyspnea, hypoxia, diminished breath sounds) following aspiration of a toluene-containing solvent, and in whom symptomatic treatment, including bronchodilators, was ineffective. A chest x-ray had revealed pulmonary hyperinflation and an initial pulse oximetry showed an O2sat of 82%. Within a few seconds of beginning HFCWO treatment, the patient developed increased agitation and severe fatigue, therefore NPPV was added via nasal mask in order to reduce the work of breathing and to avoid endotracheal intubation. After a few minutes of this combined treatment, the patient was able to expectorate bronchial casts and his O2 saturation increased to 93%. Initially, he was given 3 10-minute HFCWO treatments the first day with NPPV continued until the next morning. Then, 10-min HFCWO treatments were administered twice daily for 7 days. At the end of the HFCWO treatments (8 days after initial presentation), the patient's symptoms had resolved and a repeat chest x-ray indicated that his pulmonary hyperinflation had improved significantly (Koga et al, 2004).

C) VENTRICULAR ARRHYTHMIA

1) Epinephrine and other sympathomimetics should be used with caution due to possible increased sensitivity of the myocardium to catecholamines as a result of hydrocarbon exposure. Ventricular arrhythmias may be precipitated.

D) SEIZURE

1) SUMMARY

a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).

2) DIAZEPAM

a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .

3) NO INTRAVENOUS ACCESS

a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).

4) LORAZEPAM

a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2009; Chin et al, 2008).

5) PHENOBARBITAL

a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).

6) OTHER AGENTS

a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):

1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

E) SUPPORT

1) See also (where applicable) specific managements for benzene, carbon tetrachloride, chlorinated hydrocarbon insecticides, hexane, methylene chloride, naphthalene, nitrobenzene, organophosphate insecticides, toluene, trichloroethane, trichloroethylene, tetrachloroethylene, xylene and other hydrocarbons.

Inhalation Exposure

6.7.1)

A) Move patient from the toxic environment to fresh air. Monitor for respiratory distress. If cough or difficulty in breathing develops, evaluate for hypoxia, respiratory tract irritation, bronchitis, or pneumonitis.
B) OBSERVATION: Carefully observe patients with inhalation exposure for the development of any systemic signs or symptoms and administer symptomatic treatment as necessary.
C) INITIAL TREATMENT: Administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta-2 adrenergic agonists, if bronchospasm develops. Consider systemic corticosteroids in patients with significant bronchospasm (National Heart,Lung,and Blood Institute, 2007). Exposed skin and eyes should be flushed with copious amounts of water.

Eye Exposure

6.8.1)

A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

6.9.1)

A) DERMAL DECONTAMINATION

1) Remove all contaminated clothing to prevent further absorption. Wash all clothing and exposed areas of the body twice with soap and water.

6.9.2)

A) BURN INJURY

1) CHEMICAL

a) APPLICATION

1) These recommendations apply to patients with MINOR chemical burns (FIRST DEGREE; SECOND DEGREE: less than 15% body surface area in adults; less than 10% body surface area in children; THIRD DEGREE: less than 2% body surface area). Consultation with a clinician experienced in burn therapy or a burn unit should be obtained if larger area or more severe burns are present. Neutralizing agents should NOT be used.

b) DEBRIDEMENT

1) After initial flushing with large volumes of water to remove any residual chemical material, clean wounds with a mild disinfectant soap and water.
2) DEVITALIZED SKIN: Loose, nonviable tissue should be removed by gentle cleansing with surgical soap or formal skin debridement (Moylan, 1980; Haynes, 1981). Intravenous analgesia may be required (Roberts, 1988).
3) BLISTERS: Removal and debridement of closed blisters is controversial. Current consensus is that intact blisters prevent pain and dehydration, promote healing, and allow motion; therefore, blisters should be left intact until they rupture spontaneously or healing is well underway, unless they are extremely large or inhibit motion (Roberts, 1988; Carvajal & Stewart, 1987).

c) TREATMENT

1) TOPICAL ANTIBIOTICS: Prophylactic topical antibiotic therapy with silver sulfadiazine is recommended for all burns except superficial partial thickness (first-degree) burns (Roberts, 1988). For first-degree burns bacitracin may be used, but effectiveness is not documented (Roberts, 1988).
2) SYSTEMIC ANTIBIOTICS: Systemic antibiotics are generally not indicated unless infection is present or the burn involves the hands, feet, or perineum.
3) WOUND DRESSING:

a) Depending on the site and area, the burn may be treated open (face, ears, or perineum) or covered with sterile nonstick porous gauze. The gauze dressing should be fluffy and thick enough to absorb all drainage.
b) Alternatively, a petrolatum fine-mesh gauze dressing may be used alone on partial-thickness burns.

4) DRESSING CHANGES:

a) Daily dressing changes are indicated if a burn cream is used; changes every 3 to 4 days are adequate with a dry dressing.
b) If dressing changes are to be done at home, the patient or caregiver should be instructed in proper techniques and given sufficient dressings and other necessary supplies.

5) Analgesics such as acetaminophen with codeine may be used for pain relief if needed.

d) TETANUS PROPHYLAXIS

1) The patient's tetanus immunization status should be determined. Tetanus toxoid 0.5 milliliter intramuscularly or other indicated tetanus prophylaxis should be administered if required.

e) THERMAL

1) Consultation with a clinician experienced in burn therapy or a burn unit should be obtained.

B) FROSTBITE

1) PREHOSPITAL

a) Rewarming of a localized area should only be considered if the risk of refreezing is unlikely. Avoid rubbing the frozen area which may cause further damage to the area (Grieve et al, 2011; Hallam et al, 2010).

2) REWARMING

a) Do not institute rewarming unless complete rewarming can be assured; refreezing thawed tissue increases tissue damage. Place affected area in a water bath with a temperature of 40 to 42 degrees Celsius for 15 to 30 minutes until thawing is complete. The bath should be large enough to permit complete immersion of the injured part, avoiding contact with the sides of the bath. A whirlpool bath would be ideal. Some authors suggest a mild antibacterial (ie, chlorhexidine, hexachlorophene or povidone-iodine) be added to the bath water. Tissues should be thoroughly rewarmed and pliable; the skin will appear a red-purple color (Grieve et al, 2011; Hallam et al, 2010; Murphy et al, 2000).
b) Correct systemic hypothermia which can cause cold diuresis due to suppression of antidiuretic hormone; consider IV fluids (Grieve et al, 2011).
c) Rewarming may be associated with increasing acute pain, requiring narcotic analgesics.
d) For severe frostbite, clinical trials have shown that pentoxifylline, a phosphodiesterase inhibitor, can enhance tissue viability by increasing blood flow and reducing platelet activity (Hallam et al, 2010).

3) WOUND CARE

a) Digits should be separated by sterile absorbent cotton; no constrictive dressings should be used. Protective dressings should be changed twice per day.
b) Perform twice daily hydrotherapy for 30 to 45 minutes in warm water at 40 degrees Celsius. This helps debride devitalized tissue and maintain range of motion. Keep the area warm and dry between treatments (Hallam et al, 2010; Murphy et al, 2000).
c) The injured extremities should be elevated and should not be allowed to bear weight.
d) In patients at risk for infection of necrotic tissue, prophylactic antibiotics and tetanus toxoid have been recommended by some authors (Hallam et al, 2010; Murphy et al, 2000).
e) Non-tense clear blisters should be left intact due to the risk of infection; tense or hemorrhagic blisters may be carefully aspirated in a setting where aseptic technique is provided (Hallam et al, 2010).
f) Further surgical debridement should be delayed until mummification demarcation has occurred (60 to 90 days). Spontaneous amputation may occur.
g) Analgesics may be required during the rewarming phase; however, patients with severe pain should be evaluated for vasospasm.
h) IMAGING: Arteriography and noninvasive vascular techniques (e.g., plain radiography, laser Doppler studies, digital plethysmography, infrared thermography, isotope scanning), have been useful in evaluating the extent of vasospasm after thawing and assessing whether debridement is needed (Hallam et al, 2010). In cases of severe frostbite, Technetium 99 (triple phase scanning) and MRI angiography have been shown to be the most useful to assess injury and determine the extent or need for surgical debridement (Hallam et al, 2010).
i) TOPICAL THERAPY: Topical aloe vera may decrease tissue destruction and should be applied every 6 hours (Murphy et al, 2000).
j) IBUPROFEN THERAPY: Ibuprofen, a thromboxane inhibitor, may help limit inflammatory damage and reduce tissue loss (Grieve et al, 2011; Murphy et al, 2000). DOSE: 400 mg orally every 12 hours is recommended (Hallam et al, 2010).
k) THROMBOLYTIC THERAPY: Thrombolysis (intra-arterial or intravenous thrombolytic agents) may be beneficial in those patients at risk to lose a digit or a limb, if done within the first 24 hours of exposure. The use of tissue plasminogen activator (t-PA) to clear microvascular thromboses can restore arterial blood flow, but should be accompanied by close monitoring including angiography or technetium scanning to evaluate the injury and to evaluate the effects of t-PA administration. Potential risk of the procedure includes significant tissue edema that can lead to a rise in interstitial pressures resulting in compartment syndrome (Grieve et al, 2011).
l) CONTROVERSIAL: Adjunct pharmacological agents (ie, heparin, vasodilators, prostacyclins, prostaglandin synthetase inhibitors, dextran) are controversial and not routinely recommended. The role of hyperbaric oxygen therapy, sympathectomy remains unclear (Grieve et al, 2011).
m) CHRONIC PAIN: Vasomotor dysfunction can produce chronic pain. Amitriptyline has been used in some patients; some patients may need a referral for pain management. Inability to tolerate the cold (in the affected area) has been observed following a single episode of frostbite (Hallam et al, 2010).
n) MORBIDITIES: Frostbite can produce localized osteoporosis and possible bone loss following a severe case. These events may take a year or more to develop. Children may be at greater risk to develop more severe events (ie, early arthritis) (Hallam et al, 2010).

C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

1) Hemodialysis and hemoperfusion are not of value.

Abstracts

Case Reports

1) SPECIFIC AGENT

a) GASOLINE: A 23-year-old male developed respiratory failure, seizures, severe esophagitis and gastritis, disseminated intravascular coagulation, hepatocellular injury, and oliguric renal insufficiency after ingesting 600 mL of refined gasoline, an aliphatic hydrocarbon mixture with a small amount of aromatics (Janssen et al, 1988).

2) INSECTICIDE: A 62-year-old male developed 4 well-defined mass-like lesions detected by chest x-ray within 2 weeks of ingesting a half bottle of Black Flag insecticide (1% organophosphates in a hydrocarbon distillate) in a suicide attempt. The lesions resolved within 2 months (Scott, 1989). No cause and effect relationship could be established.
3) CARBURETOR CLEANER: Fulminant hepatic failure was reported in a 17-year-old with recent exposure (route not specified) to an engine or carburetor cleaner; he died within 24 hours after admission. Possible ingredients in the cleaners included isopropyl alcohol, mineral oil, aromatic petroleum distillates, and methyl amyl alcohol. Prior chronic butane abuse may have predisposed him to severe liver injury via microsomal enzyme induction (McIntyre & Long, 1992).

1) INGESTION

a) Two pediatric patients who ingested aliphatic hydrocarbons exhibited evidence of intravascular hemolysis (Algren & Rodgers, 1992).

1) A 3-year-old male who ingested gasoline was initially stabilized with intubation, ventilation, and fluid resuscitation, with subsequent dopamine infusion. When his serum hemoglobin decreased from 14.5 g/dL to 4.6 g/dL within the first 8 hours, a transfusion of packed red blood cells was instituted with hemoglobin recovery and stability thereafter.
2) A 1-year-old male who ingested and aspirated kerosene developed severe pneumonitis and respiratory distress syndrome, requiring 6 weeks of mechanical ventilation and 3 months of hospitalization.

Range Of Toxicity

Summary

Maximum Tolerated Exposure

1) VISCOSITY: Low viscosity hydrocarbons pose the greatest risk of pulmonary aspiration and toxicity. Products with a viscosity greater than 100 S.U.S. at 100 degrees F are not considered to present an aspiration hazard. Products with less than or equal to 35 S.U.S. present a severe aspiration hazard (Weast, 1979).
2) AMOUNT INGESTED: It is difficult to estimate amounts of hydrocarbons capable of producing severe symptomatology. Less than 1 mL of some, when aspirated directly into the trachea, has produced severe pneumonitis and death in animal studies. It is impossible to evaluate the amount ingested by a child found with an empty bottle, surrounded by a pool of hydrocarbon.

1) SIGNIFICANT SYSTEMIC TOXICITY

a) The following compounds are associated with significant CNS, renal, hepatic, bone marrow or other systemic toxicity.

1) Halogenated aromatic and aliphatic hydrocarbons
2)

a) trichloroethane
b) trichloroethylene
c) carbon tetrachloride
d) methylene chloride

3) Petroleum distillates with additives
4)

a) any hydrocarbon with dangerous additives
b) heavy metals excluding gasoline
c) insecticides
d) nitrobenzene
e) aniline

5) Benzene

2) The following compounds are unlikely to produce systemic symptoms following accidental ingestion.

1) gasoline
2) kerosene
3) charcoal lighter fluid
4) Other Petroleum Products
5)

a) petroleum ether (benzine)
b) petroleum naphtha
c) VM & P naphtha paint thinner
d) Mineral spirits (eg, Stoddard solvent, solvent, white spirit, mineral turpentine (90%), petroleum spirits)
e) Turpentine

6) Aromatic hydrocarbons
7)

a) toluene
b) xylene

3) There is no evidence that the following products are absorbed from GI tract. They are not associated with systemic toxicity, but they have the highest risk of severe aspiration pneumonitis.

1) mineral seal oil
2) signal oil
3) oils found in furniture polish or oil polishes

4) The following generally do not cause CNS or pulmonary problems. They are generally considered nontoxic, although with frank aspiration they may cause a low grade lipoid pneumonia.

1) asphalt or tar
2) lubricants (e.g., motor oil, transmission oil, cutting oil, household oil, heavy greases)
3) mineral oil or liquid petrolatum (eg, laxatives, baby oil, sun tan oil, white petroleum)

1) Three patients developed diarrhea and perianal injury with burns, blistering, redness, broken skin and severe excoriation after ingesting 350 mL to 2 L of white spirit (Cassidy et al, 2014).
2) One retrospective study of hydrocarbon ingestions in children demonstrated that the majority (800 of 950) did not develop symptoms. Gastric emptying was performed in 42 of the 950 patients (Anas et al, 1981).
3) In another study, patients who were initially asymptomatic did not develop symptoms within 18 hours, and 97 percent of symptomatic patients improved within 18 hours of home follow-up (Machado et al, 1988).
4) INDOOR AIR QUALITY: Intermittent complaints of eye irritation, nausea, and headache were associated with exposure to petroleum hydrocarbons from leaking gasoline tanks buried beneath an adjacent building. Building air had measured total (gasoline) hydrocarbon concentrations ranging from 12 to 96 milligrams/cubic meter (Kullman & Hill, 1990).

Pharmacology Toxicology

Toxicologic Mechanism

1) Similar effects have been reported when concentration of taurine is reduced (Oja & Kontro, 1983; Pasantes-Morales, 1982; Wright et al, 1986; Yanau et al, 1983).

Physicochemical

Physical Characteristics

Molecular Weight

Animal Toxicology

Clinical Effects

11.1.1)

A) Birds and mammals whose feathers, coats, and skins become contaminated in an oil spill will lose the ability to shed water and thermoregulate. The animal will be depressed, dehydrated and hypothermic.

11.1.2)

A) Animals who have ingested hydrocarbons may present depressed and lethargic with gastrointestinal upset.
B) Animals may aspirate hydrocarbons after swallowing them; do not induce vomiting.

11.1.4)

A) Severe bloat, coughing, vomiting, star-gazing, depression, recumbency, dyspnea, and death occurred in goats 4 hours to ll days after single-dose kerosene ingestions of 40 mL/kg. Postmortem analysis showed gangrenous pneumonia, pleuropneumonia, congestion in brain and kidney, perivascular and perineuronal edema in brain tissue, and renal nephrosis (Aslani et al, 2000).

Treatment

11.2.1)

A) BIRD

1) OIL-COVERED BIRD - Birds should initially receive a physical examination to determine the extent of oiling, attitude, and other injuries (Dein & Frink, 1990).

a) Flush the eyes and mouth, clean the nares, and tube feed with warm electrolyte solution. Birds are frequently 10% to 15% dehydrated.
b) A GI protectant may be administered (Pepto-Bismol(R)).

1) DOSE - 2 mL/kg

c) Keep birds in a warm, quiet environment until they can be cleaned.

11.2.2)

A) GENERAL

1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.

11.2.4)

A) GASTRIC DECONTAMINATION

1) BIRD

a) OIL-COVERED BIRD - Bird is placed in a warm (103 to 104 degree F) tub of water with a 2 to 10% concentration of liquid detergent (Dawn(R) dishwashing liquid) (Dein & Frink, 1990).
b) Pour water over the bird and squeeze through the feathers (do not scrub).
c) Move the bird to a fresh tub of water and detergent when the water gets dirty.
d) It may take 3 to 4 tubs before all the oil is removed.
e) After the final washing, move the bird through a series of clean water tubs and sprays (all should be at the same temperature).
f) Reestablishment of waterproofing will be delayed if all the soap residue is not removed during the rinsing procedure.

11.2.5)

A) BIRD

1) OIL-COVERED BIRD - Determine the fluid status of the bird. If the bird is dehydrated, fluid replacement may be given by intravenous fluid and by gavage during the first day (Dein & Frink, 1990). Fluid replacement should be reduced on the second day. Fluid replacement should be guided by fluid status assessment.
2) If it is determined that the oil was contaminated with a toxin, appropriate actions should be taken; personnel should be protected from the toxic contaminant if necessary.
3) The birds should be held in dry pens for about 24 hours then in pens with half land and half water.
4) Feed birds pellets, whole smelt supplemented with vitamins, or tube feed if necessary.
5) Birds are ready for release when they can stay in water 15 to 90 minutes (depending on the species) without becoming waterlogged.

Continuing Care

11.4.1)

11.4.1.2) DECONTAMINATION/TREATMENT

A) BIRD

1) OIL-COVERED BIRD - Birds should initially receive a physical examination to determine the extent of oiling, attitude, and other injuries (Dein & Frink, 1990).

a) Flush the eyes and mouth, clean the nares, and tube feed with warm electrolyte solution. Birds are frequently 10% to 15% dehydrated.
b) A GI protectant may be administered (Pepto-Bismol(R)).

1) DOSE - 2 mL/kg

c) Keep birds in a warm, quiet environment until they can be cleaned.

11.4.2)

11.4.2.2) GASTRIC DECONTAMINATION

A) GASTRIC DECONTAMINATION

1) BIRD

Range Of Toxicity

11.3.2)

A) BIRD

1) Body weights and cloacal temperatures were found useful in determining which of a large group of afflicted birds are more likely to survive (Dein & Frink, 1990).
2) For Ruddy ducks, weighing above the group average with a cloacal temperature of over 40 degrees C was associated with approximately 100% survival in one spill (Dein & Frink, 1990); only 38% survived in the group with parameters below the group average.

References

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HYDROCARBONS

Classification | Detailed evidence-based information

Therapeutic Toxic Class

Specific Substances

Available Forms Sources

Life Support

Clinical Effects

Laboratory Monitoring

Treatment Overview

Range Of Toxicity

Summary Of Exposure

Heent

Cardiovascular

Respiratory

Neurologic

Gastrointestinal

Hepatic

Genitourinary

Hematologic

Dermatologic

Musculoskeletal

Reproductive

Carcinogenicity

Monitoring Parameters Levels

Radiographic Studies

Methods

Life Support

Patient Disposition

Monitoring

Oral Exposure

Inhalation Exposure

Eye Exposure

Dermal Exposure

Enhanced Elimination

Case Reports

Summary

Maximum Tolerated Exposure

Toxicologic Mechanism

Physical Characteristics

Molecular Weight

Clinical Effects

Treatment

Continuing Care

Range Of Toxicity

General Bibliography