Stoddard Solvent Toxicity
CE Original Date: September 1, 1993
CE Renewal Date: October 1, 2000
CE Expiration Date: October 18, 2006
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|The following is about physiologic effects.|
Few studies of Stoddard solvent exposure have been done in humans. In addition, the existing data can be difficult to interpret because workers in most of the studies were exposed to mixtures of solvents. Acute exposure to Stoddard solvent at air concentrations below the odor threshold produces no adverse health effects. Studies in both experimental animals and humans indicate that exposure to high levels of Stoddard solvent can produce irritation of the skin, respiratory tract, and other mucous membranes and can generally cause transient neurologic effects. Some reports indicate that exposure of hydrocarbons may cause arrhythmias, myocardial depression, or even ventricular fibrillation.
Although case reports have been published of persons who were exposed to Stoddard solvent and subsequently suffered liver, kidney, or hematologic injury, a causal relationship has not been firmly established. Data from studies in humans and experimental animals provide inconsistent and inconclusive evidence of injury to these target organs.
The major effect associated with inhalation of paraffin-like solvents is CNS excitation, followed rapidly by CNS depression. In volunteers exposed to 100 ppm of white spirits over 6 hours, no subjective CNS symptoms were detected; however, acute exposure to 700 ppm produced prolonged reaction times. Workers exposed chronically to unknown concentrations of Stoddard solvent reported a variety of neurologic complaints including headaches, fatigue, memory deficits, inebriation, and subtle changes in color vision (dyschromatopsia). Most of these findings were reversible upon discontinuation of exposure. In experimental animal studies, inhalation exposures to high levels of Stoddard solvent produced incoordination, tremors, clonic spasms, and death.
A case report described a severe myocardial depression 72 hours after ingesting paint thinner. Inhalation of hydrocarbons may cause arrhythmias, possibly from sensitization of the myocardium to circulating catecholamines. In another report, an adult woman developed ventricular fibrillation and cardiopulmonary arrest after prolonged exposure to concentrated vapors from mineral spirits.
Acute exposure to high concentrations of Stoddard solvent can irritate mucous membranes and cause upper respiratory tract irritation. The only available human study of respiratory effects from chronic exposure involves house painters who were exposed to paints containing Stoddard solvent for periods ranging from 4 to 42 years. These workers had no decrease in lung vital capacity or expiratory volume compared to workers in other industries. Exposure concentrations were not recorded.
Acute ingestion and attendant aspiration of hydrocarbon mixtures similar to Stoddard solvent have resulted in chemical pneumonitis that mimics adult respiratory distress syndrome. Typically, respiratory involvement progresses during the first day, with resolution during the second through fifth days after exposure ceases. Complications of severe overexposure by the aspiration route may also include pulmonary edema, pulmonary emphysema, pneumothorax, pleuritis, pleural effusion, empyema, and pneumatoceles.
Stoddard solvent is a skin irritant, producing dermatitis, ulcerated and vesicular lesions, and desquamation on prolonged contact with the liquid. Dermal injury is reversible if contact with the solvent ceases. The dermal effects appear to be secondary to Stoddard solvent's ability to remove oils from the skin (defatting action). Stoddard solvent is associated with irritant contact dermatitis, and not with allergic contact dermatitis.
Data from studies of Stoddard solvent exposure in experimental animals (dermal exposure) and in humans (inhalation exposure) have not conclusively demonstrated that Stoddard solvent is carcinogenic. Epidemiological studies of painters and dry-cleaning workers exposed to mixed petroleum products have not consistently found elevated cancer risks, although some of these studies have noted increased incidences of respiratory tract, bladder, and kidney cancer. IARC has not classified Stoddard solvent carcinogenicity.
Stoddard solvent was not mutagenic in the Ames test, bacterial assays, mouse bone marrow studies, or in studies of human lymphocytes in vitro.
Existing data on the reproductive effects of Stoddard solvent are sparse. One study of male workers exposed chronically to mixed petroleum solvents indicated no sperm abnormalities. Because Stoddard solvent is fat soluble, it can probably cross the placenta and enter breast milk; however, this phenomenon has not been documented. Inhaled Stoddard solvent was not fetotoxic in experimental animals. The effects of Stoddard solvent on other reproductive endpoints in experimental animals have not been studied.
Are the complaints of the patient in the case study consistent with exposure to Stoddard solvent?
Could the patient's skin lesions have been caused by exposure to Stoddard solvent? If so, what actions would you advise?
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