Squamous cell carcinoma of the skin and coal tar creosote exposure in a railroad worker.

A 50-year-old male railroad worker presented to his primary care physician with an erythematous, tender skin lesion on the right knee; a biopsy of this lesion revealed squamous cell carcinoma in situ. The site of the lesion was sun-protected but had been associated with 30 years of creosote-soaked clothing. In this article, we review dermal and other malignancies associated with creosote, along with creosote occupational exposures and exposure limits. This is a unique case, given the lack of other, potentially confounding, polyaromatic hydrocarbons and the sun-protected location of the lesion.

[Relapse of Creosote poisoning: report of a case taking Seirogan tablets].

A thirty-eight year old man took about 180 tablets of Seirogan. He was unconscious and had dyspnea with dark brown urine on admission. He recovered gradually after initial treatment. Seirogan contains a phenolic component. Symptoms and signs of poisoning are unconsciousness, convulsion, digestive tract disorder, pulmonary edema, hepatic failure, renal failure, and miosis. Clinical features include dark brown urine. On day 7, he again showed signs of creosote poisoning: relapse of unconsciousness and dark colored urine. Plasma concentration of phenol determined on the day before the relapse was much higher than that expected from the half-life of blood phenol. It is reported that Creosote poisoning results in a decrease in the intestinal peristalsis, or paralytic ileus. We would like to emphasize that a relapse of Creosote poisoning may occur due to possible delayed absorption of the Seirogan tablets.

A fatal case of creosote poisoning.

A case of fatal creosote poisoning is described. On presentation, extensive oropharyngeal ulceration was noted and gastric lavage withheld. Post-mortem examination showed an intact oesophagus and stomach.

Environmentally-induced methemoglobinemia in an infant.

Acquired methemoglobinemia results from the exposure to various chemicals and drugs able to oxidize hemoglobin at a rate exceeding the normal enzymatic capacity for hemoglobin reduction. Levels of methemoglobin exceeding 60-70% may be associated with coma and death. We describe a case of complete, uneventful recovery involving a 10 week-old infant who presented to the Emergency Department with profound sudden onset of cyanosis, irritability, metabolic acidosis, and a lethal methemoglobin level of 71.4%. Intravenous administration of 12 mg methylene blue resulted in immediate resolution of the cyanosis and reduction of measured methemoglobin to 1.3%. The carboxyhemoglobin was negative. Sodium bicarbonate successfully corrected the acidosis. RBC reductase measurement was within normal limits, ruling out congenital methemoglobinemia. Family history revealed a wood-burning stove which emitted pine tar fumes as the potential environmental methemoglobin-producing source. The infant's cradle was situated five feet from the stove. The infant was discharged on day three of hospitalization with a methemoglobin level of 0.2%.

Hoja informativa: creosota

Información sobre creosota, usos, quién puede estar expuesto, contaminación, efectos a la salud, examen, reducción de riesgo de exposición, y protección. Documento en formato pdf; requiere el Acrobat Reader.