Dermal hyperemia

Contact of 0.5 g of catechol with the intact and abraded skin of rabbits for up to 24 hours produced slight to moderate erythema and slight edema of the intact areas and necrosis of the abraded areas. The single-dose skin penetration LD50 was estimated to be 0.8 g/kg. Sub-dermal hyperemia and edema were noted at autopsy, but there were no internal gross lesions. ... 

I. Mechanism of toxicity. After topical application, essential oils produce dermal hyperemia followed by a feeling of comfort, but it ingested they can cause systemic toxicity. Most essential oils cause CNS stimulation or depression. Camphor is a CNS stimulant that causes seizures shortly after ingestion. The underlying mechanism is unknown. Camphor is rapidly absorbed from the gastrointestinal tract and is metabolized by the liver. It is not known whether metabolites contribute to toxicity. 

Dermal hyperemia (acute exposure), dry, scaling skin (chronic exposure)... 

Dermal application resulted in immediate irritation characterized by erythema and hyperemia. The subjects complained of painful burning sensation, and, after 5 hours, blisters formed on the exposed areas. ... 

Renal Effects. Acute nephritis with albuminuria and oliguria, polyuria, and nitrogen retention were observed in individuals after application of a salve that contained potassium chromate. These effects disappeared in individuals who survived. Autopsy of people who died revealed hyperemia and tubular necrosis (Brieger 1920). Acute nephritis with polyuria and proteinuria were also described in a man who was admitted to a hospital with skin ulcers on both hands due to dermal exposure to ammonium dichromate in a planographic printing establishment where he had worked for a few months (Smith 1931). A 49-year-old man with an inoperable carcinoma of the face was treated with chromic acid crystals. Severe nephritis occurred after treatment with the chromium(VI) compound. Urinalysis revealed marked protein in the urine. Death resulted 4 weeks after exposure. A postmortem examination of the kidneys revealed extensive destruction of the tubular epithelium (Major 1922). 

Renal Effects. DNOC caused elevated BUN levels in a spray operator exposed to DNOC aerosols for 5 weeks (Pollard and Filbee 1951) and cloudy swelling of the kidney in one spray operator who died after drinking water contaminated with DNOC (Bidstrup and Payne 1951) and 6 workers occupationally exposed to DNOC for 2-8 weeks (Bidstrup and Payne 1951). DNOC also caused severe capillary hyperemia in the kidneys of a boy who died after an extremely large quantity of DNOC was accidentally applied to a skin rash (Buchinskii 1974). Therefore, the human data suggest that inhalation, oral, or dermal exposure to DNOC may cause renal effects. 

Ethyl benzene is extremely irritating in animal studies. Repeated skin application has caused blisters. Inhalation or ingestion of high concentrations has led to central nervous system (CNS) depression with death attributed to depression of the respiratory center. Pathological observations include pulmonary edema and generalized visceral hyperemia. The oral LD50 for ethyl benzene is 3500 mg kg The dermal... 

Animals sacrificed after a single oral dose showed hyperemia and focal ulcerations of the gastrointestinal tract. Single dermal applications of 1000-2000 mg kg to rats and 500-1000 mg kg to rabbits produced only slight skin irritation. 

A single-exposure dermal study in guinea pigs reported death from dermal administration (Spencer et al. 1948). Hyperemia, edema, and denaturation of the skin was reported in rabbits after dermal exposure (Dow Chemical Co. 1940). 

Coal Tar Products. In an acute animal study, New Zealand white rabbits that died following single dermal applications of undiluted coal tar creosote (15,800 mg/kg) exhibited hyperemia of the intestines, but animals treated with 7,950 mg/kg did not (Pfitzer et al. 1965). 

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