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Toxicological information

Direct observations: clinical cases, poisoning incidents and other

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Administrative data

Endpoint:
direct observations: clinical cases, poisoning incidents and other
Type of information:
other:
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: Study reported in EU-RAR 2006; reliability 2 assumed Phenol is a major component of the reaction mass, so that phenol hazard data are applied in the hazard assessment.

Data source

Reference
Reference Type:
publication
Title:
No information
Author:
Kania Jr., C.J.
Year:
1981
Bibliographic source:
J. Amer. Med. Technol. 43, 20

Materials and methods

Study type:
poisoning incident
Endpoint addressed:
acute toxicity: oral
acute toxicity: inhalation
acute toxicity: dermal
GLP compliance:
not specified

Test material

Reference
Name:
Unnamed
Type:
Constituent

Method

Route of exposure:
dermal
inhalation
oral

Results and discussion

Results of examinations:
Phenol is reported to cause poisoning by skin absorption, vapour inhalation and ingestion. Primary route of entry is the skin. Vapours readily penetrate the skin surface with absorption efficiency equal to that of inhalation. Absorption from spilling phenolic solutions on the skin may be very rapid, and death results from collapse within 30 minutes to several hours. Death has resulted from absorption of phenol through a skin area of 64 inch2. Where death is delayed, damage of the kidneys, liver, pancreas and spleen, and oedema of the lungs may result. The symptoms develop rapidly, frequently within 15-20 minutes following spilling of phenol on the skin. Initial skin contact produces a white wrinkled discoloration with no experience of pain due to the local anaesthetic properties of phenol, with the affected area turning brown and subsequently becoming gangrenous. Prolonged exposure may result in deposition of dark pigment (ochronosis). Phenol vapours are also well absorbed by the lungs. Inhalation causes dyspnea, cough, cyanosis, and pulmonary oedema. Ingestion of even small amounts of phenol causes severe burns of the mouth, esophagus, and abdominal pain. Patches, first white then brown with areas of necrosis, may be noted about the face and oral cavity.
Initial skin contact with phenol produces a white wrinkled discoloration with no experience of pain due to the local anaesthetic properties of phenol, with the affected area turning brown and subsequently becoming gangrenous. Ten percent solutions regularly produce corrosion, and occasionally skin necrosis is seen with solutions as dilute as 1%. Concentrated solutions are severely irritating to the eyes and cause conjunctival swelling with the cornea becoming white and hyperaesthetic; loss of vision has occurred in some cases. Concentration is more critical than volume with respect to local response

Any other information on results incl. tables

Phenol is reported to cause poisoning by skin absorption, vapour inhalation and ingestion. Primary route of entry is the skin. Vapours readily penetrate the skin surface with absorption efficiency equal to that of inhalation. Absorption from spilling phenolic solutions on the skin may be very rapid, and death results from collapse within 30 minutes to several hours. Death has resulted from absorption of phenol through a skin area of 64 inch2. Where death is delayed, damage of the kidneys, liver, pancreas and spleen, and oedema of the lungs may result. The symptoms develop rapidly, frequently within 15-20 minutes following spilling of phenol on the skin. Initial skin contact produces a white wrinkled discoloration with no experience of pain due to the local anaesthetic properties of phenol, with the affected area turning brown and subsequently becoming gangrenous. Prolonged exposure may result in deposition of dark pigment (ochronosis). Phenol vapours are also well absorbed by the lungs. Inhalation causes dyspnea, cough, cyanosis, and pulmonary oedema. Ingestion of even small amounts of phenol causes severe burns of the mouth, esophagus, and abdominal pain. Patches, first white then brown with areas of necrosis, may be noted about the face and oral cavity.

Initial skin contact with phenol produces a white wrinkled discoloration with no experience of pain due to the local anaesthetic properties of phenol, with the affected area turning brown and subsequently becoming gangrenous. Ten percent solutions regularly produce corrosion, and occasionally skin necrosis is seen with solutions as dilute as 1%. Concentrated solutions are severely irritating to the eyes and cause conjunctival swelling with the cornea becoming white and hyperaesthetic; loss of vision has occurred in some cases. Concentration is more critical than volume with respect to local response

Applicant's summary and conclusion

Conclusions:
Classification: highly corrosive (causes severe burns)