VOL.: 71 (1999) (p. 749)
CAS No.:
Chem. Abstr. Name: Phenol
5.1 Exposure data
Phenol is a basic feedstock for the production of phenolic resins, bisphenol A, caprolactam, chlorophenols and several alkylphenols and xylenols. Phenol is also used in disinfectants and antiseptics. Occupational exposure to phenol has been reported during its production and use, as well as in the use of phenolic resins in the wood products industry. It has also been detected in automotive exhaust and tobacco smoke.
5.2 Human carcinogenicity data
A study of Finnish woodworkers found a high risk of lung cancer among those exposed to phenol, although the excess risk was stronger in short-term than in long-term workers. This result was not replicated in three other studies which reported results on phenol and lung cancer, although two of them had very low statistical power. In the three studies reporting associations with multiple cancer sites, a few elevated risks were reported, but not at any cancer site in two or more studies. The pattern of results fails to demonstrate a risk of cancer due to phenol exposure.
5.3 Animal carcinogenicity data
Phenol was tested for carcinogenicity by oral administration in rats in one study and in mice in one study. An increased incidence of leukaemia was reported in male rats treated with the lower dose but not in high-dose rats or in mice or female rats. Phenol was a promoter of mouse skin carcinogenesis in two-stage protocols.
5.4 Other relevant data
Phenol is well absorbed from the gastrointestinal tract and through the skin of animals and humans. It is metabolized principally by conjugation (by sulfation and glucuronidation) with a minor oxidation pathway leading to quinone-related reactive intermediates which bind covalently to protein and are detoxified by conjugation with glutathione. Topically applied phenol is a skin irritant and systemic toxicity is seen in liver and kidney after topical and oral dosing.
After in-vivo administration, phenol induced micronuclei in mice and chromosomal aberrations in rats. It also caused oxidative DNA damage in mice, and it bound covalently to rat DNA. In cultured mammalian cells, phenol caused mutations, sister chromatid exchanges and micronuclei. It bound to cellular protein (but not to DNA) and inhibited intercellular communication. It did not induce recessive lethal mutations in Drosophila melanogaster and had only a weak effect in inducing segregation in Aspergillus nidulans. Phenol was not mutagenic in bacteria.
5.5 Evaluation
There is inadequate evidence in humans for the carcinogenicity of phenol.
There is inadequate evidence in experimental animals for the carcinogenicity of phenol.
Overall evaluation
Phenol is not classifiable as to its carcinogenicity to humans (Group 3).
For definition of the italicized terms, see Preamble Evaluation.
Previous evaluation: Vol. 47 (1989)
Synonyms
See Also:
Toxicological Abbreviations
Phenol (EHC 161, 1994)
Phenol (HSG 88, 1994)
Phenol (ICSC)
PHENOL (JECFA Evaluation)
Phenol (PIM 412)