The properties and characteristics of triclosan were presented in detail in the previous CEFIC-LRI B7 report, and so rather than duplicate the same material here the principal points will instead be summarised.
Triclosan is a chlorinated aromatic compound that has functional groups of both phenols and ethers. It has a vapour pressure of 5.33 x 10‑4 mm Hg at 20°C and a Log Kow of 4.67. Other key physiochemical properties of the compound are described in Table 2, Appendix 4 of the CEFRIC-LRI B7 report.
The kinetics of triclosan have been described in detail previously (Bakker et al, 2014). The key points are that the buccal absorption of triclosan is around 7.3% from 0.03% mouthwash (Lin, 2000), and the principal route of excretion are the in urine and faeces where, it is found primarily in the form of conjugates (Moss et al 2000). Mean percutaneous absorption in humans calculated from urinary excretion was 5.9% of the dose after a 12-hour application (Queckenberg et al, 2010), and triclosan has a half-life of about 11 hours (Sandborgh-Englund, 2006).
Triclosan is a skin and eye irritant when used in the neat form, but it is virtually nontoxic after single ingestion or single skin contact. The substance does not cause skin sensitisation, is not mutagenic or a reproductive toxicant. Several live-time studies were conducted in mice, rats and hamsters that can serve as points of departure for a risk assessment. In mice, a species-specific, receptor-mediated mechanism of action leads to peroxisome proliferation with concomitant liver hypertrophy which eventually results in the formation of liver tumours. In rats, liver toxicity is also the most prominent effect, however, peroxisome proliferation was not observed in this species and liver tumours did not occur. The hamster is the species most similar to humans in terms of distribution, metabolism and excretion of triclosan. Whereas mice and rats exhibit enterohepatic re-circulation of triclosan and excrete it via the faeces, hamsters and humans do not exhibit re-circulation and excrete via the urine. This may explain why in hamsters, triclosan toxicity is not observed in the liver but in kidneys. Based on benchmark dose modelling, nephrotoxicity in hamsters occurs at a slightly lower dose level than liver toxicity in rats and can therefore also be regarded as the most sensitive endpoint for human risk assessment.