Chlorocresol was first introduced as a bactericide in 1897 by Kalle & Co. [de][5] after scientists gradually discovered that more substituted and more lipophylic phenols are less toxic, less irritant and more powerful.

The biodegradation of p-Chlorocresol[8] is done in the liver, and then excreted primarily via the kidneys or in smaller amounts through the lungs.

In the first step, H2O2 is activated by a catalyst, such as a metal ion or an enzyme, to form a reactive oxygen species, such as a hydroxyl radical (HO•).

This reactive species can then attack the aromatic ring of the 4-chloro-3-methylphenol molecule, leading to the formation of a quinone intermediate.

[9] This process involves the use of microorganisms such as bacteria or fungi that have the ability to break down and remove halogens from compounds.

A phenolic preservative agent, the bacteriostatic mechanism of p-Chlorocresol arises from its ability to induce cytoplasmic[14] leakage in bacteria, disrupting membrane permeability to potassium and phosphate ions.

Cytoplasmic leakage also results in dissipation of the proton motive force, causing uncoupling of respiration from ATP synthesis.

[20] There has been a documented case of recurrent unilateral facial palsy of a woman after exposure to p-chlorocresol.

[21] The brief neurological disturbance was relieved by exposure to fresh air and was determined to be a result of pharmacological hyperreactivity.

Above the critical effect level (21 mg/ kg/ bw/ day), p-chlorocresol exposure may result in a decrease in absolute adrenal gland weights.

A Committee for Veterinary Medicinal Products found p-Chlorocresol to be rapidly metabolized and excreted with no potential to accumulate in tissues and of low toxicity.