[7] It is sparingly soluble in organic solvents such as benzene, diethyl ether and alcohol, but practically insoluble in water with no reaction.

[9] In 1867, Henry Bassett proved that the compound produced from benzene and antimony was the same as Julian's carbon chloride and named it "hexachlorobenzene".

[9] Victor Regnault obtained hexachlorobenzene from the decomposition of chloroform and tetrachloroethylene vapours through a red-hot tube.

Hexachlorobenzene has been made on a laboratory scale since the 1890s, by the electrophilic aromatic substitution reaction of chlorine with benzene or chlorobenzenes.

Much milder reagents than chlorine (e.g. dichlorine monoxide, iodine in chlorosulfonic acid) also suffice, and the various hexachlorocyclohexanes can substitute for benzene as well.

[15] A minor industrial phloroglucinol synthesis nucleophilically substitutes hexachlorobenzene with alkoxides, followed by acidic workup.

Animal carcinogenicity data for hexachlorobenzene show increased incidences of liver, kidney (renal tubular tumours) and thyroid cancers.

Human and animal studies have demonstrated that hexachlorobenzene crosses the placenta to accumulate in foetal tissues and is transferred in breast milk.

Most of the sick were affected with a liver condition called porphyria cutanea tarda, which disturbs the metabolism of hemoglobin and results in skin lesions.

Almost all breastfeeding children under the age of two, whose mothers had eaten tainted bread, died from a condition called "pembe yara" or "pink sore", most likely from high doses of HCB in the breast milk.

The observed clinical findings include scarring of the face and hands (83.7%), hyperpigmentation (65%), hypertrichosis (44.8%), pinched faces (40.1%), painless arthritis (70.2%), small hands (66.6%), sensory shading (60.6%), myotonia (37.9%), cogwheeling (41.9%), enlarged thyroid (34.9%), and enlarged liver (4.8%).