A modern copper immersion chiller is speculated to provide trace elements of zinc; thus care must be taken when adding supplemental zinc so as not to cause excess. Side effects include "...increased acetaldehyde and fusel alcohol production due to high yeast growth when zinc concentrations exceed 5 ppm. Excess zinc can also cause soapy or goaty flavors." Zinc sulfate is a potent inhibitor of sweetness perception for most sweet-tasting substances. Toxicity
Zinc sulfate powder is an eye irritant. Ingestion of trace amounts is considered safe, and zinc sulfate is added to animal feed as a source of essential zinc, at rates of up to several hundred milligrams per kilogram of feed. Excess ingestion results in acute stomach distress, with nausea and vomiting appearing at 2–8 mg/kg of body weight. Production and reactivity
Zinc sulfate is produced by treating virtually any zinc-containing material (metal, minerals, oxides) with sulfuric acid.Specific reactions include the reaction of the metal with aqueous sulfuric acid:

Zn + H2SO4 + 7 H2O → ZnSO4·7H2O + H2Pharmaceutical-grade zinc sulfate is produced by treating high-purity zinc oxide with sulfuric acid:

ZnO + H2SO4 + 6 H2O → ZnSO4·7H2OIn aqueous solution, all forms of zinc sulfate behave identically. These aqueous solutions consist of the metal aquo complex [Zn(H2O)6]2+ and SO2−4 ions. Barium sulfate forms when these solutions are treated with solutions of barium ions:

ZnSO4 + BaCl2 → BaSO4 + ZnCl2With a reduction potential of −0.76 V, zinc(II) reduces only with difficulty.
Worsening of symptoms during this time may be considered as an indicator of recurrent onset in patients known to have the disorder, and age of initial onset can be from early childhood to young adulthood, with attenuation of symptoms sometimes happening after age 30. Patients first exhibiting the disorder at a younger age may also experience worsened symptoms. Currently, no specific correlating factor or reason for winter-related manifestation has been established, though the coldness and dryer air common to winter conditions may be suspect. Winter onset is, however, considered to be a distinguishing feature of KWE among other erythematic skin disorders.When peeling of skin occurs, the newly exposed layer of skin underneath is moist, raw and very sensitive. While this may result in minor discomfort and inconvenience, in severe cases of KWE where large areas of raw skin are present, it is often life-altering and debilitating. KWE is inherited in an autosomal dominant manner. This means that the defective gene responsible for the disorder is located on an autosome (chromosome 8 is an autosome), and one copy of the defective gene is sufficient to cause the disorder when inherited from a parent who also has the disorder.KWE can begin as a spontaneous mutation, first appearing in an individual with no previous family history of the disorder. This may be due to a genetic predisposition for the disorder, possibly connected to the Oudtshoorn ancestral line. Genetics
KWE is inherited in an autosomal dominant manner.