REACTION OF PYRITE AND CLAYS: EXPERIMENTS IN AMD AND “PYRITE DISEASE”

Oxidation and hydrolysis of pyrite is a prime culprit in production of acid mine drainage (AMD). On a smaller scale, secondary pyrite in vertebrate fossils reacts to produce hydrous iron oxides (“pyrite disease”). The end product of this reaction is sulfuric acid, a component of AMD and a culprit in destruction of museum specimens. This is a serious problem for long-term storage of fossils and minerals. Oxidation/hydrolysis is difficult to halt once begun, and may seem to spread throughout a storage cabinet.

Polished sections of pyritized gastralia from Acrocanthosaurus atokensis were reacted at 33%, 43%, 58% and 75% relative humidity (RH) and room temperature. Humidity was buffered by saturated salt solutions. EDA analysis showed pure pyrite within the limits of detection. Pyrite particle sizes cover three orders of magnitude, from 1 micrometer to 1 mm.

After more than two years, pyrite in bone shows tarnish under reflected light microscopy, but no secondary minerals. Grain size was slightly significant in producing oxidation tarnish. By contrast, the quartz-clay-pyrite matrix in which the fossil was found reacted within months to form halotrichite, melanterite and jarosite. Potassium- and aluminum-bearing products point to the participation of clay minerals. A 7Å phase was identified by XRD, either kaolinite or (dehydrated) halloysite-(7Å). Samples coated with synthetic kaolinite failed to react, suggesting that halloysite was involved. Halloysite-(10Å) could act as donor for water, initiating a reaction that is self-perpetuating through production of hygroscopic minerals.

Under these conditions, relative humidity is unimportant: water for the reaction comes from a local source, and hydrous iron-aluminum sulfates act as “getters” for more water. Drying the materials worsens the problem by producing a dust that easily spreads to seed pyrite disease in other specimens. These seeds rapidly re-hydrate at higher humidity.