By reacting the molten mixture with chlorine gas the metals are converted to their chlorides while bismuth remains unchanged. Impurities can also be removed by various other methods for example with fluxes and treatments yielding high-purity bismuth metal (over 99% Bi). Price
The price for pure bismuth metal has been relatively stable through most of the 20th century, except for a spike in the 1970s. Bismuth has always been produced mainly as a byproduct of lead refining, and thus the price usually reflected the cost of recovery and the balance between production and demand.Prior to World War II, demand for bismuth was small and mainly pharmaceutical — bismuth compounds were used to treat such conditions as digestive disorders, sexually transmitted diseases and burns. Minor amounts of bismuth metal were consumed in fusible alloys for fire sprinkler systems and fuse wire. During World War II bismuth was considered a strategic material, used for solders, fusible alloys, medications and atomic research. To stabilize the market, the producers set the price at $1.25 per pound ($2.75 /kg) during the war and at $2.25 per pound ($4.96 /kg) from 1950 until 1964.In the early 1970s, the price rose rapidly as a result of increasing demand for bismuth as a metallurgical additive to aluminium, iron and steel. This was followed by a decline owing to increased world production, stabilized consumption, and the recessions of 1980 and 1981–1982. In 1984, the price began to climb as consumption increased worldwide, especially in the United States and Japan.
Specifically, urease-positive bacteria, such as Proteus mirabilis can produce the enzyme urease, which converts urea to ammonia and carbon dioxide. This increases the urinary pH and promotes struvite stone formation. Additionally, non-urease producing bacteria can provide bacteria components that can promote calcium oxalate crystallization, though this mechanism is poorly understood. Inhibitors of stone formation
Normal urine contains chelating agents, such as citrate, that inhibit the nucleation, growth, and aggregation of calcium-containing crystals. Other endogenous inhibitors include calgranulin (an S-100 calcium-binding protein), Tamm–Horsfall protein, glycosaminoglycans, uropontin (a form of osteopontin), nephrocalcin (an acidic glycoprotein), prothrombin F1 peptide, and bikunin (uronic acid-rich protein). The biochemical mechanisms of action of these substances have not yet been thoroughly elucidated. However, when these substances fall below their normal proportions, stones can form from an aggregation of crystals.Sufficient dietary intake of magnesium and citrate inhibits the formation of calcium oxalate and calcium phosphate stones; in addition, magnesium and citrate operate synergistically to inhibit kidney stones. The efficacy of magnesium in subduing stone formation and growth is dose-dependent. Hypocitraturia
Hypocitraturia or low urinary-citrate excretion (variably defined as less than 320 mg/day) can be a contributing cause of kidney stones in up to 2/3 of cases. The protective role of citrate is linked to several mechanisms; citrate reduces urinary supersaturation of calcium salts by forming soluble complexes with calcium ions and by inhibiting crystal growth and aggregation. Therapy with potassium citrate  is commonly prescribed in clinical practice to increase urinary citrate and to reduce stone formation rates.