Sources:
Tin is found mainly in cassiterite (SnO2) from which it is reduced with coal in a reverberatory furnace. Tin’s world supply is largely exported from Malaysia, Bolivia, Indonesia, the Republic of Congo, Thailand, and Nigeria. United States being the main consumers has some deposits in Alaska and California, but produces none. Some important alloys that utilize tin are Type metal, fusible metal, bell metal, Babbitt metal, white metal, pewter, bronze, phosphor bronze, soft solder and die casting alloy (Schäfer, 1984).
Image source can be found here.
Mechanism of Action:
Certain Organotins: Triphenyltin, tributylin, dibutyltin and dioctyltin cause Thymic atrophy by reducing the number of cortical thymocytes which decreases thymus weight. T-cell mediated responses are crushed with prolonged exposure. Thymocytes that are loss appears to cause suppression of proliferation of immature thymocytes with apoptosis of mature thymocytes at higher dosage. In thymocyte cell direct effects on thymus as both cytotoxicity and apoptosis has been seen when exposed to di-or-tributyltin and triphenyltin. Supression of DNA and protein synthesis can also be caused by cytotoxicity of butyltin compounds in thymocyte. The start of apoptosis causes an increase in cytosolic ionized calcium concentration as a result of intracellular calcium stores as well as interference of calcium transport at the cell membrane. This dysregulation of calcium level has direct effects on energy metabolism of mitochondria causes uncontrolled production of reaction oxygen species, liberating of cytochrome C to the cytosol and apoptosis (Agency of Toxic Substance and Disease Registry).
Image source can be found here.
Toxicokinetics:
Toxicokinetics on Tin and Tin compounds lack persuading evidence for expert Physiologically based pharmacokinetic model. There has been no estimates on absorption of inhaled inorganic or organotin compounds. Animal studies imply that redox state and number of alkyl moieties influence gastrointestinal absorption of tin compounds. No information on the distribution of specific inorganic or organotin compounds in humans. Quantitative estimates of rates of elimination rates of absorbed tin in human is not yet made available. Animals studies have shown that elimination rates differ with chemical across species for the tin compound of interest (Agency of Toxic Substance and Disease Registry).
Image source can be found here. Page 172. This figure depicts the tin level distribution in the Human Tissues with Bone having the highest Wet weight.
Biomarker:
There are no model that would support quantitative estimates of exposure to tin and tin compounds on the basis of blood or urine levels of tin or a specific organotin or metabolite. Further research on this can help test the prevalence and magnitude of exposure in an at-risk population (Agency of Toxic Substance and Disease Registry).
Populations that are Susceptible:
No Specific population has been observed that is unusually susceptible to the effects of exposure to organotin compounds or tin and tin compounds. Although studies have suggested that inorganic tin affects the metabolism of various essential trace elements. For example, zinc absorption is reduced when dietary tin levels are high than those in normal diets this reduces growth and reduces plasma copper levels and leads to anemia. As a result, children or adults who intake diets already poor in these mineral may have higher risks of developing signs of lack of zinc or copper if their dietary tin is excessive like in a canned food based diet. It is vital to remember that >90% of tin-lined cans used for food today are coated with lacquer (Agency of Toxic Substance and Disease Registry).
Symptoms, Exposure and Treatment
Resources:
- Schäfer SG. Tin–a toxic heavy metal? A review of the literature. Regulatory toxicology and pharmacology. 03/1984;4(1):57-69. doi: 10.1016/0273-2300(84)90006-0.
- TOXICOLOGICAL PROFILE FOR TIN AND TIN COMPOUNDS (cdc.gov)