by sanding or torching, creates lead-containing dust and fumes, it is generally safer to seal the lead paint under new paint (excepting moveable windows and doors, which create paint dust when operated). Alternatively, special precautions must be taken if the lead paint is to be removed.In oil painting, it was once common for colours such as yellow or white to be made with lead carbonate. Lead white oil colour was the main white of oil painters until superseded by compounds containing zinc or titanium in the mid-20th century. It is speculated that the painter Caravaggio and possibly Francisco Goya and Vincent Van Gogh had lead poisoning due to overexposure or carelessness when handling this colour. Soil
Residual lead in soil contributes to lead exposure in urban areas. It has been thought that the more polluted an area is with various contaminants, the more likely it is to contain lead. However, this is not always the case, as there are several other reasons for lead contamination in soil.Lead content in soil may be caused by broken-down lead paint, residues from lead-containing gasoline, used engine oil, tire weights, or pesticides used in the past, contaminated landfills, or from nearby industries such as foundries or smelters. For example, in the Montevideo neighborhood of La Teja, former industrial sites became important sources of exposure in local communities in the early 2000s.
Conversely, SIT1 mutations are believed to result in full expression of iminoglycinuria in some cases where heterozygous mutations of PAT2 would otherwise have only been sufficient to cause hyperglycinuria.Two other transport systems are believed to play subsequent roles in iminoglycinuria, when mutations in them are present. The neutral amino acid transporter SLC6A19 (affecting glycine, proline, and other neutral amino acids like cysteine and tryptophan), associated with Hartnup disease, plays a role in iminoglycinuria as a modifier to PAT2 mutations and is also directly affected by the actions of SIT1. The glycine-specific transporter, SLC6A18, also has an effect on the iminoglycinuria phenotype by either compounding or compensating for failures of glycine transport.To summarize, iminoglycinuria is primarily expressed by homozygous mutations of the PAT2 renal transporter, while the overall iminoglycinuria phenotype may be modified by normal or defective activity of SIT1 (IMINO), SLC6A19 and SLC6A18. Diagnosis
Treament
See also
Pipecolic acid
Facilitated diffusion
Oral rehydration therapy

References


== External links ==