Team:Cornell/project/background/lead

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Common effects in children: gastrointestinal distress, anemia, kidney failure, irritability, lethargy, learning disabilities, erratic behavior.<br>
Common effects in children: gastrointestinal distress, anemia, kidney failure, irritability, lethargy, learning disabilities, erratic behavior.<br>
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Common effects in adults: gastrointestinal distress, weakness, pins and needle, kidney failure  
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Common effects in adults: gastrointestinal distress, weakness, pins and needle, kidney failure <br>
Extreme cases: neurological damage, death  
Extreme cases: neurological damage, death  
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Revision as of 03:19, 16 October 2014

Cornell iGEM

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Project Background

Health Risks

Lead has no known function, and therefore no place, in the human body[4]. The lack of any robust, evolved system to deal with lead means that when it enters the organism, it will not be filtered naturally, and instead act as a disruptive, persistent, and often unnoticed antagonist to normal function. What makes lead so insidious? As it accumulates, lead will begin to take the place of other metals in biochemical reactions, replacing zinc or calcium when it is available for chemical reactions. In fact, “Lead binds to calcium-activated proteins with much higher (105 times) affinity than calcium.[10]” As a result, 75-90% of lead body load is in mineralizing tissues such as teeth and bones.

Because of these issues, the United States’ Environmental Protection Agency, which was tasked to set safe levels of chemicals in drinking water by the 1974 Safe Drinking Water Act, has set 0 as the Maximum Contaminant Level Goal for lead. The U.S. Environmental Protection Agency sets the maximum allowable lead concentration at .015 mg/L (74.8 nM)[6]. Any concentration above the set maximum requires additional treatment for removal of lead. On January 4th, 2014 a new provision of the Safe Drinking Water Act requires that any pipe used for the transport of potable water must contain less than 0.25% lead--a reduction from 8% under the previous law. Lowering levels of lead in piping will help to reduce lead in drinking water - especially since lead piping is the greatest cause of consumed lead in the US - but environmental routes of pollution still exist.

Lead is especially dangerous for children, as their porous GI tracts, and the increased vulnerability and volatility of their developing body systems make them highly susceptible to the disruptive effects of even small amounts of lead. It also takes them much more time to clear it: the half-life of lead in the adult human body is 1 month, but 10 months in a child’s [5]. Low-level exposure can be quite harmful: an increase in blood lead level from 10μg/dL to 20μg/dL is associated with an almost 3-point drop in IQ all on its own[8]. Lead has also been shown to inhibit hippocampal long-term potentiation, a neural mechanism required for learning[8].

Common effects in children: gastrointestinal distress, anemia, kidney failure, irritability, lethargy, learning disabilities, erratic behavior.
Common effects in adults: gastrointestinal distress, weakness, pins and needle, kidney failure
Extreme cases: neurological damage, death

Case Studies



Current Remediation Techniques



CBP4

The transport protein being utilized for our project is the calmodulin-binding protein CBP4 from Nicotiana tabacum. This protein is structurally similar to non-selective membrane channel proteins from other eukaryotes and has been shown to confer nickel tolerance and lead hypersensitivity.[1] Transgenic plants overexpressing NtCBP4 were found to have increased uptake of Pb2+ ions into cells, likely leading to the increased toxicity.[1] While it has been suggested that NtCBP4 could possibly be used for bioremediation purposes and other attempts have been made at lead removal from water using genetically engineered organisms, to the best of our knowledge no attempt has been made at utilizing NtCBP4 for precisely this purpose.[1],[2],[3]. We believe that the specificity of this transport protein for lead and its readily available sequence make it an ideal candidate for bioremediation.

References


  1. Arazi, T., Sunkar, R., Kaplan, B., & Fromm, H. (1999). A tobacco plasma membrane calmodulin-binding transporter confers Ni2 tolerance and Pb2 hypersensitivity in transgenic plants. The Plant Journal, 171-182
  2. Song, W., Sohn, E., Martinoia, E., Lee, Y., Yang, Y., Jasinski, M., Forestier, C., Hwang, I., & Lee, Y. (2003). Engineering tolerance and accumulation of lead and cadmium in transgenic plants. Nature Biotechnology, 914-919.
  3. Eapen, S., & Dsouza, S. (2004). Prospects Of Genetic Engineering Of Plants For Phytoremediation Of Toxic Metals. Biotechnology Advances, 97-114.
  4. "Public Health - Seattle & King County." Lead and Its Human Effects. King County Government, n.d. Web. 15 Oct. 2014.
  5. "Pathophysiology and Etiology of Lead Toxicity ." Pathophysiology and Etiology of Lead Toxicity. Medscape, n.d. Web. 15 Oct. 2014.
  6. "Consumer Factsheet on Lead in Drinking Water." Home. Environmental Protection Agency, n.d. Web. 15 Oct. 2014.
  7. "Why Lead Used to Be Added To Gasoline." Today I Found Out RSS. N.p., n.d. Web. 15 Oct. 2014.
  8. Schwartz, Joel. "Low-level lead exposure and children′ s IQ: a metaanalysis and search for a threshold." Environmental research 65.1 (1994): 42-55.
  9. "CPSC Finds Lead Poisoning Hazard for Young Children in Imported Vinyl Miniblinds." U.S. Consumer Product Safety Commission. US Consumer Product Safety Commission, n.d. Web. 15 Oct. 2014.
  10. "Lead Induced Encephalopathy: An Overview." International Journal of Pharma and Bio Sciences 2.1 (2011): 70-86. Web. http://ijpbs.net/volume2/issue1/pharma/_6.pdf.