Toxic tort claims, health risk assessments, biomonitoring, crime-scene investigations, and intellectual property cases are increasingly relying on techniques that fall under the realm of molecular biology-based science or "Toxicogenomics." Staying abreast of the rapidly evolving, cutting-edge science in this field is essential to understanding and interpreting health claims and in assessing health risks when molecular biology techniques are being used. Exponent scientists have experience in evaluating and conducting studies in the field of molecular biology, including genomics approaches such as DNA array (gene chip), real-time Q-PCR, cloning, transgenics, stem-cell therapeutics, RNA anti-sense, knock-outs, and knock-downs; and proteomics approaches such as, recombinant protein expression, cytokine assays, ELISA, radioisotope and immuno-labeling, and protein purification and identification through 1 and 2-D electrophoresis, and column chromatography.
Increasingly, "Gene Array" or DNA profiling and Cytokine arrays are being applied in an effort to understand disease mechanisms at the molecular level. In toxic tort claims, this technology is also being exploited in an to attempt to assign genetic profiles, "footprints," or "molecular signatures” to various chemical exposure scenarios, such as benzene and asbestos in order to validate an injury claim. In many cases there are considerable limitations to the design and interpretation of the scientific studies being used to support these claims. Our strong understanding of biochemistry, molecular interactions, and fate of chemicals in the body ensures a thorough scientific evaluation of molecular biology based approaches used to identify and quantify exposure and potential health effects. As part of an overall review of the science supporting a claim, Exponent scientists can critically evaluate the relevance of molecular mechanisms and techniques that are being invoked in a selected scenario.
As understanding of the molecular mechanisms behind toxicity evolves, government agencies are re-evaluating previously derived regulatory limits, and considering molecular biology-based data in deriving regulatory limits for new chemical compounds. Understanding the new molecular biology–based technology used to evaluate and assess risk of exposure to these chemicals is essential for conducting a weight-of-evidence review to determine new regulatory standards. As biotechnology patent applications increase, the need for third-party expert review is important for maintaining protection of intellectual property and "Freedom to Operate" in commercial research and development programs. Exponent scientists with experience both in the new molecular biology techniques and in regulatory toxicology can evaluate the science that will be used by regulatory agencies to derive these new limits and standards for patent protection.
Regulatory agencies and expert panels of scientists are recommending research and development of tools in the emerging field of "Toxicogenomics" for use in exposure assessment. A National Research Council committee on biomonitoring for environmental chemicals recently recommended the use of molecular biology-based biomonitoring approaches, in order "… to move beyond the traditional approaches of exposure assessment-based on one exposure to one chemical in one environmental medium" to assess multiple exposures and multiple biologic-response pathways using genetic markers of exposure and response.
Exponent has Ph.D.-level scientists who are widely published in the fields of genomics, proteomics, molecular biology, and biochemistry, with experience in designing, executing, and evaluating molecular biology-based studies. Let our scientists assist you in this rapidly evolving and complex field.
Recent Publications
Book Chapters
Dunbar BS, Chunn JL. Multimedia methods in molecular biology. In: Techniques in Electrophoresis. Roultledge (ed), Chapman and Hall, Inc., Hampshire, U.K., 1997.
Journal Articles
Chunn JL, Mohsenin A, Young HY, Lee CG, Elias JA, Kellems RE, Blackburn MR. Partially adenosine deaminase deficient mice develop pulmonary fibrosis in association with adenosine elevations. Am J Physiol Lung Cell Mol Physiol 2006; 290:579–587.
Willems L, Reichelt ME, Molina JG, Sun CX, Chunn JL, Ashton KJ, Schnermann J, Blackburn MR, Headrick JP. Effects of genetic deletion of adenosine deaminase and A1 receptors in normoxic and ischaemic hearts. Cardiovasc Res 2006; 1:71(1):79–87.
Sun CX, Zhong H, Molina JG, Belardinelli L, Zeng D, Mohsennin A, Chunn JL, Blackburn MR. Role of A2B Receptor signaling in adenosine-dependent pulmonary inflammation and injury. J Clin Invest 2006; 116(8):2173–2182.
Reichelt ME, Willems L, Molina JG, Sun CX, Chunn JC (Noble), Ashton KJ, Schnermann J, Blackburn MR, Headrick JP. Genetic deletion of the A1 adenosine receptor limits myocardial ischemic tolerance. Circ Res 2005; 18:96(3):363-367.
Chunn J, Molina JG, Mei T, Xia Y, Kellems R, Blackburn MR. Adenosine dependant pulmonary fibrosis in adenosine deaminase deficient mice. J Immunol 2005; 175:1937-1946.
Blackburn MR, Lee CG, Young HWJ, Chunn JL, Banerjee SK, Elias JA. Adenosine is an important mediator of IL-13 induced inflammation in the lung: Evidence for an IL-13-adenosine amplification pathway. J Clin Invest 2003; 112:332–343.
Chunn JL, Young WJ, Colasurdo GN, Banerjee SK, Blackburn MR. Adenosine-dependent airway inflammation and hyperresponsiveness in partially adenosine deaminase deficient mice. J Immunol 2001; 167:4676–4685.
Blackburn MR, Volmer JB, Chunn JL (Thrasher), Crosby JR, Lee JJ, Kellems RE. Metabolic consequences of adenosine deaminase deficiency in mice are associated with defects in alveogenesis, pulmonary inflammation and airway obstruction. J Exp Med 2000; 192:159-170.
Zhong H, Chunn JL, Volmer JB, Fozard JL Blackburn MR. Adenosine mediated mast cell degranulation in adenosine deaminase-deficient mice. J Pharmacol Exp Ther 2000; 298(2):433-440.
Blackburn MR, Wubah JA Chunn JL, Thompson LF, Knudsen TB. Transitory expression of the A2b adenosine receptor during implantation chamber development. Develop Dynam 1999; 216:127–136.