Laura J. McIntosh, Ph.D.

Dr. McIntosh has 18 years of multidisciplinary experience, including designing and managing multiyear research and regulatory studies for risk assessment, toxicology reports for medical devices, in vivo and in vitro neurotoxicology testing, design and analysis of biochemical assays, chemical risk assessment, literature analysis and critique, evaluation of neuronal degeneration in rodents after exposure to toxic chemicals, and experience with tissue and cellular analysis for oxidative stress.

Dr. McIntosh has conducted research and evaluated toxicology studies for government and industry (pharmaceutical, pesticide, medical device), and has also provided non-testifying expertise for a wide range of toxicology and exposure issues concerning regulation and litigation. Currently, Dr. McIntosh is conducting basic research for the British governmental agency DEFRA on the potential risk of the pesticides paraquat and maneb on Parkinson’s disease–patterned neurodegeneration, is managing a long-term series of regulatory toxicology studies intended to set an occupational exposure level for an industrial chemical (including studies for genotoxicity, metabolism and excretion, reproductive and developmental toxicity, neurotoxicity, and carcinogenicity), and manages projects to determine the toxicity of industrial chemicals and medical device components. Compounds with which Dr. McIntosh has specific expertise include pesticides, bisphenol A and choline deficiency, and asbestos.

Dr. McIntosh’s scientific background includes a Ph.D. in Environmental Toxicology from Johns Hopkins University, 5 years of postdoctoral research in the biochemistry and cell biology of stress hormones and neurodegeneration at Stanford University, and an additional 2 years at Stanford as a lecturer. While at Stanford, she was awarded a fellowship by the American Heart Association for research on the prevention of oxidative injury to stroke patients. Her international work experience includes pre-doctoral work at the Commonwealth Scientific and Industrial Research Organization in Adelaide, Australia, and post-doctoral research at the Medical Institute of Environmental Hygiene in Düsseldorf, Germany. She achieved accreditation as a Diplomate of the American Board of Toxicology in 2004.

Li AA, Baum MJ, McIntosh LJ, Day M, Liu F, Gray LE. Building a scientific framework for studying hormonal effects on behavior and on the development of the sexually dimorphic nervous system. NeuroToxicology 2008; 29:504–519.

Li AA, Mink PJ, McIntosh LJ, Teta MJ, Finley BL. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s Disease. J Occup Environ Med 2005; 47(10):1059-1087.

Patel R, McIntosh LJ, McLaughlin J, Brooke S, Nimon V, Sapolsky R. Disruptive effects of glucocorticoids on glutathione peroxidase biochemistry in hippocampal cultures. J Neurochem 2002; 82:118–125.

McIntosh LJ, Patel MK, Bliss T, Ho D, Sapolsky RM. Interactions among ascorbate, dehydroascorbate and glucose transport in cultured hippocampal neurons and glia. Brain Res 2001; 916:127-135.

McIntosh LJ, Hong KE, Sapolsky RM. Glucocorticoids may alter antioxidant enzyme capacity in the brain: Baseline studies. Brain Res 1998; 791:209-214.

McIntosh LJ, Cortopassi KM, Sapolsky RM. Glucocorticoids may alter antioxidant enzyme capacity in the brain: Kainic acid studies. Brain Res 1998; 791:215-222.

Lawrence M, Sun G, Ho D, McIntosh LJ, Kunis D, McLaughlin J, Sapolsky RM, Steinberg G. Herpes simplex viral vectors expressing Bcl-2 are neuroprotective when delivered after a stroke. J Cereb Blood Flow Metab 1997; 17:740–744.

McIntosh LJ, Trush MA, Troncoso JC. Increased susceptibility of Alzheimer’s disease temporal cortex to oxygen free radical-mediated processes. Free Rad Biol Med 1997; 23:183-190.

Wiegand H, McIntosh LJ, Gotzsch U, Kramer U. Effects of tetrandrine on spontaneous and evoked acetylcholine release at the mouse neuromuscular junction. J Pharmacol Exper Therap 1996; 279:891–901.

McIntosh LJ, Sapolsky RM. Glucocorticoids enhance oxygen radical associated neurotoxicity. NeuroToxicology 1996; 17:873–882.

McIntosh LJ, Sapolsky RM. Glucocorticoids increase the accumulation of reactive oxygen species and enhance adriamycin-induced toxicity in neuronal culture. Exper Neurol 1996; 141:201–206.

Chan R, Huey E, Maeker HL, Cortopassi KM, Howard SA, Iyer AM, McIntosh LJ, Ajilore O, Brooke SM, Sapolsky RM. Endocrine modulators of necrotic neuron death. Brain Pathol 1996; 6:481–491.

DeLuca-Flaherty C, Flaherty K, McIntosh LJ, Bahrami B, McKay DB. Crystals of an ATPase fragment of bovine clathrin uncoating ATPase. J Molec Biol 1988; 200:749 750.

Recently Published Abstracts

McIntosh LJ, Kedderis GL, Li AA. Comparison of brain exposure to paraquat in adult and postnatal day 5 C57Bl/6 mice using PBPK modeling. Teratology Society, June 2008.

McIntosh LJ, Li AA, Kedderis GL. Distribution of 14C-paraquat in brain and body tissues of C57Bl/6 mice using PBPK modeling and autoradiography toward and analysis of Parkinson’s disease–Patterned neurodegeneration. Toxicologist 2008; 97:1843.

McIntosh L, Kedderis G. Development of a physiologically based pharmacokinetic model for paraquat in C57Bl/6 mice and estimation of human brain concentrations of paraquat under field conditions. Toxicologist 2007; 96:796.

McIntosh LJ, Li AA, Webber C, Coombs DW, Kedderis GL. Paraquat concentration in the brain varies by hemisphere after intranasal dosing. International Neurotoxicology Association 2007; 11:1.6.

• Consulting Scientist, EcoAllies.com, 2002–2003
• Scientist, AvaCore (startup medical device company), 2000
• Consulting Toxicologist, Grahn Industries (startup pollution control company), 1998–2002
• Lecturer, Stanford University, 1998-2000
• Postdoctoral Fellow, Stanford University, 1993–1998
• Postdoctoral Fellow, Medical Institute of Environmental Hygiene (Dusseldorf, Germany), 1993
• Research Associate, Commonwealth Scientific and Industrial Research Organization (Adelaide, Australia), 1986
• Research Associate, University of Colorado at Boulder, 1985
  

Wrote and was awarded a grant from the Pesticides Safety Directorate in the Department of the Environment Food and Rural Affairs of the British Government. The research is intended to provide data for publication regarding whether exposure to the pesticides paraquat and maneb are risk factors for Parkinson’s disease.

Wrote the proposal for a set of studies that would determine the toxicity of an industrial chemical currently in use. The studies are designed to set an Occupational Exposure Level for the protection of personnel who inhale the compound within a manufacturing facility. The proposal was accepted in 2006, and Dr. McIntosh will direct the studies through 2010.

Acts as a Safety Officer and Project Manager for the review of chemicals handled by an electronics research and development laboratory.

Assisted in critically reviewing and interpreting animal studies for a review on the neurobehavioral effects of exposure to bisphenol A.

Critically reviewed and interpreted toxicity data (acute), and identified data gaps, for a chemical residue left on a medical device in preparation for a review by the FDA.

Assisted in preparing toxicology summary submissions to regulatory authorities in the European Union.

Assisted in literature evaluation of acute motor effects of nicotine on rodents.

Critically reviewed and interpreted animal model studies for a review publication on the role of pesticide exposure on Parkinson’s disease.

Prepared experts, supported expert witness testimony, created lines of questioning for opposing experts, and conducted literature reviews for litigation related to occupational and domestic exposure to asbestos.

Supported efforts related to asbestos litigation, including researching regulatory, legal, and scientific sources for the concept of de minimus risk as differentiated between the population as a whole and subsections within the population, analysis of the health effects of different forms of asbestos and asbestos products, state-of-the-art analysis of friction products and manufacturer warnings, evaluation of synergy with other disease risk factors, and analysis of alternative disease causation.

• Society for Neuroscience
• Genetic and Environmental Toxicology Association
• Society of Toxicology, and NorCal chapter
• Union of Concerned Scientists
• International Neurotoxicology Association