Document DGQ8BYDKwJvybakv97x8pmxVo

September 10, 2009 Mr. Michael J. Brickman Richardson, Patrick, Westbrook & Brickman, LLC 174 East Bay Street Charleston, SC 29401 Re: Rose Marie Taylor Expert Report Dear Mr. Brickman: The following is an expert report containing opinions regarding the asbestos exposure history of Rose Taylor as outlined from the testimony from the videotaped depositions of Mrs. Taylor and her husband Robert Taylor. This report is based on the information that was sent from your office, my educational background and training, research into asbestos exposure issues as well as both the published and unpublished literature. The information that you provided and that we have reviewed for this report is as follows: 1. Video Deposition of Rose M. Taylor dated March 8, 2006. 2. Video Deposition of Robert M. Taylor dated May 4, 2006. 3. Video Deposition of Robert M. Taylor dated March 27, 2009. 4. Rose Taylor's Exposure Summary Rose Marie Taylor testified that she believes her mesothelioma cancer was due to the secondary exposure she received from her direct proximity to the clothing that her husband Robert wore during his 45 year work history with Southwestern Bell Telephone. Mrs. Taylor was 82 at the time of her deposition in 2006. The Law Offices of Richardson, Patrick, Westbrook & Brickman requested that 1 review the depositions of Rose and Robert Taylor to determine if there was airborne asbestos exposure to Rose Taylor from the potential secondary asbestos exposure to Robert Taylor's work clothes during his employment at Southwestern Bell Telephone. ROBERT TAYLOR OCCUPATIONAL WORK HISTORY Prior to the breakup of AT&T in the early 1980s, AT&T owned the operating subsidiaries across the United States including Southwestern Bell Telephone where Robert Taylor worked. To ensure uniform systems across this network of phone companies, AT&T also owned Western Electric which was the sole supplier, and when necessary the manufacturer, of products used by its subsidiaries. Robert Taylor testified that Western Electric materials were used in Central Switching Offices (also known as Central Offices) across the United States. Cable Holes and Cable Hole Covers Mr. Taylor stated that the Central Office was based on a uniform design template throughout the United States. The various Central Switching Offices where Robert Taylor worked were either square or rectangular buildings of multiple floors. In Abilene, Amarillo, Dallas and other cities in north Texas these buildings were usually approximately six to ten floors. Each floor was made from two feet thick concrete and at predetermined spots along the floor in rows were 2Vi feet by 2/2 feet square holes in the floor. Every several feet there was another hole and there was row after row on each floor and the holes on each floor aligned directly with the holes in the floor below and the holes in the floor above. The purpose of these holes was to accommodate cables that were run in from the outside through the ground floor or basement and then up into the building. Each floor contained frames. These frames held the switching equipment and as phone service expanded lines were pulled in through the underground below the building and then run up into each successive floor as phone capacity expanded in the community. These holes, known as cable holes because the cables ran through them, were covered until they were needed. Each cable hole had a panel at the bottom and the top made out of transite board that covered the hole. If you were on a floor looking up through a hole in the floor above there was a panel of transite board flush with the ceiling above you and there was a transite board that covered the floor the hole was in to prevent anyone from stepping into the hole. The inside wall of the hole had a metal panel on it against which cables were attached as they were pulled through. Asbestos Pillows Robert Taylor testified that when the holes were not in use and the transite panels were in place the holes were filled with small asbestos filled pillows approximately nine inches square. Mr. Taylor stated that it required approximately 100 such pillows to fill the hole. The purpose of the pillows was to prevent air and/or fire from using the holes as conduits to go from floor to floor in the event of fire. Each time new lines were pulled through a hole the process first required removing the transite board panels in the floor and emptying the hole of the asbestos pillows. The pillows were piled up alongside the hole. Mr. Taylor testified that any time the asbestos pillows were handled they released noticeable dust. Next, the workers opened the panel at the bottom of the hole in the ceiling below to run the cables through. The cables were attached to the metal panel on the side of the hole and then the transite board panels were replaced. According to the testimony of Mr. Taylor, the "pillows" that were used to seal the pathways of the telephone cable runs contained asbestos. Robert Taylor also stated that when he handled these asbestos pillows during work activities they would produce visible dust. Based on Mr. Taylor's testimony it would be my opinion that the handling of these asbestos pillows would have exposed Mr. Taylor to significant amounts of asbestos fibers and contaminated his work clothes. Cutting and Drilling Asbestos Boards Transite Panels Robert Taylor testified that in order for the transite panels to fit flush they had to be cut to adjust the size to accommodate the cables now running through the hole that were not there before. The transite boards were cut with a small electric "band saw". According to Mr. Taylor this process generated substantial dust. Robert Taylor testified that he performed this work approximately one day a week during which time he could have worked on one hole or multiple holes running cable. However, he testified that Western Electric workers did the majority of this work in the same work spaces where he worked as first a frame man, installing the frames that held the switching equipment, and later as a switchman which involved much of the same work as a frame man with added responsibilities of maintaining the switching equipment inside the frames. This activity was regular routine activity that occurred multiple times each week because it was the principle activity associated with adding new telephone lines. Multiple individuals performed it throughout the week. When one central office was at capacity they built additional central offices. As the cable holes accommodated more cables the transite board covers had to be cut and re-cut to make room for the additional cables. Work at MAS has shown that the asbestos-containing Transite boards used for this purpose were found to contain 15 % chrysotile asbestos. It would be my opinion that when Mr. Taylor cut these boards with an electric saw he would have been exposed to substantial amounts of airborne chrysotile asbestos. His asbestos exposure levels could have exceeded the 1972 OSHA Excursion limit of 10 fibers/cc and his work cloths would have become severally contaminated with asbestos-containing dust. Additionally, it is my opinion that when he was around other workers cutting this transite board he would have had significant exposure to airborne asbestos fibers as a bystander and this exposure would have contaminated his work clothes. Ebony Board Asbestos boards were also used in the frames to hold the equipment that was added in a vertical posture. These boards were called asbestos mill boards or were sometimes referred to as Ebony board. These boards were regularly drilled to attach equipment to the boards that were housed inside the frames. Asbestos Ebony sheets and panels were manufactured by Johns-Manville and they stated that this product contain between 38 to 45 % amosite, 48 to 52 % cement and 8 % asphaltic binder.1'2 As just discussed, Mr. Taylor would routinely work with Ebony board where he would drill the material to attach equipment. Based on the composition of JM Ebony board, and the work practices described by Mr. Taylor, it is my opinion that when Mr. Taylor worked with this product he would have been exposed to significant amounts of airborne amosite fibers. It is also my opinion that when Mr. Taylor worked with Ebony panels his work clothes would have become contaminated with amosite fibers. Cutting of Cement Conduit Robert Taylor stated that another product that he worked with that created dust was cement conduit. Mr. Taylor testified that cement conduit was used at the central offices to protect cables and wires from hazards. The cement conduit would have to be cut from time to time. A cutter was used that would be affixed to the pipe and then score the pipe until it broke. Mr. Taylor stated the cutting process created dust that got on his person and his clothes and generated particles that fell on the floor. Asbestos-containing cement pipe of this nature typically contains both chrysotile and crocidolite asbestos fibers. Manufacturing Specifications for Johns-Manville's pressure and non-pressure cement pipe showed that these types of pipes contained approximately 3% crocidolite and between 15 to 20% chrysotile.2'3 Studies at MAS have shown that when asbestos-containing cement pipe (AGP) is handled and cut it can release significant amounts of both crocidolite and chrysotile fibers.4 Just as important in these same studies we have shown that ACP surfaces can have a significant amount of loose asbestos fibers that are easily re-entrained when the ACP surface is touched. When Mr. Taylor handled and cut asbestos-containing conduit it is my opinion that his work clothes would have become severely contaminated with both chrysotile and crocidolite fibers. 1 Johns-Manville Ebony Manufacturing Specifications 1967--1969 Notice of Return and Notice of Deviation Sheets 2 09/03/1969 Invoice from Johns-Manville to Western Electric for Ebony Sheets and Transite Pipe. 3 Johns-Manville, "Transite Pipe Fibre Blends" 1 MAS Work Practice Study, "Cutting of CertainTeed Asbestos-Containing Pipe", October 2002 study and video. Asbestos Cloth Soldering Pads and Bags Mr. Taylor testified that another asbestos-containing product used on a daily basis by him was used in connection with the soldering process. Any time a wire had to be attached to the switching equipment it was soldered in place. To prevent the solder from dripping down to the switching equipment below where the wire was being attached a soldering pad was placed below the area where Mr. Taylor was working. This soldering pad was raw asbestos cloth. Mr. Taylor also carried a small soldering bag on his hip made of asbestos cloth in which to put additional remnants of soldering and other debris. The soldering pad and bags were made out of asbestos cloth because of the high temperature of the soldering materials. Mr. Taylor handled these items on a daily basis for 25 years between 1946 and 1971. The daily placement of an asbestos bag on Mr. Taylor's hip to hold his soldering tools would cause the bag to be in constant contact with Mr. Taylor's work clothes. The asbestos bag was described as a cloth material and our work at MAS has shown that asbestos cloth usually contains between 50% to 85% chrysotile. It is my opinion that fabric or cloth that contains between 50% to 85% chrysotile being in constant contact with Mr. Taylor's work clothes during his work activities, would have transferred significant amounts of chrysotile fibers to his work clothes causing contamination. Asbestos Insulated Wire and Cable Robert Taylor testified that much of the wire and cable used in the central offices was insulated with asbestos insulation. This is significant because one of Mr. Taylor's primary responsibilities in attaching those cables and wires involved stripping the wire and cable of the asbestoscontaining insulation. This was an activity that he did repeatedly most days that he was working in the Central Office. In addition there were other workers in the same position as Mr. Taylor doing the same kind of work stripping these asbestos insulated wires and cables to attach to the switching equipment. Mr. Taylor also testified to using hard plastic spacers which Western Electric confirms contained asbestos-containing phenolic molding compounds. Dust Generation and Control in the Central Office Environment Mr. Taylor testified that dust was a significant problem in a Central Office environment and the principle cause of faulty telephone service and static on the lines. Dust accumulated from the use of these various asbestos-containing materials that was discussed above. To reduce the dust heavy curtains were used around each set of switching equipment and exhaust fans or vacuums were often inserted underneath the curtains to collect the dust. Mr. Taylor testified that there was compressed air on each floor that was used to blow off the switching equipment in order to disturb the dust that had accumulated on it into the environment where it could eventually be suctioned or vacuumed. It is my opinion that the asbestos dust that was generated during the cutting of the transite boards and the use of asbestos pillows would have settled onto the door area, switching equipment, and other surfaces inside these work areas. Further, it is my opinion that when Mr. Taylor was in these areas when compressed air was used to blow off the switching equipment, this asbestos-containing dust would have been re-entrained into the environmental space causing Mr. Taylor to be re-exposed to significant amounts of airborne asbestos fibers. Mr. Taylor's asbestos exposure from re-entrainment would have further contaminated his work clothes with asbestos dust. ROSE TAYLOR'S SECONDARY EXPOSURE TO HER HUSBAND'S WORK CLOTHES Robert Taylor testified that he and his_wife carpooled to work each morning. He wore the same work clothes he wore in the Central Switch Office home and he and his wife Rose rode in the same family car home from work each afternoon. Each evening when Robert Taylor arrived home he testified that the first thing he did was take off his work clothes and give them to'his wife Rose to launder. She corroborated this testimony in her deposition that she laundered his work clothes each evening after they returned home from work. Rose Taylor also testified that she followed a set routine in preparing to launder Robert's clothes. She first brushed them down with a hand brush to remove what was noticeable dust on the clothes either outside or in the laundry room which was usually adjacent to the kitchen. After brushing the clothes she would then launder them that evening. Mrs. Taylor performed that task five days a week. This occurred every day of every week that Robert Taylor worked between 1946 and 1971, a period of 25 years from the time they began living together until Mr. Taylor changed work environments to work in an area where there is presently no known asbestos exposure. Fifty work weeks a year multiplied by five work days a week over 25 years, even if miscellaneous days off are accounted, adds up to 5000 work days over a 25 year period that Rose Taylor methodically laundered her husband's work clothes that he wore in an enclosed environment containing multiple asbestos-containing materials that generated dust which accumulated on his work clothes. In addition to this regular and consistent exposure on a daily basis during a 25 year period to dust generated from asbestos-containing materials used in the central office environment, Mrs. Taylor testified that she assisted her husband on a few occasions during home remodels where he used joint compounds. Mr. Taylor testified he purchased these joint compounds from the Sherwin Williams paint stores. Rose Taylor stated in some detail that she assisted her husband in the mixing process of the joint compounds and was present when the joints were sanded where he had taped and floated the joint compound. However, there is no evidence of the specific brand of joint compound used or whether those joint compounds actually contained asbestos. Mrs. Taylor also testified that she worked as a secretary at a plumbing supply warehouse and at an oil drilling supply company but there is no evidence that she had any exposure to asbestos- containing dusts because there is limited evidence that asbestos materials were present. And those materials that may have been present were not manipulated, fabricated or disturbed to release asbestos fibers. Secondary Exposure It has been well published in the peer-reviewed literature of the significant problems of household exposure to asbestos from contaminated work clothes brought home by a family member from a work site."'36'*7"*8 A review article of this problem by NIOSH provides many examples of asbestos exposure problems to children and spouses from a family member's work clothes.9 It is my opinion that the primary mechanism of asbestos exposure to household occupants from asbestos contaminated work clothing is by the washing of the work clothes in the household. The basis of this opinion is that the above referenced studies all conclude that the route of secondary exposure to family members was from the asbestos contaminated work clothes from individuals who either worked directly with asbestos products or were bystanders around others who worked with these products. Asbestos fibers have a natural tendency to adhere to work clothes where they are then transported home to the household. Typically, during laundry activities the clothes are briefly shaken releasing some of the asbestos contamination before being put into the washing machine. If this laundry procedure is carried out in the house the environment inside the house will be contaminated over time. The Taylor's testified that the clothes washing area inside their home was next to the kitchen. Since Robert Taylor always wore his work clothes and they were washed at his house some of the asbestos on his work clothes would therefore be consistently released into his house. Over time this asbestos contamination would build up causing a continuous exposure to the occupants of that home. This would include Rose Taylor from the 1946 to 1971 time period. As discussed above it is my opinion that when Robert Taylor went to the Central Switch Office his work clothes would have been contaminated with chrysotile asbestos. It is further my opinion that this facility was most likely the primary source of the asbestos that contaminated the Taylor household. 3 Epler, G.R., Fitz Gerald, M.X., Gaensler, E.A. and Carrington, C.B.: "Asbestos-Related Disease from Household Exposure", Respiration 39:229-240 (1980). 6 Comments of Johns-Manville Corporation with respect to Notice of Proposed Rulemaking Occupational Exposure to Asbestos (Federal Register, October 9, 1975) to: OSHA, April 1976. 7 Huncharek, M., Capotoito, J.V. and Muscat, J.: "Domestic Asbestos Exposure, Lung Fiber Burden, and Pleural Mesothelioma in a Housewife", British Journal of Industrial Medicine, 1989:46, 345-355. s Miltonic, C., Pinto, C. and Mobiglia, A.: "Mesotheliomas Following Exposure to Asbestos Used in Railroads: The Italian Cases", Toxicology and Industrial Health, Vol. 7, No. 112, 1191. 9 NIOSH, Publication No. 95-123, Report to Congress on Workers' Home Contamination Study Conducted Under the Workers Family Protection Act". September 1995. Ironically, asbestos product manufacturer Johns-Manville verifies this position because they had a very good understanding of the problem with take home or secondary asbestos exposure issues in the household. In published comments to the Federal Register in 1976, Johns-Manville stated the following: "As recognized by Selikqffcmd others, the impregnation ofdrapes, rugs, furniture, etc. with asbestos fibers and the constant Resuspension offibers in the respirable range creates an exaggerated hazard. Once asbestos is carried home by the workmen, it's presence in the home is likely to be permanent. Once it gets into the rugs, for example, it becomes resuspended by movement such as brushing and walking and therefore, family members are getting 24 hour a day, 7-day a week exposures. " Johns-Manville went on to say that: , "These household exposures also provide an opportunityfor repetitive high, short peak exposures due to the shaking out ofwork clothes. "" In my opinion, it is just this type of household asbestos exposure environment that Rose Taylor would have been subjected to when she lived with her family during and after the time her husband worked for Southwestern Bell Telephone. The propensity of asbestos fibers to be released from typical work clothes has been studied extensively at MAS. Our in-house work practice studies have measured the amount of asbestos dust that can be released from work clothes that were contaminated during the routine use of asbestos-containing products. An example of two of these secondary exposure studies measured the amount of asbestos release from work clothes that were contaminated with AC pipe dust and thermal insulation.10' 11 In these studies the contaminated work clothes were brought into our testing facility in a laundry basket and then shaken out to simulate a typical washing procedure. For the AC pipe dust study we measured exposure levels of between 1.8 to 2.1 fibers/cc. Significant amounts of asbestos were released from the contaminated clothing. For the MAS thermal insulation work practice study we found secondary asbestos exposure levels between 7.1 to 9.9 fibers/cc. The use of these two MAS secondary exposure work practice studies are not intended to replicate the types of work practices that Mr. Taylor used while working for AT&T. These two secondary exposure studies are provided only as demonstrative examples on how asbestos-contaminated work clothes can easily release loosely adhered asbestos dust in the breathing zone of a person who is laundering contaminated work clothes. 10 MAS Work Practice Study, "Secondary Exposure from Work Clothes with Asbestos Cement Pipe Dust", November 2006 study and video tape. 11 MAS Work Practice Study, "Secondary Exposure from Work Clothing II", April 1999 study and video tape. Based on these results it is my opinion that when Rose Taylor washed her husband's asbestoscontaminated clothing at their house she would release significant amounts of airborne asbestos fibers into the home environment causingher to be exposed to elevated levels of airborne asbestos. ASBESTOS CONCENTRATIONS IN AMBIENT AIR It is my opinion that ambient air does not contain any appreciable amounts of airborne asbestos fibers unless there is a source for those fibers. A study by the EPA showed that the average concentration of asbestos in ambient air is approximately 0.0005 fibers/cc. Mrs. Taylor's secondary asbestos exposure would have exposed her to many times above this leveland in some cases hundreds to thousands of times above this level. All the opinions expressed in this report are held withina reasonable degree of scientific certainty and I reserve the right to modify this expert report if additional information becomes available. A copy of my resume is attached to this report along with the most recent list of my testimony over the last four years. Also my hourly rate for deposition and trial testimony is$450.00 per hour. William E. Longo, P President EXHIBIT H Produced Under Separate Cover Due to File Size EXHIBIT I Produced Under Separate Cover Due to File Size EXHIBIT J William Edward Longo, Ph.D. MAS: LLC 3945 Lakefield Court Suwanee, Georgia 30024 Work Telephone: (770) 866-3200 VITAE Education October 1980 to December 1983 June 1979 to October 1980 September 1972 to June 1977 Received Doctor of Philosophy in Materials Science and Engineering, University of Florida. Completed the requirements for a Master of Science in Materials Science and Engineering, University of Florida. Received Bachelor of Science degree; Major in Microbiology, Minor in Chemistry, University of Florida. Professional Work History September 1987 to Present President of MAS, LLC (previously Materials Analytical Services Inc) Suwanee, Georgia August 1987 to February 1988 President and Founder of Longo Microanalytical Services, Inc., Gainesville, Florida. October 1983 to August 1987 President and Founder of Micro Analytical Laboratories, Inc., Gainesville, Florida. March 1985 to December 1987 Visiting Assistant Professor; University of Florida, Department of Materials Science and Engineering. August 1983 to March 1985 Post Doctoral Associate; University of Florida, Department of Materials Science and Engineering. Patents U. S. Patent Serial No. 4,671,954 June 9, 1987. Goldberg, E.P., Iwata, H., and Longo, W.E., "Microspheres for Incorporation of Therapeutic Substances and Methods of Preparation Thereof." William E. Longo Page 2 U. S. Patent Serial No. 4871716, October 3, 1989. Goldberg, E.P., Longo, W.E., and McCluskey, R.A., "Magnetically Responsive, Hydrophilic Microspheres for Incorporation of Therapeutic Substances and Methods of Preparation Thereof." Publications and Presentations Health Effects of Welding, "The Characterization of Welding Fume Particulates and Mn Bioavailability Studies for SMAW and FCAW Consumables" Longo, W.E., Rigler, M.W., Russell, P.E., Vitarelli, J.P., Hoffmann, E.M., & Johnson, H.M. NIOSH, West Virginia, July 2005 Harris, M.D., Ewing, W.M., Longo, W., DePasquale, C., Mount, M.D., Hatfield, R.L. & Stapleton, R. "Manganese Exposure During Shielded Metal Arc Welding (SMAW) in an Enclosed Space" J. Occup. & Environ. Hyg 2(8) 375 -382, 2005. Longo, W.E., Egeland, W.B., Hatfield, R.L., Stapleton, R., and Hubbard J., "Tremolite Analysis of Chrysotile Containing Friction and Gasket / Packing Products", ASTM Johnson Conference, Johnson Vermont, July 2002. Longo, W.E., Egeland, W.B., Hatfield, R.L., and Newton, L.R., "Fiber Release During the Removal of Asbestos-Containing Gaskets: A Work Practice Simulation" Appl. Occup. Environ. Hyg. 17(1) 55-62, 2002. Hatfield, R.L., Krewer, J.A., and Longo, W.E., "A Study of the Reproducibility of the MicroVac Technigue as a Tool for the Assessment of Surface Contamination in Buildings with Asbestos Containing Materials" (M.E. Beard and H.L. Rook) in Advances in Environmental Measurement Methods for Asbestos, ASTM #STP 1342,301, January 2000. Longo, W.E., and Rigler, M.W., "Rapid Identification of Inorganic and Organic Particulate for Routine IAQ Assessment" Indoor Environment meeting April 1996. Longo, W.E., "Malignant Mesothelioma in Kent Cigarettes Smokers: Analysis of Asbestos Content in Filters. Cigarette Smoke and Lung Tissue" Society for Ultrastructural Pathology, March 1996. Longo, W.E., "The Identification of Asbestos Containing Surface Treatment Products using Standard Analytical Technigues'' Florida Environmental and Asbestos Council Meeting, January 1996. Longo, W.E., Rigler, M.W. and Slade, J., "Crocidolite Asbestos Fibers in Smoke from Original Kent Cigarettes" Cancer Research 55 11, 2232, 1995. Longo, W.E., "Occupational Exposure From In-Place Asbestos Containing Fireproofing" Environmental Information Association, April 1995. William E. Longo Page 3 ;..W:, w. Keyes, D. L., Ewing, W. M., Hays, S. M., Longo, W. E. and Millette, J.R., "Baseline Studies of Asbestos Exposure During Operations and Maintenance Activities" Appl. Occup. Environ. Hyg. 9(11) Nov, 1994. Goldberg, E.P., Quigg, J., Sitren, H., Hoffmann, E., Jayakrishnan, A., Longo, W. and Cantrell, J., "Microsphere Drug Carriers for Targeted Chemo Immunotherapy and for Intracellular Infections" 20th Annual Meeting of the Society for Biomaterials, 1994. Millette, J.R., Longo, W.E. and Hubbard, J.L., "Demonstration of the Capability of Asbestos Analysis by Transmission Electron Microscopy in the 1960's" Microscope, 41_ 15, 1993. Ewing, W. M., Chesson, J., Dawson, T. A., Ewing, E. M., Hatfield, R. L., Hays, S. M., Keyes, D. L., Longo, W. E., Millette, J. R., and Spain, W. H. "Asbestos Exposure During and Following Cable Installation in the Vicinity of Fireproofing" Environmental Choices Technical Supplement, Volume I, (2), 1993. Longo, W. E., "Sampling and Analysis of Asbestos in Dust: An Update" Environmental Information Association, April, 1993. Nashville, Tennessee. Keyes, D. L., Chessan, J., Hayes, S. M., Hatfield, R. L., Ewing, W. M., Longo, W. E. and Millette, J. R. "Re-Entrainment of Asbestos from Dust in a Building with Acoustical Plaster" Environmental Choice, Technical Support, Volume I, (6), 1992. Longo, W. E. "A Standard Method for the Analysis of Asbestos in Settled Dust by TEM" Asbestos Measurement Risk Assessment and Laboratory Accreditation, ASTM Conference, July 1992. Johnson, Vermont. Longo, W. E. and Roggli, V. L., "Mineral Fiber Content of Lung Tissue in Patients with Environmental Exposures: Household Contacts vs. Building Occupants" (B. Boland and J. Cullian EDS) in The Third Wave of Asbestos Exposure to Asbestos in Place. Annals of The New York Academy of Sciences, Volume 63, 1991. Keyes, D. L., Chessan, J., Ewing, W. M., Faas, J. C., Hatfield, R. L., Hayes, S. M., Longo, W. E. and Millette, J. R. "Exposure to Airborne Asbestos Associated with Simulated Cable Installation Above and Suspended Ceiling" Am. Ind. Hyg. Assoc. J. (52) Nov. 1991 Longo, W. E. "Sampling and Analysis of Asbestos in Settled Dust" EPA/A&WMA Symposium on "Measurement of Toxic and Related Air Pollutants", May 1991. Durham, North Carolina. Longo, W. E. "Asbestos Wipe Sampling" Industrial Hygiene Association, October 1990. West Palm Beach, Florida. Longo, W. E. "Standard Test Method for Asbestos Concentrations in Dust Samples" American Society of Testing Materials Subcommittee D22.05.07, manuscript in progress. William E. Longo Page 4 Goldberg, E. P., Yalon, M., and Longo, W. E. "Low Voltage SEM for Unique Surface Analysis of Prosthetic Devices" Materials Research Society Symposium Proceedings 110, Biomedical Materials and Devices, 1989. Longo, W. E. "Field Emission Scanning Electron Microscopy: An Alternative Technique for the Analysis of Asbestos Air Filter Samples" National Asbestos Council, September 1988. Boston, Massachusetts. Goldberg, E. P., Yalon, M., and Longo, W. E. "Low Voltage Scanning Electron Microscopy for Improved Surface Characterization of Ocular Implants and Other Prosthetic Devices" American Chemical Society Symposium, September 1988. Los Angeles, California. Longo, W. E. "Rinse Technique for Recovery of Air Samples for TEM Analysis" Asbestos Measurement Research and Laboratory Accreditation, ASTM Conference, July 1988. Johnson, Vermont. Longo, W. E. "The Presence of Inorganic Fibers in Commercial Brands of Cigarettes" American Industrial Hygiene Conference, May 1988. San Francisco, California. Longo, W. E. "Analysis of Asbestos by Transmission Electron Microscopy" Alabama Electron Microscopy Society 7th Annual Meeting, March 1988. Birmingham, Alabama Longo, W. E. "Asbestos Fiber Loss from Air Sampling Cassettes: A Study by Transmission Electron Microscopy" EPA/APCA Symposium on Measurement of Toxic and Related Air Pollutants, May 1987. Research Triangle Park, North Carolina. Longo, W. E. "Asbestos Air Sample Analysis by Transmission Electron Microscopy" American Industrial Hygiene Conference Professional Development Course, May 1987. Montreal, Canada. Longo, W. E., Jenkins, E. J., Greene, R,, and Baxter, D. "Water Refiltration: An Alternative Sample Preparation Method for the Analysis of Airborne Asbestos by TEM" National Asbestos Council, January 1987. Chicago, Illinois. Longo, W. E., and Goldberg, E. P. in "Drug and Enzyme Targeting" (K. Widder and R. Green Eds) Methods of Enzymology, 112, 18, 1985. Goldberg, E. P., Iwata, H., and Longo, W. E. "Hydrophilic Albumin and Dextran IonExchange Microspheres for Localized Chemotherapy" (S. Davis, L. Illium, J. McVie, and E. Tomlinson Eds) in Microspheres and Drug Therapy. Pharmaceutical Immunological and Medical Aspects, 10, 309, 1984. Hoffmann, E. M., Longo, W. E., and Goldberg, E. P. "Macrophage Uptake of Albumin Microsphere Drug Carriers" Proceedings of the 11th International Symposium on Controlled Release of Bioactive Materials, 1_1, 27, 1984. Longo, W.E., "Albumin Microspheres for the Controlled Release of Therapeutic Agents" Doctor of Philosophy Dissertation, University of Florida, 1983. Longo, W. E., and Goldberg, E. P. "Novel Albumin-Polypeptide-Druq Microspheres: Synthesis and Ion Exchange Drug Release Properties" Proceedings of the 10th International Symposium on Controlled Release of Bioactive Materials, 10, 245, 1983. Longo, W. E., Iwata, H., Lindheimer, T., and Goldberg, E. P. "Preparation and Drug Release Properties of Albumin-Polyqlutamic Acid-Adriamycin Microspheres" American Chemical Society, 24, 56, 1983. Longo, W. E., Iwata, H., Lindheimer, T., and Goldberg, E. P. "Preparation of Hydrophilic Albumin Microspheres Using Polymeric Dispersing Agents" J. Pharm. Sci., 71_, 1323, 1982. Goldberg, E. P., Iwata, H., Terry, R. W., Longo, W. E., Levy, M., and Cantrell, J. L. in "Affinity Chromatography and Related Techniques" (Visser, Visser and Nivard Eds), Elsevier, Amsterdam, 375, 1982. Longo, W. E., Iwata, H., and Goldberg, E. P. "Hydrophilic Albumin-Polyqlutamic AcidAdriamycin Microspheres for Localized Chemotherapy" 8th Annual Meeting of the Society of Biomaterials, 10, 60, 1982. Activities and Organizations Member of Environmental Protection Agency Workshop on Sampling and Analysis of Asbestos in Settled Dusts, July 1989. Member of Environmental Protection Agency Peer Review Group for the Asbestos Engineering Program, 1987 to present. Vice-Chairman of the National Asbestos Council Analytical Subcommittee on Transmission Electron Microscopy 1987-1988. Chairman of National Asbestos Council Analytical Subcommittee on Transmission Electron Microscopy 1988-1989. Member of ASTM D-22-05 Subcommittee for Indoor Air Pollution. William E. Longo Page 6 Lectures and Courses Instructed Longo, W.E. "Electron Microscopy for Industrial Hygiene Applications" American Industrial Hygiene Conference Professional Development Course, Atlanta GA, May 2004. Longo, W. E. "Settled Dust: Asbestos and Other Particulates" Georgia Institute of Technology Seminar, August 1991. Longo, W. E. "The Role of the Laboratory Manager, Quality Assurance Officer and the Analyst for NIST Accreditation" Georgia Institute of Technology, Transmission Electron Microscopy Asbestos Accreditation Seminar, August 1989. Longo, W. E. 24th Annual Meeting of the Microbeam Analysis Society, "Asbestos Analysis Session" Ashville. North Carolina, July 1989 (Session Co-Chairman). Longo, W. E. "Fundamentals of Asbestos Analysis by TEM" Institute in Materials Science State University of New York. New Paltz, New York, October 1988 (Course Director). Longo, W. E. "TEM Imaginq/Photoqraphv" Georgia Institute of Technology, Transmission Electron Microscopy Asbestos Analysis Course, June 1988. Longo, W. E. "Laboratory Preparation of Polycarbonate Filters for TEM Analysis" Georgia Institute of Technology, Advanced Transmission Electron Microscopy Asbestos Analysis Course, February 1988. Longo, W. E. "Transmission Electron Microscopy Laboratory Set-Up" Georgia Institute of Technology, Advanced Transmission Electron Microscopy Asbestos Analysis Course, February 1988. Longo, W. E. "Laboratory Analysis of Asbestos" Hall-Kimbrell Seminar in Asbestos Abatement in the State of Florida, January 1988. Longo, W. E. "Air Sample Preparation and Analysis by TEM" Georgia Institute of Technology, Clearance Testing for Asbestos: AHERA Regulations, October 1987. Longo, W. E. "Asbestos Air Sample Analysis by Transmission Electron Microscopy" American Industrial Hygiene Conference Professional Development Course, Montreal, Canada, May 1987. Longo, W.E. "Asbestos Air Sample Analysis by Transmission Electron Microscopy" American Industrial Hygiene Conference Professional Development Course, Dallas, TX May 1986. William E. Longo Page 7 V* Professional Memberships American Industrial Hygiene Association 1985 to Present American Society for the Testing of Materials 1987 to Present American Society of Materials 1994 to Present National Asbestos Council 1984 to 1993 Environmental Information Association 1993 to Present Materials Research Society 1988 to Present Electron Microscopy Society Association 1988 to Present Microbeam Analysis Society 1988 to Present New York Academy of Science 1985 to 1987 1989 to 1994 Air Pollution Control Association 1985 to 1987 National Institute of Building Sciences 1991 to Present The Society for Ultrastructural Pathology 1996 to Present American Society of Heating, Refrigerating and Air-Conditioning Engineers 1996 to Present The American College of Forensic Examiners - Diplomat of Forensic Engineering Technology 1999 to Present American Conference of Governmental Industrial Hygienist (ACGIH) Associate Member 2006 to Present EXHIBIT K Name: CURRICULUM VITAE Arnold R. Brody, Ph.D. Address: Department of Molecular Biomedical Sciences North Carolina State University 4700 Hillsborough St. Raleigh, NC 27606 Date and Place of Birth: March 24, 1943, Boston, MA Citizenship: United States Marital Status: Married, 2 children Education: June 1961 June 1965 June 1967 June 1969 Nashua Public High School, Nashua, NH B.S. Colorado State University, Zoology M.S. University of Illinois, Functional Vertebrate Anatomy Ph.D. Colorado State University, Cell Biology Ultrastructural Cytology Brief Chronology of Employment: 1969-1972 1972-1978 1978-1984 1984-1987 1987-1990 1978-1993 1978-1993 1985-1993 1991-1993 1993 -2006 1993 -2006 1993 -2006 1999 -2006 2006- Date Post-Doctoral Fellow (NIH) with the Acarology Laboratory, Ohio State University, Columbus, OH Assistant Professor, Department of Pathology, University of Vermont, Burlington with the Vermont Specialized Center of Research in Pulmonary Disease Senior Staff Fellow, Laboratory of Pulmonary Function and Toxicology, National Institute of Environmental Health Sciences Research Biologist (Tenured), Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences GS-14 Head, Pulmonary Pathology Group, Laboratory of Pulmonary Pathobiology, National Institute of Environmental Health Sciences Adjunct Professor, Department of Pathology, and member of Graduate School Faculty, Duke University, Durham, NC Faculty: Curriculum in Toxicology, University of North Carolina College of Medicine, Chapel Hill, NC GS-15 (Full Professor with Tenure)-NIEHS Full Professor, Department of Pathology, and Department of Environmental Health Sciences, Tulane University Medical Center, New Orleans, LA Director, Lung Biology Program, Center for Bioenvironmental Research, Tulane University Medical Center, New Orleans, LA Graduate Faculty, Molecular and Cellular Biology Program, Tulane University Medical Center, New Orleans, LA Vice Chairman, Department of Pathology, Tulane University Medical Center, New Orleans, LA Professor, Department of Molecular Biomedical Sciences, North Carolina State University, Raleigh, NC Military Service: 2 1961-1963 Army ROTC Honors and Invited Participation: 1967 Outstanding teaching assistant, Department of Zoology, University of Illinois. 1969 Sigma Xi, Biological Honorary. 1974 Visiting Scientist: Pneumoconiosis Research Center, Cardiff, Wales. 1977 Research Fellowship: Institut National de la Sante et de la Recherche Medicale, Paris, France. 1978 Invited Participant and Oral Presentation: Aspen Lung Conference on Immunology of the Lung. 1979 Chairman: Use of SEM and associated techniques (DES) in studies of pulmonary pathobiology at Annual Electron Microscopy Society Mtgs. Invited participant: IARC Mtg. on Biological Effects of Mineral Fibers, Lyon. 1980 Invited Presentation: Aspen Lung Conference on Environment and the Lung. 1981 Chairman: Use of electron microscopy and associated techniques in studies of pulmonary structure, function and disease at Annual Electron Microscopy Society Meetings. 1982 Invited Participant: Aspen Lung Conference on Pulmonary Secretions an Fluids. Invited Presentation: International Conference on Occupational Lung Disease, Chicago, IL. Invited Presentation: 4th Annual Occupational and Environmental Health Conference, Salt Lake City, UT. Invited Presentation: Conference on The In Vitro Effects of Mineral Dusts, Little Rock, AR. Invited Participant: NIH Workshop on the Fibroblast in Interstitial Lung Disease. 1983 Invited Participant and Elected Member of Committee on Basic Science: EPA Task Force on Environmental Lung Disease, Washington, DC, March. Invited Tutorial on Pathogenesis of Asbestos-Induced Lung Disease: Annual Electron Microscopy Soc., Detroit, April. Invited presentation: Aspen Lung Conference on Pathobiology of Pulmonary Emphysema, June. Invited Paper: Theodore F. Hatch Symposium on Occupational Health, U. of Pittsburgh, September. 1984 Chairman: Symposium on Mechanisms of Acute Lung Injury. FASEB, St. Louis, MO. Member NIH Study Section: Isolation and Characterization of Human Lung Cells. 1985 1986 1987 1988 3 Invited Speaker: Rochester International Conference on Environmental Toxicity, Rochester, NY, June. Faculty: Pulmonary Pathology Course, University of Vermont, Department of Pathology, August. Scientific Advisory Committee and Invited Presentation: In Vitro Effects of Mineral Dusts, Schluchsee, FRG, October. Visiting Professor: Department of Pathology, Instituto Nacional DeCardiologia, Mexico City, January. Visiting Professor: Department of Biology, University of California, Santa Barbara, April. Chairman: Symposium on Pulmonary Response Following Particulate Exposure in Experimental Animals, Annual Meeting American Thoracic Society, Anaheim, CA, May. Visiting Professor: Department of Pathology, State University of New York at Stony Brook, June. State-of-the-Art Presentation: Cellular Pathobiology of Asbestosis at 28th Annual Aspen Lung Conference, June. Awarded: John P. Wyatt Traveling Fellowship In Environmental Pathology. Invited Speaker: Depts. of Pathology and Medicine Pulmonary Seminar Program, Washington University, St. Louis, September. Standing Member of Merit Review Board: Respiratory Disease Section, Veterans Administration, Washington, DC, September 1985-88. Invited Speaker: Pathology Grand Rounds, Harvard Medical School, Boston, January. Invited Speaker: Conference on Silicosis and Mixed-Dust Pneumoconiosis Chantilly, France, April. Visiting Scientist: Institut Nationale de Sante et Recherche Medicale, Paris, France, May - June. Invited Speaker: Gordon Conference on Pulmonary Biology, New London, New Hampshire, July. Invited Speaker: Electron Microscopy Society of America, Albuquerque, August. Invited Speaker: Third International Conference on Environmental Lung Disease, Montreal, October. Appointed: National Academy of Sciences Panel on Pulmonary Toxicology. Outstanding Performance Cash Award from NIH, March. Chairman: Symposium on Cellular Mechanisms of Occupational Lung Injury. Annual Meeting American Thoracic Society, New Orleans, May. NIH Study Section: Ad Hoc Panel to review RFA on subpopulations of pulmonary interstitial cells. Invited Speaker: IARC Conference on Mineral Fibres in the Non-Occupational Environment, Lyon, France, September. Keynote Address: "Mechanisms of Particle-Induced Lung Injury" American College of Chest Physicians, Atlanta, October. Invited Speaker: Lung Dosimetry: Extrapolation Modeling of Inhaled Particles and Gases, Duke University, October. Appointed: Visiting Committee: Harvard School of Public Health, Respiratory Biology Program, March. 1989 1990 4 Outstanding Performance Cash Award from NIH, March. Visiting Scientist: University of Rochester School of Medicine, Environmental Health Sciences Center, March. Organizer and Faculty: Course on Environmental Lung Disease, Mexico City, March. Invited Speaker: Biological Interactions of Inhaled Mineral Fibers and Cigarette Smoke, Seattle, April. Chairman: Symposium on "Pulmonary Macrophage Biology and Interstitial Lung Disease" Annual FASEB Conference, May. Chairman and Invited Speaker: Symposium on "Biochemical and Molecular Mechanisms of Alveolar Fibrosis," Annual Meeting American Thoracic Society, May. Invited Speaker: VIIth International Pneumoconioses Conference, Pittsburgh, August. Scientific Advisor: Workshop on In Vitro Effects of Mineral Dusts, Sherbrooke, Canada, September. Chairman: "Mechanisms of Cellular Response to Inhale Substances," IIIrd Chicago Conference on Occupational Lung Disease, October. Science Advisory Board: Health Effects Institute, Boston. Invited Speaker: Congressional Subcommittee on Environment and Technology. Washington, DC, January. Invited Speaker: Dept. of Environmental Hygiene, University of Gothenburg, Sweden, March. Invited Speaker: 3rd Alexis Carrell Conference on Accelerated Atherosclerosis, Washington, DC, March. Invited Speaker: 2nd GERP Conference on Occupational Lung Disease, Paris, France, March. Invited Speaker: Dept. of Pathology, Baylor College of Medicine. Houston, TX, May. Conference Organizer and Speaker: Fiber Toxicology, Research Triangle Park, NC, June. International Advisory Committee: Appointed as standing member for The Annual Aspen Lung Conference. Invited Participant: XIVth Annual European Symposium on Hormones and Cell Regulation, Mont St-Odile, France, September. Invited Speaker: Symposium on Molecular Biomarkers of Disease, NIEHS, February. Invited Participant: Banbury Center Conference on Molecular Mechanisms of Fiber Cytotoxicity and Carcinogenesis, Cold Spring Harbor, NY, March. Program Committee and Session Chair: Mechanisms of Particle-Overload Induced Lung Disease, Rochester, May. Session Chair: Symposium on Cell-Cell Interactions in the Lung, World Conference on Lung Health, Boston, May. State-of-the-Art Speaker: Aspen Lung Conference on Mechanisms of Lung Repair, Aspen, CO, June. Program Committee and Invited Speaker: The Third Wave of Asbestos Disease, Exposure to Asbestos in Place, NY, June. Invited Participant: International Congress on Inflammation, Barcelona, June. 1991 1992 1993 5 Invited Participant: Alveolar Macrophages in the Clearance of Inhaled Particles, Oxford, September. Program Committee and Speaker: Biannual Symposium on Pulmonary Fibrosis, Stowe, VT, October. NIH Study Section: Specialized Centers of Research in Pulmonary Disease. Bethesda, January. Visiting Scientist: Environmental Science Center, Univ. of Calif., Davis, February. Visiting Pulmonary Scholar: Univ. of Wisconsin School of Medicine, March. Keynote Speaker: American Association of Respiratory Therapy, Providence, March. Session Chair and Speaker: Mechanisms of Pulmonary Fibrosis Amer. Assoc. of Pathologists Minisymposium, Atlanta, April. Invited Speaker and Member of the Environmental Lung Disease Working Group of the Pulmonary Diseases Advisory Council, NHLBI Workshop, Washington, DC, May. Christie Memorial Lecturer: Australian Society for Experimental Pathology, Adelaide, Australia, September. Chairman: Basic Science Symposium, Fourth International Conference on Environmental Lung Disease, Montreal, September. Chairman: Biological Reaction to Dust, Seventh International Symposium on Inhaled Particles, Edinburgh, September. Invited Speaker: Woods Hole Conference on Pulmonary Biology, October. Invited Speaker and Organizer: Environmental Pulmonary Disease, Cuernavaca, Mexico, January. Invited Faculty: Scientific Frontiers of Occupational Pulmonary Medicine, Miami, May. Scientific Committee: Workshop on Durability of Inhalable Minerals, Lyon, France, September. Invited Speaker: International Conference on Pulmonary Vascular Remodeling in Health and Disease, London, September. Scientific Committee and Speaker: Seventh International Pulmonary Fibrosis Colloquium, Cambridge, U.K., October. Visiting Professor: University of Michigan School of Medicine, October. Invited Speaker: Cochin Hospital, Paris, November. Member: American Thoracic Society Task Force Developing a Strategic Plan for Lung Research into the 21St Century. Invited Speaker: FASEB Conference on Pulmonary Pathobiology, New Orleans, April. Invited Participant: Workshop on Interactions of Particles with the Lung, ATS Meeting, San Francisco, May. Invited Speaker: 4th European Meeting of Environmental Hygiene, Wagenigen, The Netherlands, June. Invited Speaker and Organizing Committee: Cytokines and Lung Inflammation, Institut Pasteur, Paris, June. Invited Speaker: 24th International Conference in Occupational Health, Nice, September. Invited Speaker: Effects of Mineral Dusts on Cells, Paris, October. Member: Scientific Site Visit Committee to the Institut Pasteur, Paris, 1994 1995 1996 October. Invited Speaker: World Congress on Inflammation, Vienna, October. 6 Invited Participant: Colloquium on Particulate Air Pollution and Human Mortality and Morbidity, National Academy of Sciences Conference, Irvine, CA, January. Invited Speaker: European Society for Clinical Investigation, Toledo, Spain, April. Invited Speaker: American Lung Association, Science Day for the Media, New York, September. Scientific Co-Chairman and Member of Organizing Committee: Eighth International Conference on Pulmonary Fibrosis, Dijon, France, October. Ad Hoc Participant: Lung Biology Study Section, Bethesda, October. Invited Speaker: Institute of Preventive and Clinical Medicine, Bratislava, Slovakia, November. Invited Speaker: 5th International Inhalation Symposium, Hannover, Germany, February. Invited Speaker: American College of Chest Physicians, 5Th International Conference on Environmental and Occupational Lung Disease, Orlando, March. Invited Speaker: NIEHS-Sponsored Public Health Symposium, Mexico City, March. Chairman and Invited Speaker: Environmental Biology '95, Minisymposium on Environmental Pathology and Toxicology, Atlanta, April. Invited Speaker: American Thoracic Society Annual International Conference, Symposium on Interstitial Pulmonary Fibrosis, Seattle, May. Co-Chair and State-of-the-Art Speaker: 38th Annual Aspen Lung Conference, Environmental Lung Disease, Aspen, June. Chairman: Session on Fiber Dissolution, British Association for Lung Research, Edinburgh, September. Selected: Wellcome Visiting Professor in the Basic Medical Sciences, sponsored by the Burroughs Wellcome Fund, November. NIH SCOR (Fibrotic Lung Diseases) Study Section, Washington, DC, January. NIH Lung Biology Pathology Study Section, Washington, DC, February. Featured Speaker: American Thoracic Society Annual Conference, Symposium on Cell Activation in Lung Injury, New Orleans, May. Invited Speaker: NATO Advanced Study Institute, Vascular Endothelium, Crete, Greece, June. Invited Speaker and Scientific Organizing Committee: International Conference on Toxicology of Natural and Man-Made Particles, Lake Placid, NY, September. Invited Participant and Workgroup Member: Association of Occupational and Environmental Clinics, Workshop on Particulates and Chronic Airways Disease, Pittsburgh, October. Invited Speaker: Annual Woods Hole Conference on Lung Biology, Woods Hole, MA, October. Invited Speaker and Organizer: Ninth International Colloquium on Pulmonary Fibrosis, Oaxaca, Mexico, November. 1997 1998 1999 7 Invited Speaker: Dean's Distinguished Faculty Forum, Tulane University Medical Center, New Orleans, February. Participant: NIH Lung Biology and Pathology Study Section, Bethesda, MD, February. Invited Speaker and Co-Chair: Mediator and Signal Transduction in Lung Injury Models, Annual Meeting of the American Society for Investigative Pathology, New Orleans, April, 1997. Invited Speaker and Co-Chair: Cellular Mechanisms of Pulmonary Fibrosis, Annual Meeting of the ATS, San Francisco, May. Invited Speaker: World Health Organization Conference on Lung Injury, Corfu, June. Participant: NIH Special Study Section--Oxidative Lung Injury, Research Triangle Park, NC, August. Scientific Advisor and Participant: Second International Meeting on Oxygen/Nitrogen Radicals and Cellular Injury, Chapel Hill, NC, September. Invited Speaker: International Conference on Occupational Health, Kyoto, Japan, October. Visiting Professor: Tainan Medical College, Taiwan, October. Visiting Professor: Beijing Medical College, Beijing, China, October. Invited Speaker: University of California, Davis, College of Medicine, November. Study Section: Member of MIT Site Visit Team for the Environmental Science Center, Boston, March. Special Study Section: Children and Environmental Health, NIEHS, Research Triangle Park, NC, March. Invited Speaker: EurQConference on Therapeutic Approaches for Diseases of the Respiratory Tract, Institut Pasteur, Paris, April. Invited Speaker: Respiratory Biology at the American Society for Investigative Pathology, San Francisco, April. Session Chairman: Mechanisms of Lung Injury, American Thoracic Society, Annual Conference, Chicago, April. Invited Speaker and Organizer: Tenth International Colloquium on Pulmonary Fibrosis, Siena, Italy, October. Session Chairman: Symposium on Systemic Sarcoidosis, National Heart, Lung, and Blood Institute Conference, New Haven, October. Member: National Institute of Environmental Health Sciences, Environmental Health Sciences Review Committee, 1998-2002. Member: ATS Committee on Research Advocacy, American Thoracic Society, 1999-2000. Invited Speaker: 6th International Conference on Environmental and Occupational Lung Diseases, American College of Chest Physicians, Vancouver, February. Member: ATS Government Relations Committee, American Thoracic Society, 1999-2000. Invited Speaker: Signal Transduction and Growth Factors in Molecular Toxicology, National Institute of Environmental Health Sciences, Research Triangle Park, NC, March. Member: Research Grants Review Committee, American Lung Association, 1999-2000. 2000 2001 2002 8 Invited Speaker: Cytokines: Biology, Gene Regulation and Role in the Pathogenesis of Lung Disease, Society of Toxicology, New Orleans, March. Invited Speaker: Experimental Biology, Recent Advances in Molecular Mechanisms and Pharmacological Interventions of Lung Fibrosis, Washington, D.C., April. Invited Speaker: Tissue Repair and Fibrosis, 4th World Congress on Inflammation, Paris, June. Keynote Speaker: Seventh Symposium on Particle Toxicology, Maastricht, The Netherlands, October. Invited Panelist and Speaker: Advanced Research Cooperation in Environmental Health, 7th Biennial Symposium on Minorities and Cancer, Washington, D.C., February. Invited "Special Lecturer": 4th Conference on Acute Lung Injury, Tokyo, Japan, February. Invited Speaker: Update in Occupational Lung Disease, Johns Hopkins University, Baltimore, March. Invited Speaker: Andrews' 15th Annual Asbestos Conference, Andrews Publications, New Orleans, April. Chairman and Speaker: ATS-NIEHS Workshop, Toronto, Canada, May. Study Section: Cancer and Smoking Disease Program, Nebraska Department of Health and Human Services, Omaha, May. Scientific Committee and Conference Summarizer: 11th International Colloquium on Lung Fibrosis, Stockholm, Sweden, September. Member: ATS Committee on Research Advocacy, American Thoracic Society, 2000-2001. Sabbatical Leave, Duke University, Division of Pulmonary Medicine, JanuaryApril; Institut Pasteur, Paris, May-June. Study Section: University of California, Tobacco-Related Disease Research Program - PulmonaryDisease Review Committee, San Francisco, March. Invited Speaker: ATS 2Qp1 Meet-the-Professor Seminar 97th International Conference, San Francisco, May. Organizer and Speaker: EurQconference on Chronic Lung Diseases, Paris, June. Study Section: NIEHS Environmental Health Sciences Review Committee Meeting, Research Triangle Park, NC , November. Special Study Section: National Heart, Lung, and Blood Institute Conference, Chevy Chase, MD, February. Site Visit: NIEHS - National Jewish Medical and Research Center, February. Study Section: University of California, Tobacco-Related Diseases Research Program - PulmonaryDisease Review Committee, San Francisco, April. Site Visit: NIEHS Special Emphasis Panel - Harvard School of Public Health, Boston, May-June. Study Section: American Heart Association, Lung, Resuscitation, and Respiration Study Group, Chicago, October. Invited Speaker: International Conference on Lung Fibrosis, Geneva, October Invited Speaker: 7th Congress of Asian Pacific Society of Respirology, Taipei, November. Invited Speaker: Liaocheng Peoples Hospital, Peoples Republic of China, November. 2003 2004 2005 2006 9 Chairman - Study Section:National Heart, Lung, and Blood Institute Special Emphasis Panel, Molecular Targets and Interventions in Pulmonary Fibrosis, Columbia, MD, March. Study Section: University of California, Tobacco-Related Diseases Research Program - Pulmonary Disease Review Committee, San Francisco, March. Invited Lecture: Mechanism of TGF-B Activation by Reactive Oxygen Species Harvard School of Public Health, Boston, April. Invited Speaker: Andrews' 18th Annual Asbestos Litigation Conference, Andrews Publications, New Orleans, May. Site Visit: NIEHS - Harvard School of Public Health, Boston, June Invited Lecture: EPA Workshop on Mechanisms of Asbestos Fiber Toxicity and Carcinogenicity, Chicago, June. Study Section: NIH (LPBA) Lung Biology and Pathology, Washington, DC, June. Invited Speaker: XVII World Asthma Congress, St. Petersburg, Russia. July. Study Section: NIH (NHLBI) National Heart, Lung, Blood Institute, Special Review Committee for Program Project Grant/POl, Lung Fibrogenesis and the Biology of Fibroblast, Rockville, MD, February. Study Section: NIH (NHLBI) National Heart, Lung, Blood Institute, Special Review Committee for Program Project Grant/POl, Regulation of Respiratory Epithelial Cell Homeostasis, Rockville, MD, February. Chairman -Study Section: NIH NHLBI National Heart, Lung, Blood Institute, Special Emphasis Panel Granulomatous Lung Inflammation in Sarcoidosis, Rockville, MD., March. Study Section: University of California, Tobacco-Related Diseases Research Program - Pulmonary Disease Review Committee, San Francisco, April. Invited Speaker: St. Luke's Medical Center, Grand Rounds, "Asbestos-induced fibrogenesis: how unraveling of the molecular mechanisms will direct potential therapeutic approaches,"Milwaukee, WI, September. Invited Speaker and Session Chair: 13th International Colloquium on Lung Fibrosis. Banff, Alberta, Canada, October. Invited Speaker: Shanghai International Respiratory Symposium. Shanghai, China, October. Invited Speaker: 8th International Meeting on Effects of Mineral Dusts and Nanoparticles. NIH Research Triangle Park, NC, October. Scientific Advisory Board: BioMarck Pharmaceuticals Invited Speaker: University of Rochester College of Medicine, Department of Pulmonary Medicine, March Invited Speaker: 14th International Colloquium on Pulmonary Fibrosis, Frankfurt, Germany, September. Invited Speaker: International Mesothelioma Conference; Chicago, October Invited Chair: Amer Physiol Soc Conf; Physiological Genomics and Proteomics Of Lung Disease; Ft. Lauderdale, November 2007 2008 10 Invited Speaker: Univ. of Pennsylvania, Dept. of Pulmonary and Critical Care Medicine; Philadelphia, March Study Section: NIH-National Heart Lung and Blood Institute; RFA for Adult Stem Cell Biology; Bethesda, April Invited Speaker: University of California, Los Angeles, Dept. of Pulmonary and Critical Care Medicine; Los Angeles, May Invited Speaker: NIH Conference on Lung Cell Biology; Bethesda, July ATS Program Committee for 2007 Annual Meeting Invited Speaker: Duke University, Dept. of Pulm. and Crit. Care Med., October Study Section: Asthma and Allergy Cooperative Research Centers; NHLBI Bethesda, October. Invited Speaker: University of Southern California, Dept. of Pulmonary and Critical Care Medicine, Los Angeles, January. Study Section: National Institute of Allergy and Infectious Diseases, Bethesda, February Study Section: National Institute of Environmental Health Sciences, RTP, NC, April ATS Program Committee for 2008 Annual Meeting Invited Speaker: Hopital Bichat, Dept. of Lung Biology, Paris, June Study Section: National Heart Lung and Blood Inst, Bethesda, August Visiting Scientist: UC Davis College of Medicine, Davis, CA, October Committees: NIEHS Chairman: GS-9/11 Promotions Committee (1988-91) Standing Member: Animal Care Committee (1984-90) Standing Member: Tenure Review and Promotions Committee (1991-93) Tulane Department of Pathology - Tenure and Promotions (1993 - 2006) - Delegate to the Basic Science Faculty - Strategic Plan Co-Chair President's Search Committee for Senior Vice President for the Health Sciences President's Search Committee for Director of the Center for Bioenvironmental Research Chairman: Subcommittee on Training Grants Chairman: Dean's Pharmacology Department Review Standing Member: Cancer Center Steering Committee Dean's Pharmacology Chair Search Committee Elected Member: Molecular and Cellular Biology Steering Committee Chairman: Dean's Forum for Advances in Research Committee Member: Dean's Personnel and Honors Committee (1999-2006) Elected Member: Faculty Advisory Committee Appointed: Center for Bioenvironmental Research Faculty Council Editorial Board American Journal of Pathology American Journal of Physiology: Lung, Cellular, and Molecular Physiology American Journal of Respiratory, Cell, and Molecular Biology Current Respiratory Medicine Reviews Journal of Environmental Pathology, Toxicology, and Oncology Journal of Inflammopharmacology Journal of Organ Dysfunction Section Editor (Pathology) Journal of Lipid Mediators and Cell Signalling 11 Review Manuscripts for: American Journal of Respiratory and Critical Care Medicine Chemico-Biological Interactions Environmental Health Perspectives Environmental Research FASEB Journal Journal of Cellular Physiology Journal of Clinical Investigation Journal of Immunology Journal of the American Physiological Society Laboratory Investigation Science Toxicology and Applied Pharmacology American Journal of Pathology Active Memberships: AAAS - American Association for the Advancement of Science American Thoracic Society - Assembly Nominating Committee FASEB - Federation of American Societies for Experimental Biology Sigma Xi (Biological Honorary) Peer-Reviewed Publications 1. Brody, A. R. Comparative fine structure of acarine integument. J.N.Y. Entomol. Soc. 77(2):105, 1969. 2. Brody, A. R., and Wharton, G. W. Dermatophagoides farinae: Ultrastructure of lateral opisthosomal dermal glands. Trans. Amer. Micros. Soc. 89(4):499, 1970. 3. Brody, A. R. Observations on the fine structure of the developing cuticle of a soil mite, Oppia coloradensis (Acarina: Cryptostigmata). Acarologia 12(2):421, 1970. 4. Brody, A. R., and Wharton, G. W. The use of glycerol-KCL in the scanning microscopy of Acari. Ann. Entomol. Soc. Amer. 64(2):528, 1971. 5. Brody, A. R. (Ed.) Colloquium: The entomology of house-dust allergy. Proc. N. Central Branch, Entomol. Soc. Amer. 26:57, 1971. 12 6. Brody, A. R., and Wharton, G. W. The peritrophic membrane of the house-dust mite, Dermatophagoides farinae. Parasitology 58:801, 1972. 7. Brody, A. R., and Wharton, G. W. Dermatophagoides farinae: The digestive system. J.N.Y. Entomol. Soc. 80:152, 1972. 8. Brody, A. R., and Craighead, J. E. A simple perfusion apparatus for lung fixation. Proc. Soc. Biol. Med. 143:388, 1973. 9. Brody, A. R., and Craighead, J. E. Pathogenesis of pulmonary cytome-alovirus infection in immunosuppressed mice. J. Infect. Dis. 129:677, 1974. 10. Brody, A. R., Graham, W. G., Kanich, R. E., and Craighead, J. E. Cyst wall formation in pulmonary eosinophilic granuloma. Chest 66:576, 1974. 11. Murphy, G. M., Brody, A. R., and Craighead, J. E. Monocyte migration across pulmonary membranes in mice infected with cytomegalovirus. J. Exp. Mol. Pathol. 22:35, 1975. 12. Brody, A. R., and Craighead, J. E. Cytoplasmic inclusions in pulmonary macrophages of cigarette smokers. Lab. Invest. 32:125, 1975. 13. Brody, A. R., and Craighead, J. E. Preparation of human lung biopsy specimens by perfusion-fixation. Am. Rev. Respir. Dis. 112:645, 1975. 14. Harrow, E. M., Brody, A. R., Jakab, G. J., and Green, G. M. The pulmonary response to a bacteremic challenge. Am. Rev. Respir. Dis. 112:7, 1975. 15. Brody, A. R., Wharton, G. W., and McGrath, J. C. Dermatophagoides farinae: The supracoxal glands. J.N.Y. Entomol. Soc. 84:34, 1976. 16. Brody, A. R., and Craighead, J. E. Interstitial associations of cells lining air spaces in human pulmonary fibrosis. Virchows Arch. A. of Pathol., Anat. and Histol. 372:39, 1976. 17. Brody, A. R., Vallyathan, N. V., and Craighead, J. E. Distribution and elemental analysis of inorganic particulates in pulmonary tissue. Scanning Elect. Microsc. 1:477, 1976. 18. Davis, G. S., Brody, A. R., Landis, J. N., Graham, W. G., Craighead, J. E., and Green, G. M. Quantitation of inflammatory activity in interstitial pneumonitis by bronchofiberscopic pulmonary lavage. Chest 69:265, 1976. 19. Suratt, P. M., Winn, W. C., Brody, A. R., et al. Acute silicosis in tombstone sandblasters. Am. Rev. Respir. Dis. 115:521, 1977. 20. Brody, A. R., et al. The elemental content of granulomata in pulmonary sarcoidosis and hypersensitivity pneumonitis. Scan. Elect. Microsc. 2:129, 1977.21 * * 21. Davis, G. S., Brody, A. R., and Craighead, J. E. Analysis of airspace and interstitial mononuclear cell populations in human diffuse interstitial lung disease. Am. Rev. Respir. Dis. 118:7-15, 1978. 13 22. Brody, A. R., Vallyathan, N. V., and Craighead, J. E. Use of scanning electron microscopy and X-ray energy spectrometry to determine the elemental content of inclusions in human tissue lesions. Scan. Elect. Microsc. 3:252, 1978. 23. Brody, A. R., Kelleher, P. C., and Craighead, J. E. A mechanism of exudation through intact alveolar epithelial cells in the lungs of cytomegalovirus-infected mice. Lab. Invest. 39:281-288, 1978. 24. Davis, G. S., Moehring, J. M., Absher, M. P., and Brody, A. R. Isolation and characterization of fibroblasts obtained by pulmonary lavage of human subjects. In Vitro 15:612-623, 1979. 25. Davis, G. S., and Brody, A. R. Changes in human alveolar macrophage cell shape and surface morphology. Chest 75:280-282, 1979. 26. Newman, R. A., Brody, A. R., and Krakoff, I. H. Gallium nitrate induced toxicity in the rat. A pharmacologic, histopathologic, and microanalytical investigation. Cancer 44:1728, 1979. 27. Davis, G. S., and Brody, A. R. Changes in the surface morphology of human alveolar macrophages induced by tobacco and marijuana smoking. Exp. Lung Res. 1:281, 1980. 28. Brody, A. R., Roe, M. W., and Davis, G. S. Use of backscattered electron imaging to quantify the distribution of inhaled crystalline silica. Scanning Elect. Microsc. 3:301, 1980. 29. Perl, D. P., and Brody, A. R. Alzheimer's disease: X-ray spectrometric evidence of aluminum concentration in neurofibrillary tangle-bearing neurons. Science 208:297, 1980. 30. Adler, K. B., Brody, A. R., and Craighead, J. E. Studies on the mechanism of mucin secretion by cells of the porcine tracheal epithelium. Proc. Soc. Exp. Biol. Med. 166:37, 1981. 31. Brody, A. R., and Hill, L. H. Deposition pattern and clearance pathways of inhaled chrysotile asbestos. Chest 80:64-67, 1981. 32. Brody, A. R., Hill, L. H., Adkins, B., and O'Connor, R. W. Chrysotile asbestos inhalation in rats: deposition pattern and reaction of alveolar epithelium and pulmonary macrophages. Am. Rev. Respir. Dis. 123:670-679, 1981. 33. Brody, A. R., et al. Epithelial-mesenchymal association of cells in human pulmonary fibrosis and in BHT-oxygen induced fibrosis in mice. Exp. Lung. Res. 2:207-220, 1981. 34. Brody, A. R., and Hill, L. H. Interstitial accumulation of inhaled chrysotile asbestos fibersand consequent formation of microcalcifications. Am. J. Pathol. 109:107-114, 1982.35 * * 35. Brody, A. R., Roe, M. W., Evans J. N., and Davis, G. S. Deposition and translocation of inhaled silica in rats: quantification of macrophage participation and particle distribution in alveolar ducts. Lab. Invest. 4Z:533-42, 1982. 14 36. Lapenas, D. J., Davis, G. S., Gale, P. N., and Brody, A. R. Mineral dusts as etiologic agents in pulmonary fibrosis. Am. J. Clin. Pathol. 78:701-706, 1982. 37. Brody, A. R., and Roe, M. W. Deposition pattern of inorganic particles at the alveolar level in the lungs of rats and mice. Am. Rev. Respir. Dis. 128:724-729, 1983. 38. Brody, A. R., Hill, L. H., and Adler, K. B. Actin-containing microfilaments of pulmonary epithelial cells provide a mechanism for translocating asbestos to the interstitium. Chest 83:11-12, 1983. 39. Brody, A. R., George, G., and Hill, L. H. Interactions of chrysotile and crocidolite asbestos with red blood cell membranes: Chrysotile binds to sialic acid. Lab. Invest. 49:468-475, 1983. 40. Warheit, D. B., Hill, L. H., and Brody, A. R. Pulmonary macrophage phagocytosis: Quantification by secondary and backscattered electron imaging. Scan. Elect. Microsc. 4:431-437, 1983. 41. Barry, B. E., Wong K. C., Brody, A. R., and Crapo, J. D. Reaction of rat lungs to inhaled chrysotile asbestos following acute and subchronic exposures. Exp. Lung. Res. 5:1-21, 1983. 42. Pinkerton, K. E., Brody, A. R., McLaurin, D. A., Adkins, B., O'Connor, R. W., Pratt, P. C., and Crapo, J. D. Characterization of three types of chrysotile asbestos after aerosolization. Environ. Res. 31:32-53,1983. 43. Brody, A. R. Tutorial: The early pathogenesis of asbestos-induced lung disease. Scan. Elect. Microsc. I:167-170, 1984. 44. Warheit, D. B., Chang, L. Y., Hill, L. H., Hook, G. E. R., Crapo, J. D., and Brody, A. R. Pulmonary macrophage accumulation and asbestos-induced lesions at sites of fiber deposition. Am. Rev. Respir. Dis. 129:301-310, 1984. 45. Warheit, D. B., Hill, L. H., and Brody, A. R. Surface morphology and correlated phagocytic capacity of pulmonary macrophages lavaged from the lungs of rats. Exp. Lung Res. 6:1-82, 1984. 46. Lee, T. C., Wu, R., Brody, A. R., Barrett, J. C., and Nettesheim, P. Growth and differentiation of hamster tracheal epithelial cells in culture. Exp. Lung Res. 6:27-45, 1984. 47. Brody, A. R., Warheit, D. B., Chang, L. Y., et al. Initial deposition pattern of inhaled minerals and consequent pathogenic events at the alveolar level. Ann. N.Y. Acad. Sci. 428:108-120, 1984. 48. Roggli, V., and Brody, A. R. Changes in numbers and dimensions of chrysotile asbestos fibers in lungs of rats following short-term exposure. Exp. Lung Res. 7:133-147, 1984.49 49. Oghiso, Y., Kagan, E., and Brody, A. R. Intrapulmonary distribution of inhaled chrysotile and crocidolite asbestos: ultrastructural features. Brit. J. Exp. Pathol. 65:467 484, 1984. 15 50. Warheit, D. B., Hill, L. H., and Brody, A. R. In vitro effects of crocidolite asbestos and wollastonite on pulmonary macrophages and serum complement. Scan. Elect. Microsc. 2:919-926, 1984. 51. Pinkerton, K. E., Pratt, P. L., Brody, A. R., and Crapo, J. D. Fiber localization and its relationship to lung reaction in rats after chronic inhalation of chrysotile asbestos. Am. J. Pathol. 117:484-498, 1984. 52. Kouzan, S., Brody, A. R., et al. Production of arachidonic acid metabolites by pulmonary macrophages exposed in vitro to asbestos, carbonyl iron or calcium ionophore. Am. Rev. Respir. Dis. 131:624-632, 1985. 53. Warheit, D. B., George, G., Hill, L. H., Snyderman, R., and Brody, A. R. Inhaled asbestos activates a complement-dependent chemoattractant for macrophages. Lab. Invest. 52:505-514, 1985. 54. Brody, A. R., Hill, L. H., and Warheit, D. B. Induction of early alveolar injury by inhaled asbestos and silica. Federation Proc. 44:2596-2601, 1985. 55. Kouzan, S., Gallagher, J., Eling, T., and Brody, A. R. Particle binding to sialic acid residues on macrophage plasma membranes stimulates arachidonic acid metabolism. Lab. Invest. 53:320-27, 1985. 56. Kliewer, M., Fram, E. K., Brody, A. R., and Young, S. L. Secretion of surfactant by rat alveolar type II cells: Morphometric analysis and three dimensional reconstruction. Exp. Lung Res. 9:351-361, 1985. 57. Warheit, D. B., Hill, L. H., George G., and Brody, A. R. Time Course of chemotactic factor generation and the macrophage response to asbestos inhalation. Am. Rev. Respir. Dis. 134:128-133, 1986. 58. Dethloff, L. A., Gilmore, L. B., Brody, A. R., and Hook, G. E. R. Induction of intra- and extracellular phospholipids in the lungs of rats exposed to silica. Biochem. J. 133:111 118, 1986. 59. Brody, A. R. Pulmonary cell interactions with asbestos fibers in vivo and in vitro. Chest 89:155-159, 1986. 60. Roggli, V. L., Pratt, P. C., and Brody, A. R. Asbestos content of lung tissue in asbestosassociated diseases. Br. J. Ind. Med. 43:18-28, 1986. 61. Brody, A. R. and Overby, L. H.. Scientific Correspondence. Nature 324:622, 1986. 62. Hesterberg, T. W., Butterick, C. J., Oshimura, M., Brody, A. R., and Barrett, J. C. Role of phagocytosis in cytogenetic effects and cell transformation induced by asbestos and short and long glass fibers. Cancer Res. 46:5795-5802, 1986. 63. Pinkerton, K. E., Plopper, C. G., Merler, R. R., Brody, A. R., and Crapo, J. D. Airway branching patterns dictate asbestos fiber location and the extent of tissue injury at the alveolar level. Lab. Invest. 55:688-695, 1986. 16 64. Roggli, V. L., George, M. H. and Brody, A. R. Clearance and dimensional changes of crocidolite asbestos fibers isolated from lungs of rats following short-term exposure. Environ. Res. 42:94-105, 1987. 65. Hook, G. E. R., Brody, A. R., Cameron, G. S., Jetten, A. A., Gilmore, L. B., and Nettesheim, P. Repopulation by isolated Clara Cells of tracheas denuded of their own epithelium. Exp. Lung Res. 12: 11-318, 1987. 66. Gallagher, J. E., George, G. and Brody, A. R. Sialic acid mediates the initial binding of positively-charged inorganic particles to alveolar macrophage membranes. Am. Rev. Respir. Dis. 135:1345-1352, 1987. 67. Jetten, A. M., Rearick, J. I., Hook, G. E. R. and Brody, A. R. Retinoic acid and substratum regulate the differentiation of rabbit tracheal epithelial cells into squamous and secretory phenotype. Lab. Invest. 56:654-664, 1987. 68. Brody, A. R., Hook, G. E. R., Cameron, G. S., Jetten, A. M. and Nettesheim, P. The differentiation capacity of Clara cells isolated from the lungs of rabbits. Lab. Invest. 57:219-228, 1987. 69. Bauman, M. D., Jetten, A. M., Brody, A. R. Biological and Biochemical characterization of a macrophage-derived growth factor for rat lung fibroblasts. Chest 91:155-56, 1987. 70. Kouzan, S., Nolan, R. D., Eling, T. E. and Brody A. R. Stimulation of arachidonic acid metabolism by adherence of alveolar macrophages to a plastic substrate: Modulation by fetal bovine serum. Am. Rev. Respir. Dis. 137:38-43, 1988. 71. Warheit, D. B., Overby, L. H. and Brody, A. R. Pulmonary macrophages are attracted to inhaled particles through complement activation. Exp. Lung Res. 14:51-66, 1988. 72. Kumar, R. K., Bennett, R. A. and Brody, A. R. A homologue of platelet-derived growth factor produced by rat alveolar macrophages. FASEB J. 2:2272-2277, 1988. 73. Chang, L. Y., Overby, L. H., Brody, A. R., and Crapo, J. D. Progressive lung cell reactions and extracellular matrix production after a brief exposure to asbestos. Am. J. Pathol. 131:156-170, 1988. 74. Bertram, T. A., Overby, L. H., Eling, T. E., and Brody, A. R. Pulmonary intravascular macrophages metabolize arachidonic acid in vitro. Am. Rev. Respir. Dis. 138:936-944, 1988. 75. Inayama, Y., Hook, G. E. R., and Brody, A. R. et al., The differentiation potential of tracheal basal cells. Lab. Invest. 58:706-717, 1988. 76. Brody, A. R. and Overby, L. H. Incorporation of tritiated thymidine by epithelial and interstitial cells in bronchiolar-alveolar regions of asbestos-exposed rats. Am. J. Pathol. 134:133-144, 1989. 77. Inayama, Y., Hook, G. E. R., Brody, A. R., Jetten, A. M., Gray, T., Mahler, J. F. and Nettesheim, P. In vitro and in vivo growth and differentiation of clones of tracheal basal cells. Am. J. Pathol. 134:539-549, 1989. 17 78. McGavran, P. D. and Brody, A. R. Chrysotile asbestos inhalation induces tritiated thymidine incorporation by epithelial cells of distal bronchioles. Am. J. Respir. Cell Mol. Biol. 1:231-235, 1989. 79. Bonner, J. C., Hoffman, M., and Brody, A. R. A Platelet-derived growth factor homolog secreted by alveolar macrophages is complexed to an a-macroglobulin. Transplantation Proceedings 21:3704-3705, 1989. 80. Bonner, J. C., Hoffman, M., and Brody, A. R. A-macroglobulin secreted by alveolar macrophages serves as a binding protein for a macrophage-derived homologue of platelet-derived growth factor. Am. J. Respir. Cell Mol. Biol. 1:171-179, 1989. 81. Bertram, T. A., Overby, L. H., Eling, T. E., and Brody, A. R. Comparison of arachidonic acid metabolism by pulmonary intravascular and alveolar macrophages exposed to particulate and soluble stimuli. Lab. Invest. 61:457-466, 1989. 82. Pinkerton, K. E., Brody, A. R., Miller, F. J., and Crapo, J. D. Exposure to low levels of ozone results in enhanced pulmonary retention of inhaled asbestos fibers. Am. Rev. Respir. Dis. 140:1075-1081, 1989. 83. McGavran, P. D., Moore, L. M., and Brody, A. R. Inhalation of chrysotile asbestos induces rapid cellular proliferation in small pulmonary vessels of mice and rats. Am. J. Pathol. 136:695-705, 1990. 84. Nettesheim, P., Jetten, A. M., Inayama, Y., Brody, A. R., George, M. A., Gilmore, L. B., Gray, T., and Hook, G. E. R. Pathways of differentiation of airway epithelial cells. Environ. Health Perspect. 85:317-329, 1990. 85. Khan, M. F., Gallagher, J. E., and Brody, A. R. Effect of proteins and lipids of the alveolar lining layer in particle binding and phagocytosis. Toxicology In Vitro 4:93-101, 1990. 86. McGavran, P. D., Butterick, C. J., and Brody, A. R. Tritiated thymidine incorporation and the development of an interstitial lesion in the bronchiolar-alveolar regions of the lungs of normal and complement-deficient mice after inhalation of chrysotile asbestos. J. Env. Path. Toxicol. Oncol. 9:377-392, 1990. 87. Bauman, M. D., Jetten, A. M., Bonner, J. C., Kumar, R. K., Bennett, R. A., and Brody, A. R. Secretion of a platelet-derived growth factor homologue by rat alveolar macrophages exposed to particulates in vitro. Eur. J. Cell Biol. 51:327-334, 1990. 88. Brody, A. R. Asbestos, Carcinogenicity and Public Policy (Letters). Science 248:795, 1990. 89. Gendek, E. G. and Brody, A. R. Changes in lipid ordering of model phospholipid membranes treated with chrysotile and crocidolite asbestos. Environ. Res. 53:152-167, 1990. 90. Osornio-Vargas, A. R., Bonner, J. C., Badgett, A., and Brody, A. R. Rat alveolar macrophage-derived PDGF is chemotactic for rat lung fibroblasts. Am. J. Respir. Cell Mol. Biol. 3:595-602, 1990. 18 91. Bonner, J. C., Badgett, A., Osornio-Vargas, A. R., Hoffman, M., and Brody, A. R. PDGFstimulated fibroblast proliferation is enhanced synergistically by receptor-recognized a2-macroglobulin. J. Cell. Phys. 145:1-8, 1990. 92. Mangum, J. B., Everitt, J. I., Bonner, J. C., Moore, L. R., and Brody, A. R. Co-culture of primary pulmonary cells to model alveolar injury and translocation of proteins. In Vitro Cell Dev. Biol. 26:1135-1143, 1990. 93. Rom, W. N., Travis, W. D., and Brody, A. R. Cellular and Molecular bases of the asbestos-related diseases. Am. Rev. Respir. Dis. 143:408-422, 1991. 94. Kalter, V. G. and Brody, A. R. Receptors for transforming growth factor P (TGFp ) on rat lung fibroblasts have higher affinity for TGFp 1 than for TGFp 2. Am. J. Respir. Cell Mol. Biol. 4:397-407, 1991. 95. Schapira, R. M., Osornio-Vargas, A. R., and Brody, A. R. Inorganic particles induce secretion of a macrophage homologue of platelet-derived growth factor in a density and time-dependent manner in vitro. Exp. Lung Res. 17:1011-1024, 1991. 96. Brody, A. R. and Bonner, J. C. Platelet-derived growth factor produced by pulmonary cells. Chest 99:50-52, 1991. 97. Bonner, J. C. and Brody, A. R. Asbestos-induced alveolar injury. Evidence for macrophage-derived PDGF as a mediator of the fibrogenic response. Chest 99:54-55, 1991. 98. Bonner, J. C., Osornio-Vargas, A. R., Badgett, A., and Brody, A. R. Differential proliferation of rat lung fibroblasts induced by the platelet-derived growth factor (PDGF) -AA, -AB, and -BB isoforms secreted by rat alveolar macrophages. Am. J. Respir. Cell Mol. Biol. 5:539-547, 1991. 99. Osornio-Vargas, A. R., Hernandez-Rodriguez, N. A., Yanez-Buruel, A. G., Ussler, W. Overby, L. H., and Brody, A. R. Experimentally induced lung cell toxicity by a mixed dust from Mexicali, Baja California, Mexico. Env. Res. 56:31-47, 1991. 100. Coin, P. G., Roggli, V. L., and Brody, A. R. Deposition, clearance and translocation of chrysotile asbestos from peripheral and central regions of the rat lung. Env. Res. 58:97 116, 1992. 101. Brody, A. R., Overby, L. H., Badgett, A., Kalter, V., Kumar, R. K., and Bennett, R. A. Interstitial pulmonary macrophages produce platelet-derived growth factor which stimulates rat lung fibroblast proliferation in vitro. J. Leukocyte Biol. 51:640-648, 1992. 102. Roggli, V. L., Pratt, P. C., and Brody, A. R. Asbestos fiber type in malignant mesothelioma: An analytical scanning electron microscopic study of 94 cases. Am. J. Ind. Med. 23:605-614, 1993. 103. Osornio-Vargas, A. R., Kalter, V. G., Badgett, A., Hernandez-Rodriguez, N., AguilarDelfin, I., and Brody, A. R. Early-passage rat lung fibroblasts do not migrate in vitro to transforming growth factor-p. Am. J. Respir. Cell Mol. Biol. 8:468-471, 1993. 19 104. Bonner, J. C., Goodell, A. L., Brody, A. R. Chrysotile asbestos up-regulates gene expression and production of alpha-receptors for platelet-derived growth factor (PDGF) on rat lung fibroblasts. J. Clin. Invest. 92:425-430, 1993. 105. Perdue, T. D. and Brody, A. R. Distribution of transforming growth factor-01, fibronectin, and smooth muscle actin in asbestos-induced pulmonary fibrosis in rats. J. Histochem. Cytochem. 42:1061-1070, 1994. 106. Coin, P. G., Roggli, V. L., and Brody, A. R. Persistence of long thin chrysotile asbestos fibers in the lungs of rats. Environ. Health Perspect. 102:195-200, 1994. 107. Lasky, J. A., Coin, P. G., Lindroos, P. M., Ostrowski, L. E., Brody, A. R., and Bonner, J. C. Chrysotile asbestos stimulates gene expression and secretion of PDGF-AA by rat lung fibroblasts in vitro: Evidence for an autocrine loop. Am. J. Respir. Cell Mol. Biol. 12:162-170, 1995. 108. Gardner, S.Y. and Brody, A. R. Incorporation of Bromodeoxyuridine as a method to quantify cell proliferation in bronchiolar-alveolar duct regions of asbestos-exposed mice. Inhal. Toxicol. 7:215-224, 1995. 109. Brody, A. R. Perspective: Pleural Disease. Am. J. Respir. Cell Mol. Biol. 12:579-580, 1995. 110. Donaldson, K., Brown, D. M. Miller, B. G., Brody, A. R. Bromodeoxyuridine (BRDU) uptake in the lungs of rats inhaling amosite asbestos or vitreous fibres at equal airborne fibre concentrations. Exp. Toxic. Pathol. 4Z:207-211, 1995. 111. Dixon, D., Bowser, A. D., Badgett, A., Haseman, J. K., and Brody, A. R. Incorporation of Bromodeoxyuridine (BrdU) in the Bronchiolar-Alveolar Regions of the Lungs Following Two Inhalation Exposures to Chrysotile Asbestos in Strain A/J Mice. J. Environ. Pathol. Toxicol. Oncol. 14(3 & 4):205-213, 1995. 112. Badgett, A., Bonner, J. C., and Brody, A. R. Interferon-y modulates lung macrophage production of PDGF-BB and fibroblast proliferation. J. Lipid Mediat. Cell Signal. 13:9 97, 1996. 113. Corti, M., Brody, A. R., Harrison, J. Isolation and primary culture of murine alveolar type II cells. Am. J. Respir. Cell Mol. Biol. 14:309-315, 1996. 114. Liu, J.-Y., Morris, G. F., Lei, W-H., Corti, M., and Brody, A. R. Up-regulated expression of transforming growth factor-a in the bronchiolar-alveolar duct regions of asbestosexposed rats. Am. J. Pathol. 149:205-217, 1996. 115. Coin, P. G., Osornio-Vargas, A. R., Roggli, V. L., and Brody, A. R. Pulmonary fibrogenesis after three consecutive inhalation exposures to chrysotile asbestos. Am. J. Respir. Crit. Care Med. 154:1511-1519, 1996. 116. Mishra, A., Liu, J.-Y., Brody, A. R., and Morris, G. F. Inhaled asbestos fibers induce p53 expression in the rat lung. Am. J. Respir. Cell Mol. Biol. 16(4):479-485, 1997. 117. Gardner, S.Y., Brody, A. R., Mangum, J. B., Everitt, J. I. Chrysotile asbestos and H2O2 increase permeability of alveolar epithelium. Exp. Lung Res. 23:1-16, 1997. 20 118. Liu, J.-Y., Morris, G. F., Lei, W.-H., Hart, C. E., Lasky, J. A., and Brody, A. R. Rapid activation of PDGF-A and -B expression at sites of lung injury in asbestos-exposed rats. Am. J. Respir. Cell Mol. Biol. 17:129-140, 1997. 119. Warshamana, G. S., Martinez, S., Lasky, J. A., Corti, M., and Brody, A. R. Dexamethasone activates expression of the PDGF-a receptor gene and induces lung fibroblast proliferation. Am. J. Physiol., Lung Cell. Mol. Physiol. 274:499-507, 1998. 120. Lasky, J. A., Tonthat, B., Liu, J.-Y., Friedman, M., and Brody, A. R. Up-regulation of the PDGF-alpha-receptor precedes asbestos-induced lung fibrosis in rats. Am. J. Respir. Crit. Care Med. 157:1652-1657, 1998. 121. Liu, J.-Y., Brass, D. M., Hoyle, G. W., Brody, A. R. TNF-a receptor knockout mice are protected from the fibroproliferative effects of inhaled asbestos fibers. Am. J. Pathol. 153: 1839-1847, 1998. 122. Ortiz, L. A., Lasky, J. A., Hamilton, R. F., Holian, A., Hoyle, G. W., Banks, W., Peschon, J. J., Brody, A. R., Lungarella, G., and Friedman, M. Expression of TNF and the necessity of TNF receptors in bleomycin-induced lung injury in mice. Exp. Lung Res. 24:721-743, 1998. 123. Liu, J.-Y., Lei, W.-H., Brody, A. R., Hoyle, G. W. Investigation of tissue preparation conditions for nonradioactive in situ hybridization: Localization of transforming growth factor-a message in rat kidney. Histochem. J. 30:793-798, 1998. 124. Lasky, J. A., Ortiz, L. A., Tonthat, B., Hoyle, G. W., Corti, M., Athas, G., Lungarella, G., Brody, A., and Friedman, M. Connective tissue growth factor mRNA expression is upregulated in bleomycin-induced lung fibrosis. Am. J. Physiol. 275 (Lung Cell. Mol. Physiol. 19):L365-L371, 1998. 125. Ortiz, L. A., Moroz, K., Liu, J.-Y., Hoyle, G. W., Hammond, T., Hamilton, R. F., Holian, A., Banks, W., Brody, A. R., and Friedman, M. Alveolar macrophage apoptosis and TNF-a, but not p53, expression correlate with murine response to bleomycin. Am. J. Physiol. 275 (Lung Cell. Mol. Physiol. 19):L1208-L1218, 1998. 126. Brass, D., Hoyle, G. W., Poovey, H.G., Liu, J.-Y., and Brody, A.R. Reduced TNF-a and TGF-p1 expression in the lungs of inbred mice that fail to develop fibroproliferative lesions consequent to asbestos exposure. Am. J. Pathol. 154:853-862, 1999. 127. Ortiz, L. A., Lasky, J., Lungarella, G., Cavarra, E., Martorana, P., Banks, W. A., Peschon, J. J., Schmidts, H.-L., Brody, A. R., and Friedman, M. Upregulation of the p75 but not the p55 TNF-a Receptor mRNA after silica and bleomycin exposure and protection from lung injury in double receptor knockout mice. Am. J. Respir. Cell Mol. Biol. 20:825-833, 1999. 128. Hoyle, G. W., Li, J., Finkelstein, J. B., Eisenberg, T., Liu, J.-Y., Lasky, J., Athas, G., Morris, G., and Brody, A. R. Emphysematous lesions, inflammation, and fibrosis in the lungs of transgenic mice overexpressing platelet-derived growth factor. Am. J. Pathol. 154:1763 1775, 1999. 21 129. Mendoza, T., Nelson, A. B., Ghosh, S., Morris, C. B., Hoyle, G. W. , Brody, A. R., Friedman, M. and Morris, G. F. Long term survival of mice that express dominant negative p53 in the lung. J. La. State. Med. Soc. 152:181-189, 2000. 130. Liu, J.-Y. and Brody, A. R. Increased TGF-p1 in the lungs of asbestos-exposed rats and mice: Reduced expression in TNF-a receptor knockout mice. J. Environ. Pathol. Toxicol. Oncol. 20(2):97-108, 2001. 131. Warshamana, G. S., Corti, M., and Brody, A. R. TNF-a, PDGF, and TGF-p1 expression by primary mouse lung bronchiolar-alveolar epithelial and mesenchymal cells: TNF-a, induces TGF-p1. Exp. Mol. Pathol. 71:13-33, 2001. 132. Liu, J.-Y., Sime, P. J., Wu, T., Warshamana, G. S., Pociask, D., Tsai, S.-Y., and Brody, A. R. Transforming Growth Factor-p1 overexpression in Tumor Necrosis Factor-a receptor knockout mice induces fibroproliferative lung disease. Am. J. Respir. Cell Mol. Biol. 25:3-7, 2001. 133. Hoyle, G. W., and Brody, A.R. IL-9 and Lung Fibrosis: A Th2 Good Guy. Am. J. Respir. Cell Mol. Biol. 24:365-367, 2001. 134. Brass, D. M., Tsai, S.-Y., and Brody, A. R. Primary lung fibroblasts from the 129 mouse strain exhibit reduced growth factor responsiveness "in vitro." Exp. Lung Res. 27:639 653, 2001. 135. Brody, A. R. Plusieurs voies pour la fibrose interstitielle pulmonaire? (Interstitial pulmonary fibrosis). Revue Internationale de Biologie et de Medecine (Intl. J. Biol. Med.), 17:1222, 2001. 136. Ortiz, L.A., Lasky, J., Gozal E., Ruiz, V., Lungarella, G., Cavarra, E., Brody, A. R., Friedman, M., Pardo, A., and Selman, M. Tumor necrosis factor receptor deficiency alters mqtrix metalloproteinase 1 expression in murine silicosis. Am. J. Respir. Cell Mol. Biol. 163:244-252, 2001. 137. Ghosh, S., Mendoza, T., Ortiz, L. A. Hoyle, G. W., Fermin, C. D., Brody, A. R., Friedman, M., and Morris, G. F. Bleomycin sensitivity of mice expressing dominant-negative p53 in the lung epithelium. Am. J. Respir. Crit. Care Med. 166:890-897, 2002. 138. Warshamana, G. S., Pociask, D. A., Fisher, K. J., Liu, J.-Y., Sime, P. J., and Brody, A. R. Titration of non-replicating adenovirus as a vector for transducing active TGF-p1 gene expression causing inflammation and fibrogenesis in the lungs of C57BL/6 mice. Int. J. Exp. Path., 83:183-201, 2002. "third most frequently accessed original article." (2003). 139. Warshamana, G. S., Pociask, D. A., Sime, P. J., Schwartz, D. A., and Brody, A. R. Susceptibility to asbestos-induced and TGF-p1-induced fibroproliferative lung disease in two strains of mice. Am. J. Respir. Cell Mol. Biol., 27:705-713, 2002. 22 140. Pociask, D.A., Sime, P. J., and Brody, A. R. Asbestos-derived reactive oxygen species activate TGF-01. Lab. Invest., 84:1013-1023, 2004. 141. Li, J. Poovey, H.G., Rodriguez, J. F., Brody, A. R. and Hoyle, G. W. Effect of plateletderived growtn factor on the development and persistence of asbestos-induced fibroproliferative lung disease. J. Environ. Pathol. Toxicol. Oncol., 23(4)253-266, 2004. 142. David, O., Jett., J., LeBeau, H., Dy, G., Hughes, J., Friedman, M. and Brody, A.R. PhosphoAkt Overexpression in non-small cell lung cancer confers significant stageindependent survival disadvantage. Clin.Cancer Res., Oct 15;10(20):6865-6871, 2004. 143. Sullivan D. E., Ferris M-B., Pociask D.A., and Brody A. R. Tumor Necrosis Factor-alpha Induces Transforming Growth Factor-beta1 Expression in Lung Fibroblasts Through the Extracellular Signal-Regulated Kinase Pathway. Am. J. Respir. Cell Mol. Biol., Apr;32(4):342-9, 2005 143. Sullivan D. E., Ferris M-B., Pociask D.A., and Brody A. R. Tumor Necrosis Factor-alpha Induces Transforming Growth Factor-beta1 Expression in Lung Fibroblasts Through the Extracellular Signal-Regulated Kinase Pathway. Am. J. Respir. Cell Mol. Biol., Apr;32(4):342-9, 2005 144. Spees, J. L., Pociask, D.A., Sullivan, D.E., Prockop, D.J., and Brody, A.R. Bone Marrow Progenitor Cells Migrate, Proliferate and Differentiate During Asbestos-Induced Pulmonary Fibrosis. Amer. J. Resp. and Crit. Care Med. 176: 385-394, 2007 145. Qi, Y., Brody, A.R., Sullivan, D. E. Laser capture micro-dissection reveals dose-response of gene expression in situ consequent to asbestos exposure. Int J Exp Pathol. 88 (6):415-25, 2007 146. Sullivan DE, Pociask D, Ferris MB, Brody AR. The latent form of TGF-betal is induced by TNF-alpha through an ERK specific pathway and is activated by asbestos-derived reactive oxygen species in vitro and in vivo. JImmunotox. 2008; 5:145-9. Chapters and Proceedings 1. Crapo, J. D., Brody, A. R., et al. Morphologic, morphometric, and X-ray microanalytical studies on lung tissue of rats exposed to chrysotile asbestos in inhalation chambers. In: Biological Effects of Mineral Fibers (Wagner, J. C., Ed.), IARC Publications, Lyon, France, Vol. I, pp. 273-283, 1980. 2. Brody, A. R., and DeNee, P. B. Biological activity of inorganic particles in the lung. In: Critical Reviews in Environmental Control (Straub, C. P., Ed.), CRC Press, Boca Raton, FL, pp. 277-299, 1981. 3. Brody, A. R., and Davis, G. S. Alveolar macrophage toxicology. In: Mechanisms in Respiratory Toxicology (Witschi, H. and Nettesheim, P., Eds.), CRC Press, Boca Raton, FL, Vol. II, pp. 3-28, 1982. 23 4. Brody, A. R., and Hill, L. H. Interactions of chrysotile asbestos with erythrocyte membranes. In: The In Vitro Effects of Mineral Dusts (Brown, R.C. et al., Eds.), Environ. Health Perspect. 51:85-89,1983. 5. Brody, A. R. and Hill, L. H. Initial epithelial and interstitial events following asbestos inhalation. In: Health Issues Related to Metal and Nonmetallic Mining (Wagner, W. L., Rom, W. N., and Merchant, J. A., Eds.), Butterworth Publ., Boston, pp. 162-172, 1983. 6. Brody, A. R. Inhaled particles in human disease and animal models: Use of Electron Beam Instrumentation. Environ. Health Perspect. _56:149-162, 1984. 7. Brody, A. R., Roe, M. W., Evans, J. H., and Davis, G. S. Deposition and translocation of inhaled silica. In: Occupational Lung Disease (Gee, J. B. and Morgan, W. K., Brooks, S. M., Eds.), Raven Press, NY, pp. 168-170, 1984. 8. Brody, A. R. and Hill, L. H. The target cells for inhaled mineral dusts. In: In Vitro Effects of Mineral Dusts (Beck, E. G. and Bignon, J., Eds.), NATO ASI Series, SpringerVerlag, Berlin, Vol. G3, pp. 53-58, 1985. 9. Kouzan, S., Nettesheim, P., Eling, T., and Brody, A. R. Production of arachidonic acid metabolites by alveolar macrophages treated with asbestos. In: In Vitro Effects of Mineral Dusts (Beck, E. G. and Bignon, J., Eds.), NATO ASI Series, Springer-Verlag, Vol. G3, Berlin, pp. 291-295, 1985. 10. Warheit, D. B., George, G., Hill, L. H., Snyderman, R., and Brody, A. R. Inhaled asbestos fibers produce complement-derived chemotactic factors on alveolar surfaces. In: In Vitro Effects of Mineral Dusts (Beck, E. G. and Bignon, J., Eds.), NATO ASI Series, Springer-Verlag, Berlin, Vol. G3, pp. 129-138, 1985. 11. Brody, A. R., Hill, L. H., Hesterberg, T. W., Barrett, J. C., and Adler, K. B. Intracellular translocation of inorganic particles. In: The Cytoskeleton (Clarkson, T. W., Sager, P. R., and Syversen, T. L. M., Eds.), Plenum Publishing Corp., pp. 221-227, 1986. 12. Brody, A. R. Initial fiber interactions with bronchiolar-alveolar epithelium, macrophages and fibroblasts. In: Silicosis and Mixed Dust Pneumoconiosis (Le Bouffant, L., Ed.), INSERM, Paris, France, pp. 81-92, 1987. 13. Roggli, V. L. and Brody, A. R. Imagining techniques for application to lung toxicology. In: Toxicology of the Lung (Gardner, D.E., Crapo, J.D., Massaro, E.J., Eds.), Raven Press, New York, pp. 117-146, 1988. 14. Brody, A. R., McGavran, P. D., and Overby, L. H. Brief inhalation of chrysotile asbestos induces rapid proliferation of bronchiolar-alveolar epithelial and interstitial cells. In: Non-Occupational Exposure to Man-Made Mineral Fibers. IARC Publications, Lyon, Fra., (Cheney, J. Editorial Services), pp. 102-108, 1988. 15. Brody, A. R. The lung matrix and inflammation: Part II. In: Annual Meeting Highlights. Am. Rev. Respir. Dis. 138:1056-57, 1988. 16. Kumar, R. K., Bennett, R. A., and Brody, A. R. An enzyme immunoassay for plateletderived growth factor: application to the measurement of macrophage-derived PDGF. Monokines and Other Non-Lymphocytic Cytokines. Alan R. Liss, Inc. pp. 393-396, 1988. 24 17. Brody, A. R. and Overby, L. H. An animal model of asbestos-induced lung disease. In: Handbook of Animal Models of Pulmonary Disease, CRC Press, Boca Raton, FL, pp. 183-196, 1989. 18. Brody, A. R. and Yu, C. P. Particle deposition at the alveolar duct bifurcations. In: Lung Dosimetry: Extrapolation Modeling of Particles and Gases (Crapo, J.D. and Smolke, E., Eds.), Academic Press, Chapter 9, pp. 91-99, 1989. 19. Brody, A. R. and McGavran, P. D. Incorporation of tritiated thymidine by vascular, epithelial and interstitial cells in asbestos-exposed animals. In: Biological Interaction of Inhaled Mineral Fibers and Cigarette Smoke (A.P. Wehner, Ed.), Battelle Press, Columbus, OH, pp. 269-277, 1989. 20. Schapira, R., Osornio, A. R., Bonner, J. C., and Brody, A. R. Platelet-derived growth factor secretion by alveolar macrophages is stimulated by carbonyl iron and chrysotile asbestos in vitro. In: The Physiological and Pathological Effects of Cytokines. (P. Oppenheim, Kluger, Dinarello, Eds.), Wiley-Liss, Inc., pp. 189-194, 1989. 21. Nettesheim, P., Jetten, A. M., Inayama, Y., Brody, A. R., Gray, T. Mahler, J. F., and Hook, G. E. R. Pathways of differentiation in the epithelium of the conducting airways. Environ. Health Perspect. 85:317-329, 1990. 22. Brody, A. R. Production of Cytokines by particle-exposed lung macrophages. In: Cellular and Molecular Fiber Carcinogenesis (Brinkley, W., Lechner, J., Harris, C., Eds.), Cold Spring Harbor Laboratory Press, CSH, New York, pp. 83-102, 1991. 23. Brody, A. R. Asbestos-induced proliferation of bronchial and pulmonary parenchymal cells. In: Asbestos Related Cancer (Sluyser, M., Ed.), Ellis Horwood Ltd., Amsterdam, pp. 191-206, 1991. 24. Lasky, J. A., Bonner, J. C., and Brody, A. R. The pathobiology of asbestos-induced lung disease: A proposed role for macrophage-derived growth factors. In: Toxicology and Environmental Health, Proceedings of the Conference "Exposure to Asbestos in Place", (Selikoff, I., Ed.), pp. 239-244, 1991. 25. Bonner, J. C. and Brody, A. R. Cytokine Binding Proteins. In: Lung Biology in Health and Disease. (Kelly, J., Ed.), Marcel Dekker, pp. 459-490, 1992. 26. Brody, A. R. Asbestos exposure as a model of inflammation inducing interstitial pulmonary fibrosis. In: Inflammation: Basic Principles and Clinical Correlates (Gallin, J. I., Goldstein, I. M., Snyderman, R., Eds.), Raven Press, N.Y., 2nd Edition, pp. 1033 1049, 1992.27 * * 27. Roggli, V. L., Pratt, P. C., and Brody, A. R. Analysis of tissue mineral fiber content, Chap. 11. In: Pathology of Asbestos-Associated Diseases. (Roggli, V. L., Greenberg, S. D., Pratt, P. C., Eds.), Little, Brown, Boston pp. 229-345, 1992. 25 28. Brody, A. R. Asbestos Induced Lung Disease. Environ. Health Perspect. 100: 21-30, 1993. 29. Bonner, J. C. and Brody, A. R. Macrophage Signal Transduction Mechanisms. In: Lung Biology in Health and Disease. (Brody J., et. al., Eds.), Marcel Dekker, N.Y., 65: 483-520, 1993. 30. Brody, A. R. Asbestos Induced Lung Injury and Fibrosis: A Month in the Life of an Inhaled Asbestos Fiber. In: The Identification and Control of Environmental and Occupational Diseases. (Mehlman, M. and Upton, A., Eds.), Princeton Scientific Publishing, pp. 213-232, 1994. 31. Brody, A. R. Control of lung fibroblast proliferation by macrophage-derived PDGF. Proceedings of the Symposium on Cells and Cytokines in Lung Inflammation. Ann. NY, Acad. Sci. 725:193-199, 1994. 32. Roggli, V., Hammer, S. P., Pratt, P. C., Maddox, J. C., Legier, J., Mark, E. J., and Brody, A. R. Commentary: Does asbestos or asbestosis cause carcinoma of the lung? Am. J. Ind. Med. 26:835-838, 1994. 33. Bonner, J. C. and Brody, A. R. Cytokine-Binding Proteins in the Lung. Am. J. Physiol. Lung Cell. Mol. Physiol. 268:L869-L878, 1995. 34. Morris, G. F., Liu, J-Y., Lei, W-H., and Brody, A. R. Expression of genes coding for growth factors in experimental pneumoconiosis. Chest. 109:45-49, 1996. 35. Hoyle, G. W. and Brody, A. R. Gene Expression in Rodent Models of Environmental Lung Disease. Ann. N. Y. Acad. Sci. 796:162-172, 1996. 36. Kagan, E. and Brody. A.R. Immunopathology of Asbestos-Related Lung Disease. In: Immunopathology of Lung Disease. (Krandin, R. L., Robinson, B. W. S., Eds.) Butterworth-Heinemann, Boston, Chapter 20. pp 421-443, 1996. 37. Brody, A. R. Toxicology. Peptide Growth Factors in Fibroproliferative Lung Disease: In Vivo Models and In Vitro Correlates. In: Correlations Between In Vitro and In Vivo Investigations in Inhalation Toxicology, (Mohr, U., Ed.), ILSI Press, Washington, D. C. pp. 19-28, 1997. 38. Brody, A. R. Asbestos. In: Comprehensive Toxicology. (Roth, R. A., Ed.), Elsevier Science, New York, Vol. 8(25), pp. 393-413, 1997. 39. Brody, A. R., Liu, J.-Y., Brass, D., and Corti, M. Analyzing the genes and peptide growth factors expressed in lung cells in vivo consequent to asbestos exposure in vitro. In: Proceedings of the International Conference on Toxicology of Natural and Man Made Particles. Environ. Health Perspect. 105:1165-1171, 1997. 40. Brody, A. R. Occupational lung disease and the role of peptide growth factors. Curr. Opin. Pulm. Med.^:203-208, 1997.41 41. Brody, A. R. Whither goes the alveolar macrophage? Another small chapter is written on the localized response of this crucial cell. J. Lab. Clin. Med. 131:391-392, 1998. 26 42. Brody, A. R., Brass, D. M., Liu, J.-Y, Morris, G. F., and Hoyle, G. W. Asbestos-induced peptide growth factors that mediate interstitial pulmonary fibrosis. In: Advances in the Prevention of Occupational Respiratory Diseases. (Chiyotani, K., Hosoda, Y., Aizawa, Y., Eds.), Elsevier Science, The Netherlands, pp. 878-883, 1998. 43. Morris, G. F. and Brody, A. R. Molecular mechanisms of particle-induced lung disease. In: Environmental and Occupational Medicine. (Rom, W. R., Ed.) Lippincott-Raven Publishers, Philadelphia, PA, 3rd Edition, pp. 305-333, 1998. 44. Brody, A. R., Brass, D., Liu, J.-Y., Hoyle, G. W., and Warshamana, G. S. Remodelling of lung tissue consequent to chronic injury. Res. Immunol. 149:249-251, 1998. 45. Lasky, J. A. and Brody, A. R. Interstitial fibrosis and growth factors. Environ. Health Perspect. 108(suppl. 4):751-762, 2000. 46. Brody, Arnold R. Inhalation of asbestos fibers and consequent expression of peptide growth factors. Inhal. Toxicol. 12(suppl. 3):245-250, 2000. 47. Crapo, J.D., Courtney-Broaddus, V., Brody, A.R., Malindzak, G., Samet, J., Wright, J.R.. American Thoracic Society Documents. Workshop on lung disease and the environment. Where do we go from here? Am. J. Respir. Crit. Care Med., Vol. 168, pp 250-254, 2003. 48. Mutsaers, S.E., Prele, C.M., Brody, A. R., and Idell, S. Pathogenesis of Pleural Fibrosis. Respirology. 9:428-440, 2004. 49. Lasky, J. A., Ortiz, L. A., and Brody, A. R. Mediators and Mechanisms in Chronic Lung Injury and Fibrosis. In: Lung Injury: Mechanisms, Pathophysiology, and Therapy. (Notter, R. H., Holm, B. A., Finkelstein, J. N., Eds.) Marcel Dekker, N.Y., 2005. 50. Sull ivan DE and Brody AR. The asbestos model of interstitial fibrosis: TNF-a and TGF-b1 as mediators of asbestos-induced lung fibrogenesis. Donaldson and Borm P, ed. Particle Toxicology. Boca Raton, Taylor & Francis: 227-244, 2006. 51. Brody, A.R. Asbestosis and Silicosis. In Interstitial Pulmonary and Bronchiolar Disorders, (J. Lynch, Ed.), In Press, New York, Informa Healthcare, 2007. Books Published Brody, D. E. and Brody, A. R. The Science Class You Wish You Had . . . The Seven Greatest Scientific Discoveries in History and the People Who Made Them. With a Foreword by Martin Rodbell, Ph.D., Nobel Prize Recipient. The Berkley Publishing Group, New York, NY, 378 pp, 1997. EXHIBIT L LAUDERDALE ENVIRONMENTAL ENGINEERING "Engineering Solutionsfor Environmental Concerns " September 28,2009 Chrstian Hartley, Esquire Kartley Law 140 Cape May Lane Mount Pleasant, SC 29464 Re: Dorman vs Advance Auto parts INC., et al LEE Project #D82009 Dear Mr. Hartley: You have asked me to review the above referenced case and provide opinions about industrial hygiene considerations. The following is my report. I am a Certified Industrial Hygienist. Industrial hygiene is the science of identifying and preventing workplace hazards. I am now in a private consulting practice. For many previous years, I worked as an industrial hygienist for Texas State Department of Health, Occupational Health Division. In my work for the state of Texas I inspected facilities where asbestos products were manufactured and facilities where asbestos products were used. In this service I developed expertise in various areas of occupational health related to asbestos disease including, but not limited to occupational health, epidemiology, historical aspects of the development of asbestos-related disease and industrial hygiene. A true and correct copy of curriculum vitae is attached as Exhibit A. My billing rate for this project is $525.00 per hour. SCOPE OF REPORT I have been asked to review case specific information that is provided to me for the above referenced matter, and to provide a report covering my opinions covering industrial hygiene considerations relating to asbestos exposures of Mrs. Dorman. At this time, I have reviewed the following documents that were provided by The Hartley Lawfirm, LLP: Mallory Dorman Depositions, July 26,2009 and August, 2009 Western Electric transite use for closing cable holes and slots Bell Laboratories memorandum of record of potential asbestos exposure in Western electric Hartley letter to Jerry Lauderdale Lucent interrogatories 1 of 8 The information that I have reviewed is sufficient to form a reliable basis for my opinions within reasonable scientific probability. The opinions that I express in this affidavit are expressed only if I hold them to be within reasonable scientific probability. I have reviewed the above-referenced materials in order to formulate my opinions in this case. Also, I am relying on my personal knowledge about development of mesothelioma resulting from occupational and environmental exposures, as well as my educational background and professional training and experience. All of which are the types of materials that I and other occupational health experts normally rely upon to formulate our opinions. I reserve the right to amend this report if additional information becomes available to me. OCCUPATIONAL ASBESTOS EXPOSURE Asbestos has been used in industrial settings increasingly since the early 1900's. By 1930 asbestos containing dust had been well documented and established as an industrial hazard that caused a debilitating and fatal lung scarring disease, asbestosis.1 By 1939 a proposed occupational exposure limit was recommended to control asbestosis. Since this date, this standard has been reduced on numerous occasions due to increasing information about asbestos related diseases. By the late 1940's very high rates of lung cancer were associated with occupational asbestos exposures that were previously thought to be reasonably safe. Then in the early 1960's asbestos exposures were shown to produce asbestosis, lung cancer, and a very rare cancer known as mesothelioma (See Selikoff et al.2 As more information became available, increasing evidence pointed to increased incidence of lung cancer and mesothelioma in groups exposed at lower levels to asbestos in industry. The United States Occupational Safety and Health Administration (OSHA) became responsible for occupational safety and health in 1970. In light of rapidly developing new information, the occupational exposure limits for asbestos were reduced by OSHA on 5 occasions between 1970 and 1995. WORKPLACE REGULATION A federal standard for asbestos exposure was adopted for companies providing services to the United States government in 1952 under the Walsh Healy Public Contracts Act, which established a limit of 5 million particles of asbestos containing dust per cubic foot of air.3 The standard also adopted requirements for exposure control through substitution of less toxic materials, ventilation, isolation of operations, and other engineering controls and protective equipment. It also required separation of street clothing from work clothes to ensure there was no contamination taken out of the workplace. 1 Merewether, E. R. A, and C. Price: ''Report on Effects of Asbestos Dust on the Lungs and Dust Suppression in the Asbestos Industry". His Majesty's Stationery Office. London, England. (1930) 2 Selikoff, I. J., J. Churg, E. C. Hammond. "The Occurrence of Asbestosis Among Insulation Workers in the United States". Annals of the New York Academy of Sciences 3 Safety and Health Standards for Contractors performing Federal Supply Contracts under the Walsh-Healy Public Contracts Act, United States Department of Labor (1952), at p. 25. 2 of 8 The Occupational Safety and Health Administration (OSHA) also recognized the potential hazard of contaminated clothing. In 1972 OSHA required that where high asbestos exposures were present, the employer must provide full body work clothing that would not leave the workplace. These clothing were required to be handled and laundered using special precautions to prevent release of asbestos fibers. These measures were intended to prevent asbestos diseases resulting from household exposures to asbestos fibers. When this standard was revised in 1986, these provisions were strengthened. OSHA indicated in their preamble that "Evidence has shown that family members of asbestos workers face a substantially increased risk of cancer and other asbestos related diseases from exposure to asbestos carried home on work clothing." The standard adopted included specific provisions to ensure that contaminated work clothing does not leave the workplace, and that contaminated clothing be handled and laundered using appropriate precautions (see 29 Code of Federal Regulations, 1910.93a (d) (3 and 4), OSHA),4 5A6lso, employers were required to provide shower and change facilities in some instances so that workers would not leave the facility with asbestos fibers on their clothing or bodies. These provisions were not contested in the hearing process. OSHA states in the rule preamble that "Few, if any, participants in the rulemaking denied the benefits afforded by these provisions." The development of specific workplace regulations by OSHA is further evidence that such relationship has been documented and is accepted as a basis for governmental rulemaking. Further, such rulemaking was subjected to extensive public review, and was found to be a sound basis for regulation. HOUSEHOLD ASBESTOS EXPOSURE When asbestos diseases were first identified, some believed that constant, or frequently repeated, intense exposures were necessary to cause asbestosis. Epidemiologic studies that were undertaken, however, soon demonstrated that this was not the case. Increasingly, asbestos related diseases were seen in persons who had intermittent occupational exposures, and also in those with no known asbestos exposures other than living in a home with an asbestos worker. Investigations of these workers showed that due to poor conditions in many workplaces, workers' clothing was frequently heavily contaminated with asbestos fibers. When the workers returned home they carried these fibers into their residences, where fibers were dislodged and became airborne. The workers' wives and children were then indirectly exposed to these asbestos fibers. Studies have shown increased incidences of mesothelioma and asbestosis among these persons having household asbestos exposures.56 The authors concluded: "There seems little doubt that the risk of mesothelioma may arise from both occupational and domestic exposures to asbestos. " | 4 Occupational Safety and Health Administration, 29CFR1910.93a, 1986. 5 Grandjean, Philippe, and E. Bach. Indirect Exposures: "The Significance of Bystanders at Work and at Home". American Industrial Hygiene Association Journal. 47(12):819-824. 6 Newhouse, Muriel L., and H. Thompson. "Mesothelioma of Pleura and Peritoneum Following Exposure to Asbestos in the London Area". British Journal of Industrial Medicine 22:261-269 (1965) 3 of 8 This determination that asbestos fibers can be taken home on clothing was not a new concept when the above investigations were done in the mid 1960's. In fact, there were concerns about contamination on workers clothing as early as 1899, when the British factory inspectors required that workers remove contaminated work clothes before leaving the workplace to return home.7 8This has been a basic principle used by public health and sanitation professionals, and especially by industrial hygienists at least since this time. In 1952, the United States Department of Labor issued safety and health standards concerning worker safety for all contractors performing contract work under the WalshHealy Act. Among the health requirements was the provision that: "Workers who handle or are exposed to harmful materials in such a manner that contact ofwork clothes with street clothes will communicate to the latter the harmful substances accumulated during working hours should be provided with facilities which will prevent this contact and also permit thefree ventilation or drying ofthe work clothes while they are not in use. In any plant where it is necessaryfor both male andfemale employees to change clothes, separate dressing rooms should be provided. "s Industry studies indicate that household exposures can approach those found in industry. In fact, an internal report of AMOCO from 1973 indicates that such household exposures would be in excess of mandatory occupational exposure limits that were in place at that time: "We have experimentally determined that the OSHA ceiling limit may be approached and/or exceeded during subsequent wearer movement in contaminated clothing or subsequent handling ofcontaminated clothing before laundering. " 9 Due to the serious concern about household exposures, the United States Congress required the National Institute for Occupational Safety and Health (NIOSH) to conduct study of the concern. In 1995 NIOSH published its extensive report on the issue.10 The report compiled and reviewed the extensive literature on asbestos household exposure, and concluded: "Based on the studies reviewed in this section, families ofasbestos-exposed workers have been at increased risk ofpleural, pericardial, orperitoneal mesothelioma, lung cancer, cancer ofthe gastrointestinal tract, and non-malignant pleural andparenchymal abnormalities as well as asbestosis. " The NIOSH study concluded that health effects and deaths were occurring, and that they "are preventable using known effective measures, however educational measures are needed to promote their use". 7 His Majesty's stationery Office, "Annual Report of the Chief Inspector of Factories and Workshops, 1899, paragraph 15 8 Safety and Health Standards for Contractors performing Federal Supply Contracts under the Walsh-Healy Public Contracts Act, United States Department of Labor (1952), at p. 25. 9 AMOCO Industrial Hygiene Series, "Medical and Environmental Health Informatin - Asbestos Exposures", July 1975. 10 NIOSH, "Report to Congress on Workers ' Home Contamination Study Conducted Under the Workers ' Family Protection Act (29 U.S.C. 671A ", 1995, page 6. 4 of 8 Thus, there is a clear historic link between the workplace and diseases occurring in household contacts of workers who bring contaminants home on their clothing. The link has been known for over 100 years. Similarly, the methods of preventing these diseases have also been known for over 100 years. MESOTHELIOMA Studies have demonstrated that high incidences of mesothelioma are found not only in asbestos workers but also in the wives of these workers, who had only household exposure to asbestos that was brought home on their husband's clothing. Due to its rarity and its well documented relationship with asbestos exposure, mesothelioma became known as an almost certain indication that the patient had had historic exposures to asbestos either in an occupational setting or resulting from household or environmental exposures. There have been numerous studies showing mesothelioma in household contacts. In 1965, Mesothelioma was seen in 20 persons in the London area who had only household or environmental asbestos exposures.11 The authors concluded that "There seems little doubt that the risk of mesothelioma may arise from both occupational and domestic exposures to asbestos." In 2000 a summary review of mesothelioma from environmental exposures was published. It showed that the overall summary risk estimate for mesothelioma for persons with household exposures was 8.1 times higher than for unexposed persons,12 In my opinion, these and other studies are scientifically valid evaluations, and their findings demonstrate development of mesothelioma in persons having only household exposures to asbestos. DORMAN'S HOUSEHOLD ASBESTOS EXPOSURE Doris Dorman worked in a primarily in a Christian book store once or twice a week as a clerk. Early in their marriage, she also worked as a clerk, typist and did general office work according to her husband's testimony. There were no known asbestos exposures in these occupational settings. She also did all of the laundry for her husband and children. Her husband's job involved cutting and handling asbestos containing products, which resulted in deposition of asbestos fibers on his work clothing. Since his employer did not provide laundering for his work clothing, he brought it home to be laundered by his wife. Thus, this clothing was the source for Mrs. Dorman's exposure to asbestos dust. Mrs. Dorman's husband, Mallory Dorman, worked primarily for Western Electric. During his employment there, he was exposed to asbestos transite board, which he had to 11 Newhouse, Muriel L., and H. Thompson. "Mesothelioma of Pleura and Peritoneum Following Exposure to Asbestos in the London Area". British Journal of Industrial Medicine 22:261-269 (1965) 12 Bourdes, Valerie, P. Boffetta, and P. Pisani. "Environmental Exposure to Asbestos and Risk of Pleural Mesothelioma: Review and Meta-Analysis". European Journal of Epidemiology 16:411-417(2000 5 of 8 cut on many occasions using power tools, including drills and reciprocating saws. A similar transite product was made by Johns Manville between 1907 and 1985, and contained chrysotile and/or amosite asbestos at a very high concentration - from 22 to 69% by weight.13 1H4e15us1u6ally worked in enclosed rooms associated with telephone equipment, and there was usually only limited general ventilation available. Cutting, and drilling, the transite board created dust, which got on his clothes which were subsequently brought home for his wife to launder. He also frequently used vacuums to collect the dust from drilling holes in the concrete floor in the central office, but he did not ever use a vacuum for cutting of the transite boards to make cable hole covers. He described seeing dust during this operation. Other asbestos products that Mr. Dorman was exposed to in his work included; soldering wiping pads, Bakelite fuse panels, asbestos cable hole covers, and cable hole fire stop pillows. Each of these products would contribute to asbestos fiber deposition on Mr. Dorman's clothes. Studies show that cutting these types of asbestos containing materials without using dust suppression techniques can result in deposition of millions of asbestos fibers on the workers' clothes. One study in particular reported finding up to 3.5 million asbestos fibers per cm2 on the clothing worn by workers cutting asbestos cement boards similar to jobs that Mr. Dorman did^ In this study, the authors conclude that "Also, the clothing worn by the worker in this study was found to be highly contaminated with chrysotile asbestos. This contamination is yet another potential source of exposure through re entrainment of the asbestos dust from such activities as the brushing of the clothing or laundry activities." Similar studies on other asbestos cement products also reported fiber concentrations on clothing of up to 6.68 and 2.96 million fibers per square centimeter.1516 The asbestos dust transferred from these products to Mr. Dorman's clothing would have been brought home for Mrs. Dorman to launder. Mrs. Dorman was exposed to brake dust while helping and watching her husband do brake jobs on their cars. Mrs. Dorman was also exposed to asbestos from laundering her husband's clothing, which would have had brake dust on it at times. 13 Johns Manville, "Manufacturing Specification - Flat Transite ", 1983. 14 Material Analytical Services. "Cutting of Stonehenge Asbestos Contaning Cement Board", (unpublished report) 2001, Section 2 15 Material Analytical Services. "Cutting of CertainTeed AC Pipe", (unpublished report) 2002 16 Material Analytical Services. "Cutting of Flexweld Asbestos Containing Cement Board", (unpublished report) 2001 6 of 8 OPINIONS 1. Mrs. Dorman did not have any identifiable occupational asbestos exposure. 2. It is my opinion that Mrs. Dorman's husband was exposed to asbestos in his job, and unintentionally brought asbestos fibers on his clothing home with him. 3. Mrs. Dorman laundered these clothes, and received exposure to asbestos fibers that were released into their home during laundering. 4. Mrs. Dorman received exposure to brake dust from being around her husband while doing automotive brake work, and from laundering her husband's clothing. 5. The exposures that Mrs. Dorman received in her home were significant, and contributed to her risk for developing asbestos related diseases, including 7 of 8 LIST OF EXHIBITS EXHIBIT A RESUME OF JERRY F. LAUDERDA.E 8 of 8 EXHIBIT M PERSONAL RESUME JERRY F. LAUDERDALE, P.E., M.S., C.I.H., R.S. Education: Bachelor of Science in Mechanical Engineering, University of Texas at Austin - 1970 Master of Science in Industrial Hygiene, Texas A&M University, College Station 1976 Professional Qualifications Registered Professional Engineer, Texas - 1975 - #38500 Certified Industrial Hygienist - 1976 - #1027 Registered Professional Sanitarian, - 1987 - #2459 Employment History: Lauderdale Environmental Engineering, 1995 - Present. Principal. Responsible for all aspects of performance of industrial hygiene services, including recognition, evaluation, and control of occupational health hazards, including indoor air pollution. Licensed Mold Assessment Consultant in Texas. Control aspects include design of ventilation systems for contaminant control, noise reduction controls, and other aspects of engineering control methods. Provide expert opinion and testimony related to occupational and environmental health concerns. Provide Comprehensive risk assessment and risk control services. Environmental Technologies, Incorporated, 1995 - 2000 (Part-time). Executive Consultant. Responsible for initiating, bidding, planning, and conducting industrial hygiene, forensics, and environmental health projects for a broad spectrum of clients. Texas Department of Health, 1971 - 1995. Director of the Division of Occupational Health - 1990-1995. Responsible for implementation of statewide consultation and regulatory programs covering environmental health, occupational health, indoor air pollution, asbestos, polychlorinated biphenyls, lead paint poisoning and hazard communication. Programs include four contracts with the United States Environmental Protection Agency totaling over $800,000. Programs which license asbestos abatement professionals and register hazardous chemical storage facilities collect over $3,000,000 annually. Program staff included 98 professional and support staff, with an operating budget of $4,200,000. Director of the Division of Occupational Safety and Health - 1987-1990. State Safety Engineer - Directed safety and industrial hygiene programs. Responsible for implementation of a consultation program under a grant from the United States Department of Labor, Occupational Safety and Health Administration, to provide comprehensive safety and health services to Texas industries. JERRY F. LAUDERDALE, P.E., M.S., C.I.H. 3804 CLOUDY RIDGE RD. AUSTIN, TEXAS 78734 PHONE: 512/266-8933 FAX: 512/266-8933 1 Chief Industrial Hygienist - 1976-1987. Division of Occupational Health and Radiation Control -- Responsible for program development and for coordination of central and regional environmental health and industrial hygiene activities for Texas. Staff Industrial Hygienist - 1971-1976. Division of Occupational Health and Radiation Control - Performed comprehensive and complex industrial hygiene and environmental health inspections throughout Texas. Responsibilities included preparation for and conduct of inspections, hazard recognition, evaluations, and control. Texas Water Commission, 1970 - 1971. Engineering Assistant - 1970. Performed tasks relating to development of a program to track releases of chemical pollutants from industrial facilities. Professional Activities: President, Texas Hill Country Section, American Industrial Hygiene Association, 1981 Adjunct Associate Professor, Environmental Sciences, The University of Texas School of Public Health, Houston 1980 - 1996. Member, American Industrial Hygiene Association JERRY F. LAUDERDALE, P.E., M.S., C.I.H. 3804 CLOUDY RIDGE RD. AUSTIN, TEXAS 78734 PHONE: 512/266-8933 FAX: 512/266-8933 2 PUBLICATIONS 1. Air sampling Instruments (5th Edition), 1978, Part V, Section U; "Direct Reading Instruments for Analyzing Airborne Gases and Vapors (John S. Nader, Jerry F. Lauderdale) pp U-1 - U-164. 2. "Environmental and Occupational Health in Texas", East Texas Medicine / Vol. 2 No. 1, pg 12-14, by Jerry Lauderdale, P.E. Janet Pichette, BS, Jean Brender, RN, Ph.D., Dennis Perotta, Ph.D., Laurel Schulze, BS 3. "Formaldehyde: Public and Industrial Exposures" by Jerry F. Lauderdale, American Society of Safety Engineers, Region III, Tenth Annual Professional Development Conference Proceeding, Feb. 1982. 4. "Measurement of Noise Levels in the Vicinity of Occupationally Exposed Workers", Jerry Lauderdale, M.S., Richard Konzen, Pg.JD., American Industrial Hygiene Conference, May 26, 1977. 5. "Quantification of Fiber Releases for Various Floor Tile Removal Methods", R. N. Crossman, Jr., M. Williams, Jr., J. Lauderdale, K. Schosek, R. Dodson., Applied Occupational and Environmental Hygiene, Vol. 11, No. 9, September 1996. JERRY F. LAUDERDALE, P.E., M.S., C.I.H. 3804 CLOUDY RIDGE RD. AUSTIN, TEXAS 78734 PHONE: 512/266-8933 FAX: 512/266-8933 3