Document a4YnkJDaeo7x0m1GO4oz2gjZY

VRD 0062013229 L. de Tollenaere - Brussels F. Kennedy - Ponca City April 1, 1975 Thanks for the information re VCM in air and residual VCM in polymers. Vinatex provided Saddle urook with a copy recently which v/as forwarded to me. We have since ordered copies for the VCM and PVC plants. Flynt Kennedy 1m Interoffice Communication To Mr. F. Kennedy - Ponca City From l, de Tollenaere Dat March 24, 1975 Subject (conoco) CHEMICALS RESEARCH APR 1 197! As is shown on the attached correspondence, the British Federation has published a guide about analysis methods regarding VCM in the air and residual VCM in polymers. We have ariered a guide like this for our information in Brussels and we wonder whether this is of interest to you. Please let us know if you want.to order one on your behalf. -\ e l' VRD 0002013231 FEDERATION OF CHEMICAL INDUSTRIES OF BELGIUM Mr. Calhoun CONOCO February 24, 1975 PS./143 Dear Sir, The British Federation has recently published a very interesting practical guide about analysis measurements of vinyl chloride in the air as well as residual vinyl chloride in the polymers. This work can be obtained at a price of 20 Pounds Sterling a piece at the following address: Publications Department Chemical Industries Association Alembic House 93, Albert Embankment London SE1 7TU Ltd. I thought that in view of the interest of this work, it was worthwhile to have you informed personally. Yours faithfully, Translation: dd Paul F. Smets General Manager FEDERATION DES INDUSTRIES CHIMIQUES DE BELGIQUE a$bi Monsieur CALHOUN CONOCO SQUARE MARIE-LOUISE 49 1040 BRUXELLES le 24 fevrier 1975 N.|r. PS./143 Cher Monsieur, La FSdSration britannique vient de publier un trSs intSressant guide pratique des mesures d*analyse du chlorure de vinyle dans l'air et du chlorure de vinyle r^siduel dans les polymeres. Cet ouvrage pidce, au peut etre obtenu au prix de 20 livres Publications Department Chemical Industries Association Ltd Alembic House 93 , Albert Embankment London SE1 7TU sterling, J'ai cru que l'interet de 1*ouvrage m#ritait que je vous en informe personnellement. Je vous prie de croire, cher Monsieur, en raes sentiments les meilleurs. Paul-*'. amets " Directeur gSnSral VRD 9402013233 (conoco) CK^CALS , <2 Interoffice Communication To * From Date Subject Distribution K. L. Schurter February 19, 1975 Solvay Q'cF / <=> 1 _____ i ~ i ii UJ ---------- OJ } ___ _______ -: ______ i The purpose of my meeting with Messrs. Klatt and Secousse of Solvay on 2/10/75 was to determine their progress in reducing residual VCM and to determine whether we could find a basis of working together on this problem. Solvay is working on the problem in two ways. The first is "heat treatment" (steam stripping), and where this approach hits limits, they try to make the resin more porous (especially for bottle resins). Solvay may cooperate with Conoco on steam stripping (see below), but they would not disclose their formulation technology for porous,low molecular weight resins unless we took out a full license. Among the things I learned are: 1. They can achieve 100 ppm in a 5385 type resin without steam stripping. They do have separate recovery vessels in their plants which may explain this low level. They believe it will be easy to get below 10 ppm in this type of resin using steam stripping. 2. They now have part of their plant set up on a temporary basis with steam stripping (in the recovery vessel) . They have been able to get from below 10 ppm residual VCM in very porous resins to about 300 ppm for low molecular weight resins using this system. They do experience quality degradation (including resin color) with extreme steam stripping. 3. The main objective of this work is to get a bottle resin with less chan 10 ppm residual VCM with no degradation in quality. 4. They are about to launch production trials to confirm their laboratory work. They have looked at both batch and continuous steam stripping, but will not decide which approach to commercialize until the trials are made. They expect to have the trials complete in about eight weeks. 5. They want to wait until they get the results of the trials before attempting to work out a cooperative program with Conoco. Obviously, if they are very successful, they will probably want to talk about a license with us. If they are not too successful, they would entertain a cooperative development pro gram. 6. Solvay has both rotary and fluid bed dryers. Although the differences are marginal, they find that lower residual VCM comes out of the rotary versus fluid bed dryer for equal slurries. V'RD 000201 3234 Distribution 2/19/75 Page Two *7. There is no truth to the ECN report of a major bottler of mineral water in France moving away from PVC bottles. Even if this company wanted to make such a change, it would take three years to get in new equipment. 8. Maltoni's feeding study of rats shows no problems after 50 weeks. Secousse couldn't recall the doses involved. I plan to follow up with Solvay on my next trip in about three months. mj Distribution: F. Kennedy, L.N. Vernon, J.F. Gabbett, W.R. Sorenson, R.D. Gamblin, R.T. Ferrell, W.R. Beaty, D.H. Sanders, Claude De Rie - cc: JBB, JJL VRD 0002013235 <MiMr DEPARTMENT OF HEALTH, EDUCATION. AND WELFARE PUBLIC HEALTH SERVICE CENTER FOR DISEASE CONTROL -:A FEB 19 1975 Dr. Flynt Kennedy Manager Chemical Research Division Research and Development Department Conoco Box 1267 Ponca City, Oklahoma 74601 NATIONAL INSTITUTE FOR OCCUPATIONAL SAFETY AND HEALTH 5600 FISHERS LANE ^ ROCKVILLE, MARYLAND 0EMlOALa RESEARCH FEB 2 4 >975 Dear Dr. Kennedy: * On January 22, 1974, the National Institute for Occupational Safety anl__ Health was advised of three deaths from angiosarcoma of the liver at a L single vinyl chloride polymerization plant. Since that time, we have received reports of twenty-nine additional cases among polymerization workers in the United States and nine other nations. Details on these cases are given in attached Table I. Review of these cases according to date of diagnosis shows that all but three were diagnosed within the last seven years. Although the cases have clustered since that time, it is probable that the high risk of this disease for polymerization workers might have gone unnoticed except for the observation of a case in 1973 by a plant physician who reviewed earlier records and identified four cases during the prior ten-year period. The difficulty of making an early determination of an associa tion of such a rare disease with an occupational exposure, even when the exposed worker is at very high risk, is also pointed up by the distribution of cases over time. Of the first eight cases diagnosed between 1961 and the end of 1968, six were from four plants in the United States, one was from France and one was from West Germany. While an exact estimate of the incidence of liver angiosarcoma among polymerization workers cannot be determined until exposed-to-risk figures become available, it is already apparent that these workers are at very high risk of this disease. Approximately 5,600 men are currently employed at 36 facilities in the United States. To date, 15 cases of angiosarcoma of the liver have been reported from four of these facilities, all of which have been in operation for more than 25 years. Nine cases have been reported from a single facility which employs less than 300 workers. A further indication that the earliest cases are coming from the older plants is seen in the distribution by date of initial exposure. All but one case was initially employed prior to 1958 and more than 70 percent of the cases were initially employed 20 or more years ago. Page 2 - Dr. Flynt Kennedy Since the average latent period from first exposure to diagnosis is about 19 years, we would not expect to see many cases at this time from the newer plants. Preliminary findings from continuing epidemiological investigations of U.S. polymerization workers Indicate that these men also may be at high risk for other malignant neoplasms, particularly of the brain where a significant excess has been noted. Details of reported cases of angiosarcoma of the liver among other workers with exposure to vinyl chloride are shown In attached Table 11. It should be noted that in two of these cases primary angiosarcoma of the liver cannot be definitely confirmed. While too few cases have been reported to draw any definitive conclusion regarding a cause and effect relationship, the age at diagnosis for these cases, which like that for the polymerization workers is considerably lower than that observed for cancer of the liver in the general population, suggests the possibility of a common etiology. It also should be pointed out that with such a rare disease it may be some time before we can determine whether workers exposed to lower levels of vinyl chloride are at excess risk for angiosarcoma of the liver or other malignancies. It is, therefore, imperative that the non-polymerization workers be kept under .continued surveillance. Enclosures Office of Occupational Health Surveillance and Biometrics TABLE X REPORTED CASES OF ANGIOSARCOMA OF THE LIVER AMONG VINYL CHLORIDE POLYMERIZATION WORKERS COUNTRY CASE Canada 01 Canada 02 Canada 03 Canada 04 Czechoslovakia 01 Czechoslovakia 02 France 01* Great Britain 01* Great Britain 03 Italy 02* Norway 01* Rumania 01 Sweden 01* United States 01* United States 02* United States 03* United States '04* United States 05* United States 06* United States 07* United States 08* United States 09* United States 10* United States 11* United States 12* United States 13* BIRTH DATE 1st VC or PVC EXPOSURE DX ANGIO SARCOMA AWAITING DETAILS AWAITING DETAILS AWAITING DETAILS AWAITING DETAILS AWAITING DETAILS AWAITING DETAILS 00-00-00 00-00-00 00-00-00 00-00-01 00-00-46 12-00-72 06-00-37 02-00-66 no-00-74 11-13-29 00-00-57 12-13-72 12-23-15 03-00-50 12-20-71 AWAITING DETAILS 06-23-27 08-14-51 02-00-70 10-17-23 12-09-48 . 03-03-73 ` 08-19-33 11-15-55 05-00-70 05-25-15 11-28-45 12-19-73 01-15-24 07-06-52 08-19-67 01-25-12 06-19-44 04-09-64 00-00-29 01-17-62 02-00-74 05-03-22 08-00-44 00-00-68 05-06-20 10-07-46 08-00-61 11-08-31 09-09-54 03-01-74 08-16-13 06-12-51 05-00-68 05-27-09 10-14-46 03-00-70 11-17-18 09-13-49 05-02-69 12-01-21 08-19-44 05-00-74 AGE AT DX 43 71 38 43 56 43 49 36 58 43 52 45 45 41 43 55 61 50 53 YRS 1st EXP TO DX TOT YRS EXP 19 19 26 20 84 15 6 22 21 19 18 22 16 14 13 28 28 15 15 20 18 12 12 24 18 15 15 17 17 17 17 23 23 20 15 30 30 NIOSH January 22, 1975 i DATE OF DEATH / 00-00-67 12-00-72 12-24-74 12-00-72 01-04-72 10-20-70 03-03-73 09-28-71 12-19-73 01-07-68 04-09-64 ALIVE 03-23-68 08-29-61 ALIVE 05-10-68 03-16-70 05-02-69 07-04-74 COUNTRY CASE # United States United States W. Germany V. Germany W. Germany W. Germany 16* 17 01* 02* 04* 05* TABLE X (continued) REPORTED CASES OF ANCIOSARCdKA OF TlIE LIVER AMONG VINYL CHLORIDE POLYMERIZATION WORKERS BIRTH DATE 11-04-27 05-06-31 07-26-31 06-24-30 00-00-00 00-00-00 1st VC or PVC EXPOSURE 05-08-50 06-23-55 10-14-57 10-01-57 00-00-00 00-00-00 DX ANGIO SARCOMA 00-00-69 10-11-74 09-25-70 09-19-68 00-00-00 00-00-00 ACE AT DX 41 43 40 38 44 49 YRS . 1st EXP TO DX 17 19 11 13 17 11 TOT YRS EXP 4 19 11 13 11 11 DATE OF DEATH 03-27-69 ALIVE 12-14-71 01-25-69 00-00-00 ALIVE Total Reported Cases * 32 Median Values: 15 U.S. Cases 10 Non-U.S. Cases 25 Total Cases 45.0 43.0 44.0 19.0 16.0 17.0 17.0 12.0 16.0 * Indicates microscopically confirmed angiosarcoma of the liver. ''00" Indicates unknown data COUNTRY CASE ft Great Britain Italy Sweden United States United States U. Germany 02* 01 02* 14 15* 03* TABLE II REPORTED CASES OF ANGIOSARCOMA OF THE LIVER AMONG NON-POLYMERIZATION WORKERS EXPOSED TO VINYL CHLORIDE BIRTH .DATE 09-08-14 ,06-15-34 11-27-11 00-00-13 00r00-25 07-16-30 1st VC or PVC EXPOSURE 00-00-46 00-00-65 00-00-45 08-18-38 00-00-00 00-00-00 DX ANGIO SARCOMA 02-00-70 04-19-71 05-15-72 06-00-73 07-00-72 02-00-68 AGE AT DX 55 36 61 60 47 43 YRS 1st EXP TO DX 24 6 27 36 00 14 TOT YRS EXP 11 3 23 00 no 14 NIOSH January 22, 1975 DATE OF DEATH 12-00-70 04-16-71 08-16-72 07-03-73 02-15-73 10-10-73 Note 1 Note 2 & Note 3 Note 4 A Note 5 Note 6 Note 1 Note 2 Note 3 Note 4 Note 5 Note 6 Pouring PVC oil mixture onto fabric bases Production of PVC sacks Production of Vinyl Chloride Machine operator covering electrical wire with PVC plastic insulation Accountant at plant making PVC fabric Loading pesticide cans with VC propellant Note 7 Note 8 Angiosarcoma involving liver, lung, and pericardium. Although difficult to determine, primary site seems to be pericardium. Diagnosis: Sarcoma (possibly "angiosarcoma"), liver. Possibility of generalized neoplasm of the reticuloendothelial cell system cannot be ruled out. * Indicates microscopically confirmed angiosarcoma of the liver. "00" Indicates unknown data. " / : S* 6CZU0Z000 flUA VRD 0002013240 u. BACKGROUND INFORMATION ON CHLOROPRENE Office of Occupational Health Surveillance and Biometrics National Institute for Occupational Safety and Health January 20, 1975 VRD 80P20 1324 1 Jr.vfnil. A Introduction CHLOROPRENE In a letter to Mr. Edward J. Baler, Agting Director, NIOSH, dated December 16, 1974, Dr. John A. Zapp, Director, Haskell Laboratory, E.I. du Pont de Nemours and Company (Du Pont), Louisville, Kentucky, expressed concern over the potential carcinogenicity of chloroprene (2-chlorobutadiene) . Du Pont had begun looking closely at this substance recently because of the similarity in chemical structure with vinyl chloride. Du Pont has utilized chloroprene in the pro duction of neoprene (polychloroprene) since 1931. In the course of a literature search on chloroprene toxicity, Du Pont uncovered two recent Russian articles that suggest an increased incidence of skin and lung cancer in workers exposed to chloroprene. Also, two other articles in the Russian literature were located that described animal experi ments in which chloroprene adversely affected embryo development in rats and mice. Du Pont has informed its employees of the Russian reports and has alerted its customers to the possibility of "escaping chloroprene'1 during the processing of neoprene. The Company is conducting epidemiological studies in humans and animals to ascertain the carcinogenic potential of chloroprene. Background Information Chloroprene is a colorless liquid that is slightly soluble in water. It is soluble in alcohol and diethyl ether, and has a vapor density of 3.0, three times that of air, with a boiling point of 59.4C. Chloroprene is used as a chemical intermediate largely as a monomer for the manufacture of a synthetic rubber.* It is a chlorine-substituted derivative of 1,3-butadiene. Chloroprene can polymerize spontaneously at room temperature, the process being catalyzed by VRD 0002013242 ___ .. .A light, peroxides, and other free radical initiators. It can also react with oxygen to form polymeric peroxides. Because of its instability, flammability, and toxicity, chloroprene has no end product uses. It is produced in large quantities mainly for polymerization and marketing under the trade name of Neoprene. ^ 3 Neoprene was developed in the U.S. by Carothers and was originally intro- 4 duced by Du Pont in 1931 under the brand name Duprene. Although during recent years other suppliers have come on the market with their own brand name, neoprene is generally used as a generic name for polychloroprene rubbers. Neoprene is obtained by emulsion polymerization of chloroprene (2-chlorobutadiene and consists mainly of 1,4-transpolychloroprene. There are two main classes, the sulfur modified type and the non-sulfur modified type, indicating the dif ferences in polymerization techniques. Several subtypes of both are available, 4 differing in viscosity and crystalization rate. Neoprene's most valuable properties are its resistance to weathering and oil. It is also resistant to abrasion, heat, flame, oxygen, ozone, and solvents. The main applications of neoprene are in high performance articles such as cable sheaths, hoses, fabrics, adhesives, and a large number of technical rubber articles. The automotive industry is the largest consumer of neoprene.^ Toxicity Human: The primary responses to chloroprene appear to be central nervous system depression and significant injury to lungs, liver, and kidneys.3' Humans exposed to chloroprene have been reported to develop dermatitis, conjunctivitis, 6 corneal necrosis, anemia, temporary loss of hair, nervousness, and irritability. Two Russian reports suggest that chloroprene exposure is associated with an 78 increased incidence of skin and lung cancer. * '\ VRO 080 2013243 3 These studies concern a large-scale epidemiological investigation of industrial workers in the Yerevan region of Russia. During the period 1956-1970, 137 cases of skin cancer were discovered through examination of 24,989 persons over age 25. The population was subdivided into five subgroups according to the character of their employment! Group I: Persons who never worked in industrial plants Group II: Persons working in non-chemical industries Group III: Persons with extended work experience in chloroprene production Group IV: Persons working in industries using chloroprene derivatives Group V: Persons working with chemicals unrelated to chloroprene The following table depicts the results of the study: Exposure Group I II III IV V Number examined 8520 8755 684 2250 4780 Number of cases 11 35 21 38 32 Percent 0.12 0.40 3.00 1.60 0.66 Average age of cases 72.1 68.9 59.6 59.1 64.4 Average duration of employment for cases (in years) 16.3 15.4 9.5 8.7 13.8 As can be seen from the table, "the incidence of skin cancer was greatest in the chloroprene exposed group, and was substantially greater than that for the three unexposed groups. Persons exposed only to chloroprene derivatives also showed an increased incidence of skin cancer. A gradient in the skin cancer incidence is seen among the five groups reflecting the potential for exposure to toxic chemicals in the work environment. The average age of the cases in both the chloroprene and chloroprene derivative groups was signifi \ VRD 0002013244 cantly less than that for the other groups. The average duration of employment was .much shorter for the chloroprene and chloroprene derivative groups than for the other non-exposed groups. The investigators concluded that development of chloroprene-induced skin cancer is preceded by chronic dystrophic and inflam matory skin ailments which are caused by the binding of chloroprene to the free SH groups in the cells, with the formation of RS-CH compound types. The incidence of lung cancer among 19,979 workers in the same region was also studied. During the period 1956-1970, 87 cases of lung cancer were identified from the records of the local oncology department. The population was subdivided into four subgroups according to type of employment: Group I: Workers who had extended contact with chloroprene and/or its derivatives Group II: The first "control group" consisting of truck drivers, polishers, cabinet makers, stokers, gasoline station attendants, typesetters, painters, and others Group III: The second "control group" consisting mainly of electricians, carpenters, joiners, arc welders, tinsmiths, furnace workers, etc. Group IV: The third "control group" consisting of persons who worked in professional occupations \ VRD 0002013245 5 The following table summarizes the results of the analysis: Number at risk Number of cases Percent Average age of cases ! Average duration of employment I 2934 34 1.16 44.5 Exposure Group II III IV 4780 6045 6220 22 11 4 0.46 `0.18 .064 54.9 59.3 60.2 for cases (in years) 8.7 10.3 19.9 18.5 As can be seen from the table. the group with exposure to chloroprene or its derivatives experienced the highest incidence of lung cancer. A gradient in the lung cancer incidence is seen according to exposure group which reflects (roughly) the potential for exposure to toxic chemicals in the work environment. As with the results for skin cancer, the average age and duration of employment for the cases in the chloroprene exposure group is substantially less than for the non-chloroprene control groups. It is interesting to note that the average age of the lung cancer cases in the chloroprene group (44.5) is significantly less than the average age of the skin cancer cases in the same group (about 59). The authors note that the magnitude of the lung cancer risk in chloroprene-exposed workers is about the same as for chromate workers in the same district. Of the 34 cases of lung cancer in workers exposed to chloroprene or its derivatives, 18 were among persons having direct and prolonged exposure to chloroprene monomer. The remaining 16 cases were persons whose exposure was to chloroprene latexes. If this breakdown is applied h ( 4 to the two chloroprene subgroups shown in the skin cancer table (Groups III & IV), the lung cancer rates would be 2.6 (18-f-684) for the group with exposure to chloroprene monomer and 0.7 (16*f- 2,250) for the group exposed to chloroprene latexes. This difference presumably reflects the gradient in total amount of exposure to chloroprene. Animal: Animal experiments have shown that a concentration of 250ppra in air is toxic and a concentration of 75ppm may be toxic with continued exposure. Exposure to vapor first causes irritation of the respiratory tract, followed by depression of respiration and, if exposure is continued, asphyxia. The vapor is a central nervous system depressant. It causes severe degenerative changes in the vital organs, particularly the liver and kidneys. In addition, blood pressure is lowered and lung .changes accompany exposure, especially at the higher concentrations.^ Chloroprene has caused hyperplasia of lymph nodes and a decrease in 9 the number of lymphocytes in rats. During acute and chronic chloroprene 10 exposure, changes in adrenal gland function have also been noted. Even in low concentrations, chloroprene affects male reproductive organs causing degenerative changes resulting in reproduction interferences. Male reproductive organs appear to be more susceptible to 11 the effect of chloroprene than female, Chloroprene has an effect on embryogenesis. In rats and mice, it causes an increase in the total embryonal mortality and reduction in the 12,13 fetal weight of offspring of females exposed during pregnancy. Permissible Occupational Exposures: The American Conference of Governmental Industrial Hygienists established 3 14 the threshold limit of chloroprene at 25ppm (90mg/m ). This level was based VRD 0002013247 7 fA on the work of Cook and Von Oettingen, and is the current Occupational Safety and Health Administration, Department of Labor standard. Priority List Status Chloroprene is listed as number 412 on the NIOSH Priority List for Criteria Development for Toxic Substances and Physical Agents. An estimated 2,500 workers are exposed to chloroprene in the United States. The severity rating for chloroprene is 325 on a scale of 0 to 6,000. Producers and Suppliers The following is a list of the major producers and suppliers of chloroprene and neoprene in the U.S.: Chloroprene Location Dupont Victoria, Texas Laplace, Louisiana Petro-tex Chemical Corp. Petro-tex Chemical Subsid. Houston, Texas Dupont Petro-tex Chemical Corp. Petro-tex Chemical Subsid. *Shut Down in 1972 Neoprene Location Laplace, Louisiana Louisville, Kentucky Montague, Michigan* Houston, Texas Source: Adapted from 1974 Directory of Chemical Producers, USA, Stanford Research Institute, Menlo Park, California, 1974. 8 Annual production figures for chloroprene are not available. Following are the annual figures for neoprene: Year Neoprene Production (millions of pounds) 1968 340 1969 350 1970 325 1971 340 1972 370 1973 385 o xa .'J* *+ iM 9 06 Source: Chemical Economics Handbook, Stanford Research Institute, Menlo Park, California, 1974. VRD 0002013249 BIBLIOGRAPHY 1. Patty, F.R.: Industrial Hygiene and Toxicology. Interscience Publishers, New York, Vol. II, pp. 1319-1321, 1963 2. Van Oss, J.F.: Chemical Technology: An Encyclopedic Treatment, Barnes and Noble Books, New York, Vol. IV, pp. 211-212, 1972 3. Carothers, W.H., Williams, I., Collins, A.M., Kirby, J.E.: Acetylene Polymers and Their Derivatives. II. Anew synthetic rubber: Chloroprene and its polymers. J. Amer. Chem. Soc., Vol. 53:4203-4225, 1931 4. Van Oss, J.F.: Chemical Technology: An Encyclopedic Treatment, Barnes and Noble Books, New York, Vol. V, pp. 482-483, 1972 5. Chemical Economics Handbook. Stanford Research Institute, Menlo Park, California, Vol. A-B, p. 620 5022R-S, 1974 6. Sax, N.I.: Dangerous Properties of Industrial Materials. Van Nostrand Reinhold Company, 3rd Edition, p. 567, New York, 1968 7. Khachatryan, E.A.: The role of chloroprene in the process of skin neoplasm formation. Gig. Tr. Prof. Zabol., Vol. 18, pp. 54-55, 1972 8. Khachatryan, E.A.: The occurrence of lung cancer among people working with chloroprene. Problems in Oncology, Vol. 18, p. 85, 1972 9. Agakhanyan, A.G., Fridenshtein, A.Y., Allverdyan, A.G.: Iramunomorphology of chloroprene toxicosis. Zh. Eksp. Klin. Med., Vol. 13, pp. 3-7, 1973 10. Allaverdyan, A.G.: Changes in adrenal glands during acute and chronic chloroprene poisoning. Tr. Klin. Otd. NAUCH., Vol. I, pp. 150-157, 1970 11. Von Oettingen, W.F., Hueper, W.C., Deichmann-Grubler, W., and Wiley, F.H.: 2-Chloro-Butadiene (Chloroprene): Its toxicity and pathology and the mechanism of its action. J. Ind. Hyg. and Toxicology, Vol. 18:240-270, 1936 12. Salnikova, L.S.: Embryotropic effects of volatile substances given off by polychloroprene latices. Toksikologiya Novykh Promyshlennykh Khimicheskikh Veschestv, No. 11, pp. 106-111, 1968 13. Salnikova, L.S., Fomenko, V.N.: Experimental investigation of the influence of chloroprene on embryogenesis. Gig. Tr. Prof. Zabol., Vol. 8, pp. 23-26, 1973 14. American Conference of Governmental Industrial Hygienists, Documentation of the Threshold Limit Values for Substances in Workroom Air, 3rd Edition, pp. 54-55, 1971 15. Cook, W.A.: Maximum allowable concentrations of industrial atmospheric contaminants. Ind. Med., Vol. 14, p. 936, 1945 \ While in the vicinity, I stopped at Tulane Medical School to talk to Dr. DiLuzio primarily about the potential applications of his work on mechanisms and prevention of chemically induced liver injury to the VCM problem. We also discussed his cancer research and the possibilities for reversing existing cases of angiosarcoma and spotting potential cases early. Several branches of his work jnay be of interest: (1) Vitamin E supplementation has been shown to essentially eliminate thp effects of ethyl alcohol, carbon tetrachloride and several other chemicals on the liver at encountered exposure levels. This effect is quite likely to apply to VCM and is probably the most promising area for work which could have an immediate impact on the problem. (2) His work with ethyl alcohol showed that certain metabolites, rather than the alcohol itself, are linked to liver damage. Selective blocking of those metabolic paths eliminates liver damage. (This may be the answer to safe and economic alcoholism. One glass of wine would maintain a long term state of intoxication with no danger of liver damage. Sell your stock in Seagrams'.) While correlaries may exist with VCM which would help in understanding the mechanism of the problem, direct practical significance is not as likely as with the Vitamin E work. (3) It may be that VCM exposure is only one correlate of the problem. Work by DiLuzio and others has shown that interactive effects can be much more significant than direct effects. For instance, simul- taneous lead or calcium and endotoxin levels can cause precipitous death with each at levels orders of magnitude below that which would cause problems with independent exposure. It could be that some other co-factor is involved in cases where angiosarcoma has been linked to VCM exposure. A co-factor could also be a deficient state such as an inadequate antioxidant state which could be corrected with Vitamin E supplementation. (4) DiLuzio's model of natural bodily defenses against cancer (probably simplified for my sake) is that macrophages in the blood cannot recognize and destroy malignant ce.lls unless those cells are labeled with a chemical referred to as "recognition factor" (RF) which apparently complexes with malignant cell walls. Cancer is accompanied by a depression f | J 0062013251 Dr. Charles Whetstone . January 16, 1975 Page Two of RF levels usually before other symptoms are apparent. Thus, monitoring RF levels could provide a means for early or potential cancer detection. DiLuzio has used a chemical he calls "Glucan" (a biochemically produced polymer--dimers, trimers, tetramers, etc.--of glucose) to stimulate the macrophage-RF system. Such stimulation was shown to destroy and prevent recurrence of tested types of leukemia and tumors in rats. It was recently used in treating acute tumors in humans with similar results. Monitoring of RF levels of the blood in plant workers could provide both an early warning system for angiosarcoma (although low RF levels would presumably be observed with other forms of cancer unrelated to VCM exposure) and a broader statistical base for determing the correlates of angiosarcoma. Within the next week or two, DiLuzio will send us an analysis of how he feels these concepts might best be applied to work on the VCM problem. The Tulane Medical School has a new toxicology laboratory in which animal studies on VCM exposure could be done safely and efficiently. His analysis will include an evaluation of Tulane's ability to allocate manpower and facilities to this problem while meeting other research commitments. In mid-February, Dr. DiLuzio will be in New York and would be glad-to visit Saddle Brook for further discussions. CC: DAK, FK, KLS, LNV, JFG, DVP. WBC, JDBu, JJL, RWG, GWI, JWS V VRD 00(1 20 132 52 Interoffice Communication To J. D. Burns F rom D. A. Kuhn ate January 10, 1975 Suiaject Supporting Cancer Research on Vinyl Chloride Received JAH i s j9?5 MEQJCAi, Oiv. I received a package of information from Bob Gerwig from Dr. Charles Shaw at M.D. Anderson Hospital in Houston concerning a proposed pro gram as well as a discussion of what he is currently doing, a re pring and some information about his cancer prevention center. These are attached. I believe our objective in supporting any research should be directed towards determining the chemicals causing cancer and what kind of cancer they produce as well as determining which of the population are susceptible to cancer, primarily those caused by chemicals. There has been a long standing program to accomplish the first objective and no doubt it will continue into the future. Many studies are. in progress now especially on vinyl chloride. A novel approach is just beginning to accomplish the second objective, determining who is susceptible. This is the thrust of the research of Dr. Shaw at M.D. Anderson Hospital. Here is where Conoco can make a special contribution for the prevention of cancer and pro tection of our workers. The basic idea behind Dr. Shaw's work is that there is an enzyme in the body of some people that will prevent cancer. This has been found in work he has done on cigarette - smoking. Based on one's heredity, he either has it or doesn't. If we could test for this enzyme we would know whether anyone was susceptible or not. In addition, the work suggests that any test animal should also be screened for this enzyme. If the test animal has it, then he will be resistant to cancer and would be analogous to a human who has this enzyme. If not, he would be analogous to a human without the enzyme and presumably susceptible. Thus, we could make better judgements of extrapolating animal data to the human condition. During my conversation with Dr. Whetstone he indicated he was very much in favor of Conoco supporting this program because he per ceived the work to be high quality. This was based in part on the mutual assistance Dr. Shaw and Dr. Whetstone have given each other within the recent past. He was lead to Dr. Shaw through his readings of all the literature he could find on cancer caused by chemicals. As he progressed, he found himself directed to Dr. Shaw by the quality and subject of his papers. (szemm <nu J. !). Hum?; Jo^'iary 10, 1975 Po Two There are likely other places of equal quality that we could place our support. However, M.D. Anderson Hospital is in Houston near one of our major offices. Many of our Houston executives are in volved in public service in the Houston area, and here we have a chance to support an exciting new area if we choose this route. Dr. Shaw's budget indicates $41 M for the first year, but I under stand this has been inflated now to $50 M. Apparently there is no commitment beyond the first year, so we could review it the end of the first year to see if we should support him further. As Dr. Shaw's work progressed, we would be able to obtain the benefits early. Through our Medical Department we could keep in touch with what he is doing. I recommend we defer discussing this with our top management until the February meeting. However, this should provide enough background to initiate the subject with them at the Innisbrook meeting in January. I recommend we consider supporting this proqram. D. A. Kuhn' ee Attachments cc: Dr. Whetstone/Ponca City*^ Dr. Lembke/Ponca City (conoco) Interoffice Communication To From Date Subject R.W. Gerwig C.H. McGlothlia January 8, 1975 CC: JDBu, WBC, HRF, RWG, ACK, GJK, WCK, JJL, RWM, JWS, KLS, MX, LNV, RDW F. Kennedy Special Work Projects Undertaken by MSA, SPI, etc As you know, there have been several recent instances where such organizations as the SPI or the MCA have undertaken specific work or research projects on behalf of the represented companies. They bill these companies for their agreed shares of the specific project cost. Where this is clearly the case, I have obtained agreement of Tom Pickrell, Controller's Department, that these items can be charged to operating expenses rather than contributions. Since this is a sensitive area from a policy standpoint, this procedure of charging these to operating expense should be followed only when advance assessment for the individual project has been specifically agreed to by Conoco. It would not apply to special assessments that cover generally increased associated expenses* I recommend that any such agreements for special projects or work be limited to your approval in advance. Chemicals Research JAM 10 1-75 jb CC: T.R. Pickrell m u 008i t an CHEMICALS RESEARCH JAN 8 1975 January 3, 1975 N* R. SI Luclo, Ph*D. Chairman, Sept* of Physiology 1430 Tulane Avenue Tulane University New Orleans, La* 70112 Sear Doctor Si Luzlo: December 16, 1974, you sent a communication to Gaylord Greenfield, Saddle Brook, New Jersey, relevant to antioxidants, polyvinyl chloride and angio sarcoma of the liver* Ur* Greenfield and I are quite enthusiastic about your work in this area* For some time I have attempted to get more back ground material on antioxidants but to date the Information made available to me is quite scanty* X am requesting from your extensive publication list the following reprints, initially, until X get some background information on your work* Perhaps then at some future date it would be possible for Hr, Greenfield and I to meet personally with you and explore various areas for future experimenta tion relevant to our areas of interest* PUBLICATION NUMBER Protective influence of UPPD on hydrazine induced lipid peroxidation & hepatic injury* Recognition factors & cancer Peroxidation of lipids in alveolar macrophages & pulmonary protective factor by aqueous extracts of cigarette smoke Pyrazole inhibition of ethanol, allyl alcohol & ellyl formated induced hepatic injury Alcohol & teh liver Prevention of hydrazine induced lipid peroxidation & hepatic injury by DPFD Comparative uptake of BSP by isolated Kupffer & paren chymal cells* Factors modifying susceptibility to bacterial endotoxin: the effect of lead & Glucan mediated macrophage-induced necrosis of human malignant cells #320 #930 #331 #334 #344 #365 #354 #359 #360 S1"%ecJ& SIGNS. CHARLES L WHETSTONE M0 ASSISTANT MEDICAL DIRECTOR Charles L* Whetstone, M.D* Assistant Medical Director ccj Mr* Gaylord Greenfield - Saddle Brook bje VRD 010020 13256 CHEMICALS RESEARCH ft Interoffice Communication % To K. L. Schiirter From J. F. Gabbett fad Ctfih / Date December 23, 19.74 subject NIOSH Listing of Liver Angiosarcoma - 14 November 1974 Attached, for your information, is an up to date world listing of angiosarcoma cases published by NIOSH on 11/14/74. It does not, however, include the four Canadian cases released on 11/13/74. J. F. Gabbett cc: GJK, JSC, LNV, DAK, JJL, JDBu, RWG,- FK TABLE 1 REPORTED CASES OF LIVER ANGIOSARCOMA IN WORKERS EXPOSED ro VINYL CHLORIDE OR POLYVINYL CHLORIDE ' COUNTRY CASE if Czechoslovakia 01 .Czechoslovakia 02 Great Britain 01* Italy 01 Italy 02 Norway 01* Sweden 01* United States 01* United States 02* United States 03* United States 04* United States 05*' United States 06* United States 07* United States OS* United States 09* United States 10* United States 11* United States 12* United States 13* United States 16* United States 17 W. Germany 01* W. Germany 02* . BIRTH DATE 1st VC or PVC EXPOSURE DX ANGIO SARCOMA , AGE AT DX POLYMERIZATION WORKERS. YRS 1st EXP TO DX TOT YRS EXP *. AWAITING DETAILS AWAITING DETAILS 00-00-01 00-00-46 AWAITING DETAILS AWAITING DETAILS 12-23-15 03-00-50 06-23-27 10-17-23 08-14-51 12-09-48 08-19-33 11-15-55 05-25-15 11-28-45 01-15-24 07-06-52 01-25-12 06-19-44 00-00-29 01-17-62 05-03-22 08-00-44 05-06-20 10-07-46 00-00-31 05-28-45 03-16-13 06-12-51 05-27-09 10-14-46 11-17-18 09-13-49 - 12-01-21 08-19-44 11-04-27 05-08-50 05-06-31 06-23-55 07-26-31 ' 10-14-57 06-24-30 10-01-57 ' ; ^12-00-72 12-20-71 02-00-70 03-03-73 05-00-70 12-19-73 08-19-67 04-09-64 02-00-74 00-00-68 08-00-61 03-01-74 ' 05-00-68 03-00-70 05-02-69 05-00-74 00-00-69 10-11-74 09-25-70 09-19-68 71 . 26 20 56 22 ' 21 43 19 18 49 22 16 36 ` 14 13 58 28 28 43 15 15 52 20 18 45 12 12 45 24 18 - 41 - 15 " * 15 43 29 17 ' 55 17 17 61 23 23 50 20 15 53 30- 30 41 17 4 43 19 19 40 11 11 38 13. 13 NIOSH November 14, 1974 R_S.A3C.-I ^ u_, decig ;:-7i VV. ' DATE OP DEATH t*. 1 f i i, l it r* t' - - - . f: *; 12-00-72 01-04-72.10-20-70 ` 03-03-73 09-28-71 12-19-73 01-07-68 04-09-64 ALIVE 03-23-68 08-29-61 ALIVE 05-10-68 03-16-70 05-02-69 ' . . 07-04-74 03-27-69 . ALIVE 12-14-71 01-25-69 ' \ . ; C; i : / >, t %' [ !' i; t V: 1t * ^ v -.* ; .1!^ j. fj p k iim.gj.ojL. ml' Sweden 02* Great Britain United States United States 02* 14 15* W. Germany 03* 11-27-11 09-08-14 00-00-13 00-Q0-25 07-16-30 VC MONOMER PRODUCTION WORKERS 00-00-45 05-15-72 61 27 23 COMPOUNDERS FABRICATORS, ETC. 00-00-46 08-18-38 00-00-00 02-00-70 06-00-73 07-00-72 55 60 47 24 36 00 11 00 00 OTHER VC EXPOSURE- 00-00-00 02-00-68 43 14 . 14 . 08-16-72 12-00-70 07-03-73 02-15-73 I t l p Note 1 Note 2 & 5 ^ Note 3 10-10-73 - Note 4 f Note 1 Note 2 Note 3 Note 4 Note 5 Pouring PVC oil mixture onto fabric bases Machine operator covering electrical wire ..with PVC.plastic insulation Accountant at several fabrication plants (work history under review) Loading pesticide cans with VC propellant Diagnosis: Sarcoma (possibly "angiosarcoma"), liver.' Possibility of generalized neoplasm of the reticuloendothelial cell system cannot be ruled out. i * Indicates microscopically confirmed angiosarcoma of the liver "00" Indicates unknown data s' j i J VRD 0002013259 To From FK (* Date 8:05 am 1/8/75 Dr. Kirk stopped by with the following message: Dr. Sharrah is interested in the work of the fellow at Baylor on antioxidants to aid in metabolizing chlorinated hydrocarbons. However, MLS does not have it budgeted. If RWG and FK want to proceed, they will have to arrange for necessary funding. 4 09ZH0Z000 MEMORANDUM Ponca City, Oklahoma December 16, 1974 Subject: J. C. Kirk D. B. Burrows W. R. Beaty 0. C. Kerfoot A. J. Lundeen W. R. Sorenson G. Perkins C. L, Whetstone, M.D. D. V. Porchey (E.A. Setzkom-R.E.Laramy) R. G. Weiss VCM/PVC OSHA Regulation The 2nd Distrist Federal Appeal Court held Friday, December 13, 1974 that the VCM/PVC OSHA Regulation effective date by STAYED, pending litigation. I do not know when the three-man appeal bench will have com pleted its review of the facts and be prepared to rule on the petition. Flynt Kennedy lm interoffice Communication To Dr. Charles Whetstone From Gaylord G Greenfield Date December 20, 1974 Subject VITAMIN E AND VCM TOXICITY * /- S-7S s&* /fV / oJL&y^ ^J<Mj ' In my market research study on Vitamin E last year (G.G. Greenfield IOC to W.B. Carter, October 19, 1973), several references were found on the role of Vitamin E in increasing bodily tolerances to various chemicals which affect the liver. One of the main chemicals studied was CCI4. With the possible implications for the VCM health problem, I recently contacted Dr. N.R. DiLuzio (Professor and Chairman of the Department of Physiology, Tulane University), who has been the primary researcher in the area. He h'ad taken a cursory .look at the VCM problem, concluded that similar mechanisms would be quite likely, and was planning on writing a proposal for federal research funding. A letter from DiLuzio is attached along with an impressive list of his three hundred and sixty publications which are mainly devoted to mech anisms and prevention of chemically induced liver itijury, and some .re lated studies on mechanisms of tumor growth and activation of bodily defense systems to destroy malignant tissue. He is particularly interested in the VCM problem because it involves both areas of his past work and could lead not only to a means of preventing angiosarcoma, but of curing existing cases. DiLuzio`s credentials and expertise are well documented in the attachments and would seem to uniquely qualify him to work on these aspects of the VCM problem. I^recommend that CONOCO give serious consideration to funding w6rk along the/lines he proposes either directly or through the SPI. G. Greenfield ab Attachments CC: DAK, FK, LNV, D^P, WBC, GWI, JDBu, RWG, JJL, KLS v. im u u n ov Department of Physiology 1430 Tulane Avenue TULANE UNIVERSITY School of Medicine NEW ORLEANS, LA. 70112 December 16, 1974 Gaylord Greenfield Conco Chemical Division Continental Oil Company Park 80, Plaza East Saddle Brook, New Jersey 07662 Dear Mr. Greenfield: It was indeed a pleasure to chat with you recently relative to the problems of polyvinyl chloride. I have read with significant interest the recent article in Barron's relative to the impact of polyvinyl chloride exposure on industrial economics. As indicated to you, we have previously considered the possibility that antioxidants could be employed in the modifications of polyvinyl chloride . induced hepatic angiosarcoma. There appears to be little question that the most effective resolution of the PVC problem would not only be reduction in exposure which is already well under way in industry, but also to consider the possibility of providing a chemical protective agent. An agent such as vitamin E, if it were found to function as a prophylactic agent possessing the ability to inhibit the development of hepatic .lesions in PVC exposed animals, could be readily utilized. The unique- advantage of vitamin E is that it is essentially non-toxic and the fact that it has been available for clinical use for a considerable period of time. The time and cost of new drug development could well be avoided. We would be interested in the possibility of assisting Conco in their endeavors not only in the resolution of the PVC problem, but also in view of our interest in determining whether or not polyvinyl chloride acts perhaps like other hepatotoxic agents -in free radical mechanisms of hepatic injury. I have enclosed for your information a copy of my curriculum vitae which you will note, relates to mechanisms of chemical induced liver injury with emphasis on alcohol, carbon tetrachloride, and hydrazine. It also defines our more recent studies in mechanisms of tumor growth and development as influenced by alterations in host defense systems. As indicated to you during our conversation, it may be possible to tie some of these aspects together in the investigation of polyvinyl chloride induced hepatic injury and development of angiosarcoma. Please let me know if I can be of further assistance. Sincerely yours. NRD/mgl Enclosure N\ R. Di Luzio, Ph.D. Professor and Chairman G m m aaa CURRICULUM VITAE Nicholas Robert Di Luzio: Born May 4, 1926, Hazelton, Pennsylvania DEGREES: B.S., with honors. University of Scranton, 1950 Ph.D., University of Tennessee Medical Units, 1954 MILITARY SERVICE: U.S. Army Air Force, 1944-1946 SCHOLARSHIPS AND FELLOWSHIPS: 1. Laboratory assistant. Department of Biology, University of Scranton, 1948-1950. 2. Predoctoral Research Fellow of the Public Health Service National Institutes of Health (University of Tennessee) 1952-1954. AWARDS: 1. Lederle Medical Faculty Award, 1958-1961. 2. Research Award, International Society for Research on.Reticuloendothelial System (Gold Medal and Scroll for Outstanding Achievement and Research), 1964. SOCIETIES: 1. American Association for the Advancement of Science (Fellow) 2. Reticuloendothelial Society 3. American Physiological Society 4. Council on Arteriosclerosis of the American Heart Association (Fellow) 5. Society for Experimental Biology and Medicine 6. American Association for the Study of Liver Diseases -7. International Conference on the Biochemistry of Lipids 8. International Society of Parenteral Nutrition 9. Transplantation Society 10. American Heart Association 11. Experimental Hematology V \n i\M H QM* ACADEMIC APPOINTMENTS: 1. Instructor, Dept. Physiology, University of Tennessee Medical Units 1955-1956. 2.. Assistant Professor, Department Physiology, University of Tennessee Medical Units, 1957-1959. 3. Associate Professor, Dept. Physiology, University of Tennessee Medical Units, 1959-1962. 4. Professor, Department of Physiology, University of Tennessee Medical Units, 1962-1964. 5. Professor and Chairman, Department of Physiology and Biophysics, University of Tennessee Medical Units, 1964-1968. 6. Professor and Chairman, Department of Physiology, Tulane University School of Medicine, 1968-present. VISITING INVESTIGATOR: ' 1. Dorn Laboratory for Medical Research, Bradford Hospital, Bradford, Pa. Summer, 1954. 2. Research Participant, Pathology and Physiology Section, Oak Ridge National. Laboratory, Summer, 1956. 3. Research Participant, Biochemistry Branch, Biology and Medical Division U.S., Naval Radiological Defense Laboratory, San Francisco, Summer, 1958. 4. Visiting Professor, The Graduate School, New England Institute, Ridgefield, Connecticut (1966-1970). CONSULTANT: Member-Tennessee Advisory Committee on Atomic Energy (1958-1968). Scientific Advisory Committee of National Council on Alcoholism (1963-1968). Riker Laboratories (1961-1970). Naugatuck Chemical (1965-1968). Immunology and Microbiology Study Committee - American Heart Association (1966-1971). Alcoholism and Alcohol Problems Review Committee - National Institute of Mental Health (1971-1974) (Chairman, 1974). General^ Electric (1974). x VRD 0002013265 PATENTS: (#3,081>226) on a reticuloendothelial stimulant (#3,658,070) on a tobacco smoke filter SOCIETY OFFICES: President - Reticuloendothelial Society (1965-1967). Vice President - International Society for Research on the Reticuloendothelial System (1965-1969). EDITORIAL BOARD Advances in Experimental Medicine and Biology (Plenum Press). V aha (ft ADDITIONAL ACTIVITIES - N.. R. Di- LuziO, Ph.D. 1. Medical Student Admission Committee (1968 ) 2. Pounder and Director, Tulane University School of Medicine Negro Summer Research Fellowship Program (1968-1972). 3. Executive Faculty Committee (1968 - ) 4. Basic Medical Science Council (1968 - ), Chairman (1970-1972) 5. Louisiana Heart Association (1968 - ) Chairman, Research Committee (1972-197*0 Trustee (1971 - ) .6. Leukemia Society of American (New Orleans Chapter) (1970- Member, Board of Trustees . . .. Chairman, flesearch Committee (1970-1973). ) 7. Tulane Medical CenterDevelopment Fund Executive Committee (1971 ) 8. Tulane Medical Center Planning Committee (1970-197?) 9- Personnel and Honors Committee (1968-197*0 10. ' Scientific Review Committee of CTinical Cancer Research Centers 11. Committee to evaluate establishment of Lung Center 12. Consultant-New Orleans Alcohol Safety Program (1969-1972). v PUBLICATIONS OF DR. N. R. DI LUZIu 1. Action of choline on in vivo and in vitro synthesis of phospholipids. D. B. Zilversmit and N. R. Di Luzio. Fed. Proc. 10:151> 1951 (abstract). \ 2. Synthesis of phospholipids in diabetic dogs. D. B. Zilversmit and N. R. Di Luzio. J. Biol. Chem. 194:673-683, 1952. 3. Phospholipid metabolism in phlorizinized dogs. N. R. Di Luzio and D. B. Zilversmit. Fed. Proc. 11:34, 1952 (abstract). > 4. The turnover of liver and plasma phospholipids of phlorizinized dogs. N. R. Di Luzio and D. B. Zilversmit. Am. J_. Physiol. 170:472-476, 1952. k- 5. Influence of choline on phospholipid metabolism of normal and choline deficient dog liver slices. N. R. Di Luzio and D. B. Zilversmit. Am. J,: -Physiol. 171:720, 1952 (abstract!. 6. Action of cortisone and desoxycorticosterone acetate on the plasma lipids of adrenalectomized dogs. N. R. Di Luzio, M. L. Shore and D. B. Zilversmit. Fed. Proc. 12:197, 1953 (abstract). 7. The effect of cortisone and desoxycorticosterone acetate on the turnover of plasma and tissue phospholipids of adrenalectomized dogs. D. B. Zilversmit, N. R. Di Luzio and M. L. Shore. XIX Internatl. Physiol. Congress, p. 914, 1953 (abstract). ^ 8. The in vitro stimulation of phospholipid synthesis by choline in choline deficient dog liver slices. N. R. Di Luzio and D. B. Zilversmit. J. Biol. Chem. 205:867-8/1, 1953. 9. The role of tissue phospholipids in the metabolism of fats. N. R. Di Luzio. Doctoral Thesis, 1954. 10. The effect of cortisone and desoxycorticosterone on the plasma lipids of adrenalectomized dogs. N. R. Di Luzio, D. B. Zilversmit and H. L. Shore. Metabolism 3:424-432,1954. 11. The effect of adrenalcortical hormones on phospholipid turnover of adrenalectomized dogs.- D. B. Zilversmit, N. R. Di Luzio and M. L. Shore. Metabolism 3:433-437, 1954. ^'12. Protein-induced inhibition of colloidal gold uptake by liver. N. R. Di Luzio and D. B. Zilversmit. Am. J_. Physiol. 179:630, 1954 (abstract).' 13. Influence of exogenous proteins on blood clearance and tissue distribution of colloidal gold. N. R. Di Luzio and D. B. Zilversmit. Am. J. Physiol 180:563-565, 1955. 14. The effect of x-irradiation and choline on the reticuloendothelial system. N. R. Di Luzio. Am. 0. Physiol. 181:595-598, 1955. v m u a m a flaf ^15. Cortisone and epinephrine effect on plasma, liver and aortic lipid partition and phospholipid turnover. A. Dury and N. R. Di Luzio. . Fed. Proc. 14:40, 1955 (abstract). 16. Plasma lipid and lipoprotein alterations in adrenalectomized dogs. N. R. Di Luzio. Fed. Proc. 14:38, 1955 (abstract). y' 17. The influence of cortisone and epinephrine on liver, plasma and aortic lipid partition and phospholipid turnover. A. Dury and N. R. Di Luzio. Am- J- Physiol.. 182:45-50, 1955. 18. Is the cholesterol-fed rabbit choline deficient? N. R. Di Luzio, M. L. Shore and D. B. Zilversnit. Circulation 12:495, 1955 (abstract). 19. The effect of choline on the tissue phospholipid metabolism of the choline deficient rabbit. N. R. Di Luzio, M. L. Shore and D. B. Zilversmit. ' M- 1* Physiol . 183:609, 1955 (abstract). 2CT. The effect of choline deficiency on the reticuloendotehlial system of the rat. N. R. Di Luzio. Fed. Proc. 15:49, 1956 (abstract). ^21. The effect of choline, heparin and aureomycin on fatty .livers of dogs. N. R. Di Luzio and D. B. Zilversmit. Proc. Soc. Exp. Biol. Med. . 91:338-341 ,' 1956. 22. The role of the kidney in the etiology of renal hyperlipemia. N. R. Di Luzio and C. Riley Houck. Fed. Proc. 15:50, 1-956 (abstract). 23. The effect o.f choline on phosphatide metabolism of choline deficient and cholesterol-fed rabbits. N. R. Di Luzio and D. B. Zilversmit. Proc. Soc. Exp. Biol. Med. 92:454-456, 1956. 24. Reticuloendotehlial function and radiation response. N. R. Di Luzio. Rad. Res. 5:475, 1956 (abstract). 25. The effect of starvation on the phagocytic activity of the RES. It. R. Di Luzio. IV Internatl. Congress Hematol. p. 294, 1956 (abstract). 26. The role of the kidney in the etiology of renal hyperlipemia. N. R. Di Luzio and C. R. Houck. J. C>in. Invest. 35:1381-1384, 1956. 27. The effect of starvation on the phagocytic activity of the RES. N. R. Di Luzio and B. S. Powers. RES Bulletin 11:25-27, 1956. 28. The effect of cholsterol feeding on the plasma lipid fractions of adrenalectomized dogs. B. S. Powers and N. R. Di Luzio. Fed.Proc. 16:234, 1957. 29. RE function during alimentary lipemia. N. R. Di Luzio. Fed. Proc. 16:31, 1957. 30. The effect of x-irradiation on the plasma lipid fractions of the rabbit. N. R. Di Luzio and A. K. Simon. Rad. Res.. 7:79-84, 1957: 31. The effect of trypan blue and x-irradiation on the RES of the rat. N* R. Di Luzio, A. K. Simon and A. C. Upton. Arch Pathol. 64:649-656, 1957. 69ZCT0Z000 32. Dietary cholesterol and the endocrine regulation of plasma lipids. N. R. Di Luzio and B. S. Powers. Circulation 16:486, 1557 (abstract). 33. The role of choline in the turnover of phospholipids. D. B. Zilversmit, and N. R. Di Luzio. Am. J. Clin. Nutrition 6:235-241, 1958. *'34. The effect of acute ethanol intoxication on liver and plasma lipid fractions of the rat. N. R. Di Luzio. Am. J_. Physiol. 194:453-456, 1958. *^35. Bone marrow, plasma and liver lipids following x-irradiation. E. E. Elko, and N. R. Di Luzio. Fed. Proc. 17:41, 1958 (abstract). ^36. Liver and plasma metabolism in acute ethanol intoxication. N. R. Di Luzio. Fed. Proc. 17:35,.1958 (abstract).- 37. Dietary cholesterol and adrenal regulation of plasma lipids. B. S. Powers, and N. R. Di Luzio. Am. J_. Physiol. 195:165-170, 1958. 38. Effect of single and chronic choline supplements on phospholipid metabolism of the dog. N. R. Di Luzio and B. Zilversmit. Am. d_. Physiol. 196:887-889, 1959. ^39. Effect of x-irradiation on plasma, liver and bone marrow lipids of the rabbit. E. E. Elko and N. R. Di Luzio. Rad. Res. 11:1-6, 1959. 40. Lipid composition of Kupffer cells. N. R. Di Luzio. Am. J. Physiol. 196:884-886, 1959. 41. Isolation and lipid composition of liver parenchymal and Kupffer cells in normal and 'lipemic dogs. N. R. Di Luzio. Fed. Proc. 18:37, 1959 (abstract). a/42. Isolation and lipid composition of liver parenchymal and Kupffer cells following oral and intravenous fat administration. N, R. Di Luzio. XXI Internatl. Physiol. Congress, p. 76, 1959 (abstract). ^ 43. Lipid composition of liver parenchymal and Kupffer cells and hepatic uptake of administered lipid. N. R. Di Luzio. Am. Oil. Chem. 33rd Fall Meeting, p. 10, 1959 (abstract). 44. The effect of x-irradiation on plasma and adipose tissue lipids of the rabbit. E. E. Elko and N. R. Di Luzio. Rad. Res. 10:440, 1959 (abstract). ^45. Hepatic participation in lipid metabolism. N. R. Di Luzio. J. Am. Oil Chem. 37:163-165, 1960. 46. Modification of cholesterosis and lipidosis of rats maintained on an atherogenic diet. N. R. Di Luzio. Nature 185:616-618, 1960. l/47. Modification of hypercholesterolemia and hepatic cholesterosis. N. R. Di Luzio. Fed. Proc. 19:15, 1960 (abstract). 48. Reticuloendotehlial involvement in lipid metabolism. N. R. Di Luzio. Ann. N.Y. Acad. Sci. Art. 1 88:244-251, 1960. B L U l'ilB B B (JjP 49. Reticuloeridothe)ia i involvement in lipid metabolism. N. R. Di Luzio. N.Y. Acad. 5ci. Conference on the RES. p. 9, 1959 (abstract). 50. Influence of zymosan on tissue lipids of normal and cholesterol-fed animals Symposium, "Drugs Affecting Lipid Metabolism." Milan, Italy, p. 45, 1960. 51. Plasma lipid metabolism in x-irradiated rabbits. E. E. Elko and N. R. Di Luzio. Rad. Res. 12:432, I960 (abstract). 52. Reticuloendothelial involvement in lipid'metabolism. N. R. Di Luzio. RES Bulletin 5:21, 1960 (abstract). 53. The effect of intravenously administered phospholipid and triton on lipids of normal and ethanol-treated rats. N. R. Di Luzio and D. B. Zilversmit. Am. Physiol. 199:991-994, 1960). 54. Influence of zymosan on tissue lipids of normal and cholesterol-fed rats, ft. R. Di Luzio, J. Houston and E. E. Elko. Drugs Affecting Lipid Metabolism. Elservier Publishing Co., Amsterdam, 228-232, 1961. 55. Lipid mobilization in x-irradiated rabbits. E. E. Elko and N. R.Di Luzio. Rad. Res. 14:760-766, 1961. 56. Alcoholism and liver disease. (A Conference Summary). Gastroenterology 39:643, 1960 (abstract) N. R. Di Luzio. 57. Identification of a RE stimulating agent in zymosan. S. J. Riggi and N. R. Di Luzio. Am. J_. Physiol. 200:297-300, 1961 . UO. Acute ethanol intoxication and lipid mobilization. E. L. Elko and N. R. Di Luzio. fed. Proc. 20:276, 1961. (abstract). 59. Characterization of a RE stimulating agent in zymosan. S. J. Riggi and N. R. Di Luzio. Fed. Proc. 21:265, 1961 (abstract). 60. Influence of dietary lipids on RE function. N. R.Di Luzio, J. A. Logue and S. 0. Riggi. Fed. Proc. 20:266, 1961 (abstract). 61. Effect of x-irradiation on triglyceride metabolism of the rabbit. N. R. Di Luzio, E. Elkp, ft. Seidenverg and E. Entenman. Experientia 17:321-324, 1961. ^ 62. Effect of RE stimulating agents on hepatic and plasma lipids. N. R. Di Luzio, and S.. J. Riggi. Circulation Res. 24:1088, 1961 (abstract). 63. Lipid alterations in normal and RE stimulated rats following CCI4. N. R. Di Luzio. J. Am. Oil Chem. 35th Fall Meeting p. 16, 1961 (abstract). < 64. Alterations and mobilization of lipids in acute ethanol-treated rats. E. Elko, W. R. Woo.les and N. R. Di Luzio. Am. J. Physiol. 201:923-926, 1961 . ^65. Hepatic function during RE hyperfunction and hyperplasia. S. J. Riggi and N. R. Di Luzio. Am. J. Physiol. 201:923-926, 1961. V im im e e (lift 66. Influence of pre- and post- x-irradiation zymosan administration on RE function. W. R. Wooles,' E. Elko and N. R. Di Luzio. Rad. Res. 16:546, 1962. . 67. The rapid development of arterial lesions in dogs fed an "infarc producing" diet. N. R. Di Luzio and R. M. O'Neal; Exp. Mol. Pathol. 1:122-132,1962. y* 60. Triglyceride alterations in normal and RE stimulated rats following CCl^. N. R. Di Luzio. J. Am. Oil Chem. 39:194-196, 1962. 69. Influence of pre- and post x-irradiation administration of RE stimulating agents on RE activity. W. R. Wooles, E. Elko and N. R. Di Luzio. Fed. Proc. 21:279, 1962 (abstract). 70. Removal of chylomicra and fat emulsions by the RES. A new functional test for RE activity. S. 3. Riggi and-N. R. Di Luzio. Fed. Proc. 21:279, 1962 (abstract). 71. Reticuloendothelial participation in bone marrow transplantation. W. R. Wooles and N. R. Di Luzio. 2nd Internatl. Congress Radiation Res. p. 169. 1962 (abstract). 72. Comparative study of'alcoholic beverages on the development of the acute ethanol induced fatty liver. N. R. Di Luzio. Quart. J. Studies on Alcohol 23:557-561., 1962. 73. The influence of RE stimulation on the response of rats to dietary cnolesterol. S. J. Riggi and N. R. Di Luzio. J_. Li pi u Res. 3:339-343, 13G2. 74. Homo- and hetero-graft rejection by RE stimulated x-irradiated mice. W, R. Wooles and N. R. Di Luzio. Rad. Res. 16:569, 1962 (abstract). 75. Lipid biosynthesis in x-irradiated rabbits. E. Elko, W. R. Wooles and N. R. Di Luzio. Rad. Res. 16:557, 1962. (abstract). 76. Influence of RE hyperfunction on bone marrow transplantation. W. R. Wooles and N. R. Di Luzio. Am. J. Physiol. 203:404-408, 1962. 77. Effect of x-irradiation on plasma lipids and lipoproteins. N. R. Di Luzio. The Encyclopedia of X-and Gamma Rays. G; L. Clark, ed. Reinhold Publ. Co. New York, p. 560," 1963^ 78. Effect of x-irradiation on the RES. N. R.'Di Lzuio. The Encyclopedia of X- and Gamma Rays. G. L. Clark, ed. Reinhold Publ. Co., N.Y., p. 937, 1963. v/79. Role of liver and adipose tissue in the pathogenesis of the ethanol fatty liver. N. R. Di Luzio and M. Poggi. Fed. Proc. 22:398, 1963 (abstract). 80. The effect of RE stimulation on radiation chimeras and on the primary and secondary response. W. R. Wooles and N. R. Di Luzio. Rad. Res. 19:193, 1963 (abstract). oifA f 81. Evaluation of RE function in man. N. K. Salky, A. J. Sutherland* D. B. P'Pool, J. A. Chapman and N. R.Di Luzio. J_. Am. Med. Assoc. 184:221, 1963 (abstract). ^ 82.. A morphologic study of the effect of reticuloendothelial stimulation upon hepatic removal of minute particles from the blood of rats. C. T. Ashworth, S. J. Riggi and N. R. Di Luzio. J_. Exp. Mol. Pathol. Supplement 1:83-103, 1963. 83. Oimodal response of the functional state of the RES following glucan administration. W. R. Wooles and N. R. Di Luzio. The Physiologist. 6:299, 1963 (abstract). t^84. Prevention of the acute ethanol-induced fatty iiver by antioxidants N. R. Di Luzio. The Physiologist 16:169, 1963 (abstract). 85. Reticuloendothelial function and the immune response. W. R. Wooles and N. R. Di Luzio. Science 142:1078-1030, 1963. 86. Abnormal lipid tolerance and hyperlipemia in acute ethanol-treated rats. N. R. Di Luzio and M. Poggi. Life 5ci. 10:751-758, 1963. 87. Electron microscopic observations of human liver after intravenous administration of a RE test lipid emulsion. A. J. Ladman, N. K. Salky and N. R. Di Luzio. J_. Appl Physics 34:2504, 1963 (abstract). 88. The influence of RE stimulation and depression on antibody formation and on transplantation of bone marrow in 1ethally-irradiated mice. W. R. Wooles and N. R. Di Luzio. IV International Symp on RES. 69, 1964 (abstract). 89. The development and employment of a lipid emulsion for the experimental and clinical evaluation of RE function. N.R. Di Luzio, S. J. Riggi, and N. K. Salky. IV International Symp. RES 78-79, 1964 (abstract). 90. The effect of methyl cellulose on the RES. D. A. Blickens and N. R. Di Luzio. J_. Reticuloendothel. Soc. 1 :68-74, 1964. 91. The development of a lipid emulsion for the measurement of RE function. N. R. Di Luzio and S. 0. Riggi. 0_. Reticuloendothel.. Soc. 1:136-149, 1964. 92. Effect of whole body x-irradiation upon palmitate-l-C^ metabolism in the rabbit. E. E. Elko, W. R. Wooles and N. R. Di Luzio. Rad. Res. 21:493-500, 1964. ^ 93. Prevention of the acute ethanol-induced fatty liver by the simultaneous administration of antioxidants. N. R. Di Luzio. Life Sci. 3:113-118, 1964. 94. The phagocytic and proliferative response of the RES following glucan administration. W. R. Wooles and N. R. Di Luzio. J. Reticuloendothel. Soc. 1:160-169, 1964. V 4PKD 000 20 13273 95. Use of an anion exchange resin in treatment of two siblings with familial hypercholesterolemia. J. M. Horan, N. R. Di Luzio, and J. N. Etteldorf. J. Pediat. 64:201-209, 1964. 96. The role of liver and adipose tissue in the ethanol fatty liver. M. Poggi aid N. R. Di Luzio. 0_. Lipid Res. 5:437-441 , 1964. 97. Evaluation of reticuloendothelial function in man. N. K. Salky, N. R. Di Luzio, D. B. P'Pool and A. J. Sutherland. 0, Am. Med. Assoc. 187:744-748, 1964. 98. Depression of phagocytic activity and the immune response by methyl palmitate. W. R. Wooles and N. R. Di Luzio. Am. J. Physiol. 206:939- 943, 1964. 99. Inhibition of homograft acceptance and homo and heterograft rejection in. chimeras by RE stimulation. W. R. Wooles and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 115:756-759, 1964. v-^lOO. Inhibition of the CC14 induced fatty liver by antioxidants. . N. R. Di Luzio and F. Costales. Fed. Proc. 23:520, 1964 (abstract). . 101. The relative participation of hepatic parenchymal and Kupffer cells in the metabolism of chylomicrons. N. R. Di Luzio and S. J. Riggi. j. Reticulcendothel. Soc. 1:248-263. 1964. 102. Behavior of C^-labeled particulate plasma triglyceride and "RE test emulsion" in RE hyperfunctional rats. N. R. Di Luzio and E. L. Bierman Proc. Soc. Exp. Biol. Med. 116:1045-1047, 1964. 103. - The intravascular clearance and tissue distribution of methyl palmitate in mice. D. A. Blickens and N. R. Di Luzio. The Physiologist. 3:91, 1964 (abstract). 104. The influence of restraint stress on the development of the ethanolinduced fatty liver and gastric ulceration. N. R. Di Luzio and J. P. Quigley. The Physiologist 3:209, 1964 (abstract). 105. Vascular clearance and organ distribution of sheep red cells in mice with altered reticuloendothelial function. S. H. Morrow and N. R. Di Luzio. The Physiologist 3:209, 1964 (abstract).. 106. Investigation of the mechanism of methyl palmitate induced-depression of the RES. D. A. Blickens and N. R. Di Luzio. 0_. Reticuloendothel. Soc. 1:351, 1964 (abstract). 107. Behavior of particulate antigens in mice with altered RE function N. R. Di Luzio and S. H. Morrow. J.. Reticuloendothel. .Soc. 1 :359, 1964. 108. Electron microscopic observations of sinusoidal lining cells and fatstorage cells in normal human liver after intravenous administration of a RE test lipid emulsion. A. J. Ladroan, N. K, Salky and N. R. Di Luzio. J. Reticuloendothel. Soc. 1:365, 1964 (abstract). n ifim n e aW 109. Clinical evaluation of RE phagocytic activity, N, K* Salky and N. R. Di Luzio. 0, Reticuloendothel. Soc, 1:365, 1964 (abstract), 110. The effect of splenectomy and x-irradiation on antibody formation in RE hyperfunctional mice. N. R. Di Luzio, W. R. Wooles and S. H. Morrow. J. Reticuloendothel. Soc. 1:429-441, 1964. 111. Reticuloendothelial function in thymectomized rats. S. H. Morrow and N. R. Di Luzio. Nature 205:193-194, 1965. y'112. Inhibition of the ethanol and CCl* induced fatty liver by antioxidants. N. R. Di Luzio and F. Costales. 3, Exp. Mol.Pathol. 4:141-154, 1965. i/"113. Cellular aspects of ethanol fatty liver. A correlated ultrastructural and chemical study. C. T. Ashworth, F. Wrightsman, B. Cooper and N. R. Di Luzio. J. Lipid Res. 6:258-268, 1965. 114. Experimental and clinical evaluation of'RE function by means of a specific lipid emulsion. N. R. Di Luzio, N. K. Salky, S. J. Riggi and A. J. Ladman. IVth Internatl. Symp. RES May 29-0une 1, 1964, pp 15-31. (abstract). ix"115. 116. Modification of CCI4 toxicity by antioxidants. N. R. Di Luzio and B. Lyons. Gastroenterology 4:509, 1965 (abstract), The metabolism of palmitic acid-l-C14 in acute ethanol-treated rats, N. R. Di Luzio, M. Poggi, B. Lyons and K. Hedblom. Gastroenterology. 4:509, 1965 (abstract). 117. Metabolism of methyl palmitate, a phagocytic and immunologic depressant, ,and its influence on tissue lipids. 0. A. Blickens and N. R. Di Luzio. J_. Reticuloendothel. Soc. 2:60-74, 1965. 118. Influence of RE depression on neoplastic challenges. N, R. Di Luzio. Fed. Proc. 24:614, 1965 (abstract). 119, The fate of foreign red cells in mice with altered RE function, S. H. Morrow and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 119: 647-652 1965. 120. An evaluation of plasma triglyceride formation as a factor in the develop ment of the ethanol-induced fatty liver. N. R. Di Luzio. Life Sci. 4:1373-1382, 1965. ^ 121. The employment of N-Nl-diphenyl-P-phenylenediamine (DPPD) in the preven tion and treatment of experimentally induced liver injury. N. R. Di Luzio. 2nd International Symp. Drugs Affecting Lipid Metabolism 50-51, 1965. v-"' 122. The effect of vitamin E on the development of the ethanol and CCl^-induced fatty liver. N. R. Di Luzio. 2nd Internatl. Symp. on Drugs Affecting Lipid Metabolism 32, 1965 (abstract). /* 'j:, The role of RES in the remc .1 of chylomicrons and artificial lipid { emulsions. N. R. Di L.uzio. Soc. Ital. del'Artheriosclerosi. ' Giornale del*Arteriosclerosi 3:12, 1965 (abstract). S 124. Induction of phagocytic inhibition and the generalized Schwartzman 'phenomena by the administration of plasma from RE hyperfunctional mice. ^ D.A. Blickens and N. R. Di Luzio. 0_. Reticuloendothel. Soc. 2:187 (1965).~ 125. Activity of the RES in diseases of altered immunity. N. K.Salky, D. Mills and N. R. Di Luzio. J_. Lab., Clin. Med. 66:952-960, 1965. 126. Activity of the RES in neoplastic disease. N. K. Salky and N. R. Di Luzio. Proc. Central Soc. Clin. Res. 38:68, 1965 (abstract). 127. Modification of the graft versus host reaction.by methyl palmitate depres sion and glucan stimulation of the RES. K. K. Hedblom and N. R. Di Luzio. J. Reticuloendothel. Soc. 2:356, 1965 (abstract). 128. Kate of soluble and particulate antigens in RE hyperfunctional and RE hypofunctional mice. S. li. Morrow and N. R. Di Luzio. J_. Reticulo- endothel. Soc. 2:355, 1965 (abstract). 129. Phagocytic depression and the generalized Schwartzman.reaction (GSR) induced in normal mice by the administration of plasma from RE hypofunctional mice. D. A. Blickens and N. R. Di Luzio. J_. Reticulo endothel . Soc. 2:356, 1965. (abstract). 130. Development of an in vitro technique for evaluating hepatic phagocytic mechanisms and the role of opsonins as a factor in particulate behavior. T. A. Saba.and N. R. Di Luzio. J_. Reticuloendothel. Soc. 2:343. 1965 (abstract). . 131. Experimental and clinical evaluation of RE function by means of a specific lipid emulsion. N. R. Di Luzio, N. K. Salky, S. J. Riggi and A. J. Ladman. Proc. Japan. Soc. Reticuloendothel. Soc. 4:389-404, 1965. 132. Kupffer cell phagocytosis and`metabolism of a variety of particles as a function of opsonization. T. M. Saba and N. R. Di Luzio. J. Reticuloendothel. Soc. 2:437-453, 1965. ^ 133. An evaluation of the pathogenesis of the acute ethanol-induced fatty liver. N. R. Di Luzio and M. Poggi. j_n Biochemical Factors in Alcoholism, ed. B. B. Brodie and R. Mackel, Academic Press, 127-138, 1966. ^ 134. A mechanism of the acute ethanol-induced fatty liver and the modification of liver injury by antioxidants. N. R. Di Luzio. Lab. Invest 15:50-63, 1966. iX '135. Inhibition of CCl4-induced liver injury and lethality by coenzyme Q. G. H. Kalish and N. R. Di Luzio. Gastroenterology 50:392-393, 1966 (Abstract). 136. Enhanced peroxidation of lipid in the pathogenesis of acute ethanolinduced liver injury. N. R. Di Luzio and G. H. Kalish. Gastroenteroloqv. 50:392-393, 1966 (abstract). v VRD 00028132,76 V u/. 138. Peroxidation uf liver ripKij as a factor in the pathogenesis of the acute ethanol-induced fatty liver. 6. H. Kalish and N. R. Di Luzio. Science 152:1390-1392, 1966. A Method for collection and determination of 14CO2 for in vitro metabolic studies. Thomas M. Saba and N. R. Di Luzio. J.. Lipid Res. 7:566-567, 1966 139. Mechanism of gelatin inhibition of RE function. J. P. Filkins and N. R. Di Luzio. Proc. Soc. Exp. BjoX- Med. 122:131-133, 1966. 140. The role of opsonins in the in vitro phagocytosis of colloidal gold by hepatic, macrophages. J. P. Filkins. T. M. Saba and N. R.Di Luzio. Fed. Proc. 25:479, 1966 (abstract). HI. Effects of heparin and sulfated polysaccharides on in vitro hepatic phagocytosis. J. P. Filkins and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med_. 122:548-551, 1966. ^142. A. mechanism of the acute ethanol-induced fatty liver and the modification of liver injury by antioxidants. N. R. Di Luzio. In Biochemical Pathology, ed., E. Farber and P. N. Magee. The Williams and Wilkins Co.Baltimore, 50-63, 1965. The employment of antioxidants in the prevention.and treatment of experimentally induced liver injury. N. R. Di Luzio. Prog. Biochem. Pharmacol. vol 111:325-342, 1967. 144. The metabolism of cholesterol in RE hyperfunctional rats maintained on normal or high cholesterol diets. N. R. Di Luzio and S. J. Riggi. J. Rc ti cul oerricanc h* soc. ^: > -j-u~ 1 *+0, 1966. 145. The influence of intravenously administered lipids on RE function. N. R. Di Luzio and D. A. Blickens. J,. Reticuloendothel. Soc. 3:250-270, 1966. 146. The role of the RES in the metabolism of cholesterol. N. R. Di Luzio. Internatl. Symp. Atherosclerosis and Reticuloendothelial System. Summaries, p. 24, 1966. ^ 147. The influence of intravenously administered hexahydrocoenzyme Q4 on liver injury. N. R. Di Luzio. Life Sci. 5:1467-1478, 1966. 148. The influence of RE stimulation and depression on the fate of soluble and particulate antigens. S. H. Morrow and N. R. Di Luzio. Texas Reports on Biology and Medicine 24:518* 1966. (Selected for excellence of research at the 7th Annual Student Research Forum, ilniv. Texas Med. Branch* Galveston, Texas, April 9, 1966). 149. Comparative metabolic activity of hepatic parenchymal and Kupffer cells. T. M. Saba and N. R. Di Luzio. The Physiologist 9:280, 1966. (abstract). 150. The influence of heparin on intravascular phagocytosis. J. P. Filkins and N. R. Di Luzio. The Physiologist. 9:178, 1966 (abstract) VRD 000 20 132 7 7 151. Effects of ethanol administration on the peroxidation cf liver lipids. M. Comporti and N, R. Di Luzio. The Physiologist 9:157, 1966. 152. Are the opsonins involved in carbon-gel phagocytosis reacting to a 'contaminating pyrogen. 0. P. Filkins and N. R. Di Luzio. J_. Reticuloendothel Soc. 3:359-360, 1966. 153. Properties of the "opsonic system 11 regulating in vitro hepatic phago cytosis. T. M. Saba, J. P. Filkins and N. R. Di Luzio. J. Reticulo endothel Soc..3:398-414, 1SG6. 154. Hepatic phagocytosis and the opsonin system governing its activity. T. M. Saba, J. P. Filkins and N. R. Di Luzio. J. Reticuloendothel. Soc. 3:359, 1966. 155. Evaluation of the mechanism of the hyperphagocytic state in the graftversus-host reaction. N. R. Di Luzio. J. Reticuloendothel. Soc. 3:357, 1966. U'-"' 156. Peroxidation of lipids in the pathogenesis of acute ethanol-induced liver injury. A. 0. Hartman, M. Comporti and N. R. Di Luzio. Gastroenterology. 52:316, 1967 (abstract). 157. Activity of the RES in diseases.of altered immunity. N. K. Salky, D. M. Mills and N. R. Di Luzio. Arthritis Rheumatism 8:465, 1965. 158. Participation of hepatic parenchymal cells in chylomicron and cholesterol metabolism. In Advances in Experimental Biology and Medicine, ed. N. R. Di Luzio and S. J. Riggi. Plenum Publishing Co. pp 382-403, 1967. 159. Effects of gelatin and heparin on intravascular phagocytosis. 0. P. Filkins and N. R. Di Luzio. 3_. Reticuloendothel. Soc. 3:471-485, 1966. 160. Effect of in vivo and in vitro ethanol administration on liver lipid peroxidation. M. Comporti, A. D. Hartman and N. R. Di Luzio. Lab, Invest. 16:616, 1967. 161. Antioxidant modification of carbon tetrachloride induced impairment in triton response and bromsulphalein removal. C. G. Crafton and N. R. Di Luzic. Fed. Proc. 26:773, 1967, 162. "Nutrition and Hepatic Disease" Letter to the Editor. * N. R. Di Luzio. J. Internatl. Pathol. 8:16, 1967. Antioxidant maintenance of hepatic triglyceride secretory activity and hepatic function in CCI4 poisoned rats. C. G. Crafton and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 124:1321-1323, 1967. 164. Comparative evaluation of the influence of opsonins on hepatic, splenic and pulmonary phagocytosis. T. M. Saba and N. R. Di Luzio, Proc, Soc. Exp. Biol. Med. 125:630-634, 1967. 9LH191999 UHA k 165. Phagocytic arid opsonic activities of germfree rats. T. M. Saba, J. P. Fi1 kins and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 125:634-636> 1967. 166. Comparative effects of endotoxin and gelatin on reticuloendothelial activity. 3. P. Filkins and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 125:908-912, 1967. 167. Phagocytic activity of the RES in neoplastic disease. N. K. Salky, N. R. Di Luzio. A. G. Levin and H. S. Goldsmith. J. Lab. Clin. Med. 70:393-402, 1967. ^^163. Role of atnioxidants in prevention and treatment of chemical induced" alterations in lipid metabolism. N. R. Di Luzio, A. D. Hartman and C. G. Crafton. Conf. Biochemistry of Lipids. Jerusalem. Israel, Session 7, 1967. 169. The protective effect of heparin on endotoxin lethality. M. L. Walker, R. F. Suitor, J. P. Filkins and N. R. Di Luzio. Texas Reports on Biology and Medicine. 8th Annual Student Research Forum, University of Texas Med. Branch, Galveston, Texas 25, 501, 1967. - 170- Role of.lipid peroxidation in the pathogenesis.of the ethanol-induced fatty liver. N. R. Di Luzio and A. D. Hartman. Fed. Proc. 26:1436, 1967. 171. In vitro and in vivo assessment of RE phagocytic activity of control and hypercholesterolemia rabbits. N. R. Di Luzio and T. M. Saba. Circulation 36:8-9, 1967. 172. Heparin modification of endotoxin activation of RE function'and shock lethality. J. P. Filkins and N. R. Di Lzuio. The Physiologist 10:169, 1967. 173. Opsonic involvement in RE phagocytic "blockade" and recovery. T. M. Saba and N. R. Di Luzio. The Physiologist 10:296, 1967. 174. Evaluation by the graft-versus-host reaction of the immune competence of lymphoid cells of mice with altered reticuloendothelial function. N. R. Di Luzio. 0. Reticuloendothel. Soc. 4:459-475, 1967. f^175. Prevention of the chronic alcohol-induced fatty liver by antioxidants. A. D. Hartman and N. R. Di Luzio. The Physiologist 10:196, 1967. 176. Mechanism of particle-induced RE blockade. T. M. Saba and N. R. Di Luzio. J. Reticuloendothel. Soc. 4:436, 1967 (abstract). 177. Heparin-opsonin interaction in endotoxemia. J. P. Filkins and N. R. Di Luzio. J. Reticuloendothelial Soc. 4:421, 1967 (abstract). 178. Development and evaluation of a method for the isolation of Kupffer cells. J. C. Pisano, J. P. Filkins and N. R. Di Luzio, J. Reticuloendothel. Soc. 4:431, 1967 (abstract). t iu m & w - <nu 179. The influence of removal of various endocrine glands on the prolifera tion and hyperphagocytic induced by glucan or zymosan. N. R. Di Luzio. J. Reticuloendothel. Soc. 4:429, 1967 (abstract). iXfao. inhibition of the chronic ethanol-induced fatty liver by antioxidant administration. A. B. Hartman and N. R. Di Luzio. Proc. Soc. Exj3. Biol. Med. 127:270-276, 1968. ^^181. Inhibition of chronic CCI4 hepatic injury by antioxidants. A. D. Hartman, M. Trumbull and. N. R. Di Luzio. Gastroenterology 54:154, 1968 (abstract). 182. Evaluation of RE activity in the "graft-versus-host reaction." N. R. Di Luzio. _J. Reticuloendothel. Soc. 5:368-377, 1968. 183. Heparin protection in endotoxin shock. J. P. Filkins and N. R. Di Luzio. - Am. J. Physiol. 214:1074-1077, 1968. 184. Mechanism of x-irradiation induced depression of RE function. T. M. Saba and N. R. Di Luzio. Fed. Proc. 27:507, 1968 (abstract). 185. Evaluation of humoral and cellular mechanisms of methyl palmitatc induced RE depression. T. M. Saba and N. R. Di Luzio. Life Sciences 7:337-347, 1968. . ^'186. Lipid peroxidation - antioxidants - and ethanol-induced liver injury. Letters to the Editor (invited) Exp. Mol. Pathol. 8:394-402, 1968. 187. Involvement of the opsonic system in starvation induced depression of the RES. T, M. Saba and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 128:869-375, 1968. 188. Phagocytic and metabolic activities of isolated rat Kupffer cells, 0. C. Pisano, J. Filkins and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 128:917-922, 1968. ,. 189. The comparative influence of methyl palmitate and glucan administration on endotoxin lethality. C. G. Crafton and N. R. Di Luzio. 24th Int. Physiol. Congress (abstract), p. 95, 1968. 190. Evaluation of the comparative roles of splenic macrophages and lympho cytes in the graft-versus-host reaction. J. C. Pisano and N. R. Di Luzio. Transplantation Soc. 2nd Internatl. Congress, 1968. 191. Reticuloendothelial Blockade: effect of puromycin upon opsonindependent recovery from blockade. J. C. Pisano, J. T. Patterson and N. R. Di Luzio. Science 162:565, 1968. 192. Endotoxin induced hypothermia and tolerance in the rat, J. P. Filkins and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 129:724-726, 1968. -f 09!U0Z0M f 0 s'S\. . Modification, of chronic CCI4 .nduced hepatic injury by N-n'-diphenylp-phenylene diamine. A. D. Hartman, N. R. Di Luzio and M. L. Trumbull. Ex. .MoT_- Pathol. 9:349, 1968. V ^ 194. The influence of ethanol or CCI4 administration on lipid soluble anti oxidant activity of Viver mitochondria and microsomes. N. R. Di Luzio and A. D. Hartman. Am. Assoc. Study of Liver Disease. 14, 1968 (abstract). 195. Mechanism of puromycin inhibition of recovery from particle-induced RE blockade. U. R. Di Luzio and''J. C. Pisano. J.. Reticuloendothel. Soc. 5:590, 1968 (abstract). 196. Influence of methyl palmitate or glucan administration on endotoxin lethality. C. G. Grafton and N. R. Di Luzio, J.. Reticuloendothel. Soc. 5:589, 1968 (abstract). 197. Metabolic status of isolated rat Kupffer cells. J. C. Pisano and N. R. 01 Luzio. J. Reticuloendothel. Soc. 5:583, 1963. 198. Reticuloendothelial blockade and recovery as a function of opsonic activity. T. M. Saba and N. R. Di Luzio. Am. J. Physiol. 216:197-205, 1969. 199. Effect of x-i mediation on RE phagocytic function and serum opsonic, activity. T. M. Saba, and N..R. Di Luzio. Am. J. Physiol. 216:910* 1969. 200. Surgical stress and RE function. T. M. Saba and N. R. Di Luzio. Surgery 65:802-307, 1969. 201. The comparative roles of splenic macrophages and lymphocytes in the graft-versus-host (GVH) reaction. J.-C. Pisano and N. R. Di Luzio. 'Fed. Proc. 28:449, 1969 (abstract).. 202. Influence of reticuloendothelial system (RES) stimulation and depression on immunological phenomena. N. R. Di Luzio. J. Am. Chem. Soc., Invited paper., 1969 (abstract). 203. Effect of selective stimulation and depression of the RES on endotoxin lethality. N. R. Di Luzio and C. G. Crafton. IV. International Congress Pharmacology, 1969 (abstract). 204.. Influence of opsonins and heparin on intravascular carbon clearances following endotoxin. J. P. Filkins and N. R. Di Luzio. J. Reticulo endothel. Soc. 6:287-299, 1969. 205. Relationship of reticuloendothelial functional activity and endotoxin lethality. C. G. Crafton and N. R. Di Luzio. Am. J_. Physiol. 217:736, 1969. ^ ^206. The effect of ethanol and CCIa administration and hepatic lipid soluble antioxidant activity. N. R. Di Luzio and A. D. Hartman. Exp. Mol. Pathol. 11:38-52, 1969. 207. Purification of an opsonic protein fraction from rat serum. J. C. Pisano and N.R. Di Luzio. J_. Reticuloendothel. Soc. 7:386-396, 1970. im tB iB B B iTHA 208. Metabolic characterization of actively phagocytizing isolated rat Kupffer cells. J. C. Pisano, J. P. Filkins and N. R.Di Lzuio. 0. Reticuloendothel. Soc. 8:25-36, 1970. '* 209. Modification of acute and chronic ethanol-induced hepatic injury and the role of lipid peroxidation in the pathogenesis of the ethanol-induced fatty liver. N. R. Di Luzio and A. D. Hartman. Biochemical and Clinical Aspects of Alcohol Metabolism, ed. V. M. Sardesai and C. C. Thomas pp. 133-154. 210. Effect of acute and chronic administration of ethanol and alcoholic beverages on tissue triglyceride concentrations. N. R. Di Luzio. Quart. J. Stud. Alcohol. Suppl. 5 pp 26-33, 1970. 211. Influence of altered RE function on vascular clearance and tissue dis tribution of S. enteritidis endotoxin. N. R. Di Luzio and C. G. Crafton. Proc. Soc. Exp. Biol. Med. 132:686, 1969. 212. Depression of phagocytic activity of the RES by anti lymphocytic serum. J. C. Pisano, J. T. Patterson and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 132:517, 1969. 213. Evaluation of the mechanism of glucan-induced stimulation of the RES. N. R. Di Luzio, J. C. Pisano and T. M. Saba. J. Reticuloendothel. Soc. 7:731-742, 1970. ^^214. The potential role of chemical-induced free radical mechanisms in the induction of hepatic injury. N. R. Di Luzio. Magnetic Resonances in Biological' Research* University of Cagliari, Lab di Spettroicopia' Molecolore, 1969. 215. Influence of altered reticuloendohtelial (RE) function on the fate of SlCr S. enteritidis endotoxin. C. G. Crafton and N. R. Di Lzuio. The Physioloqist 12:202, 1969. 216, Influence of antilymphocytic serum (ALS) upon the functional activity of the reticuloendothelial system (RES). N. R. Di Luzio, 0. T. Patterson and J. C. Pisano. J. Reticuloendothel. Soc. 7:637, 1970. 217. A consideration o'f the role of the RES in endotoxin shock. N. R. Di Luzio and C. G. Crafton. Internatl. Symp. Biochemistry and Pharmacology of Shock, 1969 (abstract). '-'"218. Prevention of acute ethanol-induced fatty liver by pyrazole. 0. C. Morgan and N.R: Di Luzio. Gastroenterolooy 58:308, 1970. 219. Depletion of serum opsonic, activity in humans with neoplastic disease. J. C. Pisano, N. R. Di Luzio and N. K. Salk.y. J. Reticuloendothel. Soc. 7:659, 1970 (abstract). 220. Comparative influence of methyl palmitate and glucan pretreatment on survival following endotoxin and tourniquet shock. R. Trejo, C. G. Crafton and N. R. Di luzio. J. Reticuloendothel. Soc. 7:662, 1970 (abstract). 221. Evaluation of serum opsonin depletion in the induction of the primary immune response. R. A. Evans, J. C. Pisano, and N. R. Di Luzio. i). Reticuloendothel. 5oc. 7:629, 1970 (abstract). 222. The influence of endotoxin administration on plasma lysosomal enzyme activity in rats with altered RES activity. C. G. Crafton and N. R. Di Luzio. J_. Reticuloendothel. Soc. 7:664, 1970 (abstract). 223. A consideration of the role of the reticuloendothelial system (RES) in endotoxin shock. N. R. Di Luzio and C. G. Crafton. Adv. Exp. Med. Biol. pp 27-57, 1970. 224. Recognition factor dysfunction - a new disease entity? J. C. Pisano and N. R. Di Luzio. Fed. Proc. 29:758. 1970 (abstract). 2.25. The employment of antioxidants in the prevention and treatment of experimentally induced liver injury. Progr. in Biochem. Pharmacol. 3:327, 1967. 226. The importance of ethanol metabolism to the development of the acute' ethanol-induced fatty liver, hyperlipemia and the contribution of congeners to the development of the chronic ethanol-induced fatty liver. N. R. Di Luzio. In Biological Affects of Alcohol. Univ of Texas Press .1970. Ed. R. J. Creavent' and'M. K. Roach. 227. Inhibition of the.acute ethanol induced fatty liver by pyrazole. J. C. Morgan and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med, 134:462466, 1970. 228. Effect of RE functional modification upon host response to endotoxin. C. G. Crafton and N. R. Di Luzio. Presented at South Central Branch of Am. Soc. Microbiol, by C. G. Crafton- recipient of the Strawinsky Memorial Award. 229. Absence of macrophage humoral recognition factors in patients with carcinoma. J. C. Pisano, N. R. Di Luzio and N. K. Salky. J_. Lab. Clin. Med. 76:141-150, 1970. 230. Inability of plasma from patients with, neoplasia to support macrophage recognition of foreignness. 0. C. Pisano, N. K. Salky and N. R. Di Luzio. Nature 226:1049-1050, 1970. 231. Recognition factor dysfunction - a new disease entity? J. C. Pisano and N. R, Di Luzio. Tuiane Medicine 2:7, 1970. 232. Role of free radicals in chemically-induced hepatic cell injury. N. R. Di Luzio. Fed. Proc. 29:239, 1971. 233. Phagocytic activity and antibody formation in Gunn rats. B. B. Lozzio, E. A. Machado and N. R. Di Luzio. VI. Internatl. Meeting of the RE Society. Book of Abstracts, p. 90, 1970. X VRD 0002013283 !* 234. Macrophage reversal of ALS immunosuppression. J. C. Pisano, J. T. Patterson and N. R. Di Luzio. VI Internatl. Meeting of the RE Socidty, Book of Abstracts, p. Ill, 1970. 235. x Macrophage recognition mechanism-experimental and clinical considerations. N. R. Di Luzio and J. C. Pisano. VI Internatl. Meeting of the RE Society. Book of Abstracts, p. 37, 1970. 235. Effect of splenectomy upon restoration of opsonic activity following reticuloendothelial (RE) blockade. 0. I. Patterson, J. C. Pisano and N. R. Di Luzio. J. Reticuloendothel. Soc. 7:633, 1970. 237. Influence of reticuloendothelial functional alterations on mortality patterns in-endotoxin and tourniquet shock. R.- A. Trejo, C. G. Grafton and N. R. Di Luzio. J. Reticuloendothel. Soc. 9:299-306, 1971. 238. The effects of laminarian, sulfated glucan and oligosaccharide of glucan on RE activity. N. R. Di Luzio and S. J. Riqqi. J. Reticuloendothel. Soc. 8:465-473, 1970. 239. Effect of anti-Kupffer cell serum on phagocytosis and humoral antibody formation. 0. C. Pisano and N. R. Di Luzio. J_. Infect. Immun. 2:488-452,1970. 240. Reversal of anti-lymphocytic serum induced immunosuppression by macrophage administration. J. T. Patterson, J. C. Pisano, and N.R. Di Luzio. Proc. Soc. Exp. Biol. Med. 135:831-835, 1970. 241. RE phagocytic function and antibody formation in Gunn rats B. B. Lozzio R. A. Machado and'N. Di Luzio. .1 ' Cvn . . ru t . It 57-66, 1971. 242. Biochemical characterization of Kupffer and parenchymal cells isolated from rat liver. P. E. Lentz and N. R. Di Luzio. Exp.' Cell Res. 67:17- 26, 1971. 243. Impaired detoxification as a mechanism of lead acetate induced hyper sensitivity to endotoxin. R. A. Trejo and N. R. Di Luzio. Proc. Soc. Ex. Biol. Med. 136:889-893, 1971. 244. Influence of P_. berghei infections on phagocytic and humoral recognition factor activity. A. G. Kitchen and N. R. Di Luzio. J. Reticuloendothel. Soc. 9:237-247, 19/1. 245. Alterations in humoral-and cellular aspects of the RES in malaria infection. N. R. Di Luzio and A. G. Kitchen. J_. Reticuloendothel. Soc. 9:606, 1971. 246. Biochemical composition of Kupffer and parenchymal cells isolated from normal, RE stimulated or depressed rats. P. E. Lentz and N. R. Di Luzio. J_. Reticuloendothel. Soc. 9:605, 1971 (abstract). 247. Effect of lead acetate pretreatment on the intravascular clearance of colloidal carbon and on endotoxin detoxification. R. A.. Trejo and N. R. Di Luzio. J. Reticuloendothel. Soc. 9:611, 1971 (abstract). N m tt0Z000 248. Antl-Kupffer cell serum: an immunological mechanism for the selective removal of macrophages. J. C, Pisano and N. R. Di Luzio. J. Reticuloendothel. Soc. 9:630, 1971 (abstract). 249. ' Modification of antilymphocytic (ALS) induced immunosuppression by macrophage transplantation. J. T. Patterson, J. C. Pisano and N. R. Di Luzio. J. Reticuloendoth&l. Soc. 9:634, 1971 (abstract). 250. RE phagocytic function and antibody formation in Gunn rats. B. B. Lozzio, E. A. Machado and N. R. Di Luzio. J. Reticuloendothel. Soc. 9:643, 1971 (abstract). 251. Dimensions of humoral recognition factor depletion in carcinomatous patients. J. C. Pisano, J. P. Jackson, N. R. Di Luzio and H. Ichinose. Cancer Res. 32:11-15, 1972. 252. The role of lipid peroxidation in the induction of hepatic injury. N. R. Di Luzio. J_. Am. Cheni. Soc. (abstract), 1971. 253. The protective effect if Vitamin E on plasma lipid dienes in man. N. R. Di Luzi J_. Am. Oil Chem. Soc. (abstract), 1971. 254. Effect of-glucan and methyl palmitate pretreatment on endotoxin detoxification by liver and spleen. R. A. Trejo and N. R. Di Luzio. Fed. Proc. 30:374 (abstract) #1015, 1971. 255. Influence of reticuloendothelial functional modification on endotoxin detoxification by liver and spleen. R. A. Trejo and N. R. Di Luzio. J. ReticuloendothelSoc. 10:515-525, 1572. 256. Impaired endotoxin detoxification as a factor in endotoxin hypersensitivity of malaria infected mice. L. D. Loose, R. A. Trejo and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 137:794-797, 1971. 257. Macrophage recognition mechanisms: experimental and clinical considera tions. N. R. Di Luzio, J. C. Pisano and N. K. Salky. Adv. Exp. Med. Biol. 15:373-390, 1971. 258. Macrophage reversal of ALS-immunosuppression. J. C. Pisano, J. T. Patterson and N. R. Di Luzio. Advi Exp. Med. Biol. 15:237, 1971. 259. Liver parenchymal and Kupffer cell metabolism of ^C-labeled acetate, palmitate and triglyceride. N; R. Di Lu2io and T. M. Saba. <1. Reticuloendothel. Soc. 10:392-402, 1971. 260. RE blockade and ALS. Lancet, Letter, 1:309, 1970. 261. The protective effect of Vitamin E on plasma lipid dienes in man. N. R. Di Luzio. J_. Agricul. Food Chem. 20:486-490, 1972, 262. Influence of DES on RE function, tissue distribution and detoxification of S. enteritidis endotoxin. R. A. Trejo, L. D. Loose and N.R. Di Luzio. O. Reticuloendothel. Soc. 11:38-97, 1972. m U 0 l0 0 0 263. Humoral recognition factor activity and neoplasia: clinical and experimental considerations. N. R. Di Luzio. J. C. Pisano and N. K. Salky. Laryngoscope (invited paper) 81:737-749, 1971. 264. Comparative behavior of soluble and particulate antigens and inert colloid in RE stimulated or depressed mice. N. R. Di Luzio and H. S. Morrow III, J. Reticuloendothel. Soc. 9:273-287, 1971. 265. The effect of prostaglandin Ei on cellular and humoral immune responses. L. D. Loose and N. R. Di Luzio. J. Reticuloendothel. Soc. 11:419-420, 1972. 266. Evaluation of recognition factor depletion following administration of soluble or particulate agents and leukemic cells. N. R. Di Luzio and J. C. Pisano. J_. Reticuloendothel. Soc, 11:416-417, 1972. (Abstract). 267. Reticuloendothelial (RE) functional and ultrastructural alterations following lead acetate administration. R. Trejo, N.R. Di Luzio and E. Hoffmann. 11:435-437, 1972 (abstract). J. Reticuloendothel. Soc. 268. Hepatic functional and ultrastructural alterations following lead acetate administration. R. Trejo, N. R. Di Luzio and E. Hoffmann. Gastroenterology 62:199y 1972 (abstract). 269. Antilymphocyte serum-induced impairment of hepatic function. J.C. Pisano and N. R. Di Luzio. Gastroenterology 62:185, 1972 (abstract). ^ 270. Hepatic cellular functional alterations in acute lead intoxication. R. Trejo, L. i-ioiTmaim ami N. R. ui Luzio'. VIII Congreso Latino-Ajnericano de Anatomia Pathologies, Maracaibo, Venezuela (abstract), 1971. ^ 271. Hepatic ultrastructural alterations in acute lead intoxication. E. 0. Hoffmann, R. Trejo, J.Lamberty and N. R. Di Luzio. VIII Congreso Latino-Americano de Anatomia Pathologica, Maracaibo, Venezuela (abstract), 1971. 272. Alterations in plasma recognition factor activity in experimental leukemia. N. R. Di Luzio, F. Miller, R. McNamee and J. C. Pisano. Reticuloendothel. Soc. 11:186-197, 1972. 273. Macrophage recognition factor depletion following administration of particulate agents and leukemic cells. N. R. Di Luzio, R. McNamee, E. F. Miller and J. C. Pisano. J_. Reticuloendothel. Soc. 12:314-323, 1972. 274. Effect of prostaglandin E-i on cellular and humoral immune responses. L. D. loose and N. R. Di Luzio. ^3. Reticuloendothel. Soc. 13:70, 1973. ^"t^275. Antioxidants, lipid peroxidation and chemical-induced liver injury. H. R. Di Luzio. Fed. Proc. 32:1875-1881, 1973. 276. Employment of lipids in the measurement.and modification of cellular, humoral and immune responses of the RES. N. R. Di Luzio. Adv. Lipid Res. 10:43-86, 1972. m I0 Z 0 0 0 HA 277. Effect of DES on the intravascular clearance, tissue distribution and detoxification of S. enteritidis endotoxin. R. A.Trejo, L. D. Loose, and N. R. Di Luzio. The Physiologist 14:274, 1971 (abstract). 278. Isolation of immunogenic RNA from rat macrophages. P. E. Lentz and N. R. Di Luzio. The Physiologist 14:182, 1971 (abstract). 279. Influence of endotoxin administration on hepatic function of rats with altered endotoxin sensitivity. N. R. Di Luzio, R. Trejo and C. G. Crafton. J. Reticuloendothel. Soc. 11:637-653, 1972. 200. Reticuloendothelial function in immune-suppressed animals. J. C. Pisano, J. T. Patterson and N. R. Di Luzio. J. Reticuloendothel..Soc. 12:361-370, 1972. 281. Hepatotoxic effects of horse anti-mouse lymphocyte serum. 0. C. Pisano, J.* T. Patterson and N. R. Di Luzio. J.- Reticuloendothel. Soc. 12:361370, 1972. 282. Reticuloendothelial and hepatic function alterations, following lead, acetate administration. R. A. Trejo, H. R. Di Luzio, L. D. Loose and E. Hoffmann. Exp. Mol. Pathol. 17:145-159, 1972. 283. Influence of tobacco-smoke on the phagocytic, bactericidal and metabolic activities of rat alveolar macrophages. P. E. Lentz and N. R. Di Luzio. J. Reticuloendothel. Soc. 11:425-426, 1972 (abstract). 284. Comparative evaluation of macrophage inactivation of endotoxin. 0 A Trejo and N. R. Di Luzio. 1 rC`( :CC. Exp. Biol. Med. 144:901-905, 1973 285. Ultrastructural alterations of liver and spleen following acute lead administration in rats. E. 0. Hoffmann, R. A. Trejo, N. R. Di Luzio and J. Lamberty. J. Exp. Mol. Pathol. 17:159-170, 1972. 286. Surgery induced alterations in plasma recognition factor activity in normal renal donors and renal recipients. N. R. Di Luzio and E. S. Lindsey. Proc. Soc. Exp. Biol. Med. 143:715-718, 1973. 287. Influence of endotoxin tolerance on detoxification of S. enteritidis endotoxin by mouse liver and spleen. R. A. Trejo and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 141:501-505, 1972. 288. Malarial immunosuppression - a macrophage mediated defect. L. D. Loose, 0. A. Cook and N. R. Di Luzio. Proc. Helminth. Soc. 39:484-491, 1972. 289. Protective influence of pyrazole on ally] formate and allyl alcohol induced hepatic injury. T4 Working Session - Fatty Liver. U. R. Di Luzio and E. Hoffmann, 1972 (abstract). 290. Functional and ultrastructural modifications of Kupffer and parenchymal cells of acute lead-treated rats. N. R. Di Luzio, R. A. Trejo and E. 0. Hoffmann (abstract). 0I H U Z004JJHA 29 i. Mechanism of lead-induced endotoxin hypersensitivity. 5th International Congress of Pharmacology. R. A. Trejo, N. R. Di Luzio and E. 0.Hoffmann, (abstract), 1972. 292. Macrophage surveillance mechanisms in clinical and experimental neoplasia. H. R. Di Luzio and 0. C. Pisano. Internatl . Symposium. (Milan) (abstract), 1972. iX293. The effect of controlled hepatic insult on phagocytic activity in the subhuman primate liver. K. Holper, R. Trejo, M. R. Di Luzio and L. Brettschneider. Surgical Forum (abstract), 1972. 294. Endotoxin sensitivity in malaria infected mice. L. D. Loose, R. A. Tre.io and N. R. Di Luzio. The Plivsioloqist 14:186, 1971 (abstract). 295. Lead-cadmium endotoxin interactions. N. R. Di Luzio. Invited Testimony. Toxic Substances Control Act of 1973 - Hearings before the Environment Subcommittee of the Committee of Commerce - U.S.Senate #93-18, pp 216-234, 1973. -" 296. Survival following prolonged hepatic ischemia in the primate. L. Brettschneider, K. Helper, I. 01 cay, R. Trejo and N. R. Di Luzio, 4th Internatl. Congress Transplantation Soc., 1972 (abstract). 297. Role of macrophages in malaria induced immunosuppression. L. D. Loose, J. A. Cook and N. R. Di Luzio. The Physiologist 15:202, 1972. ^ 298. Enhanced endotoxin detoxification ability of liver and spleen during the state of endotoxin tolerance. R. A. Trejo and N. R, Di Luzio. . me Physiologist 45:289, 1972 (abstract). 299. Effect of prostaglandin E] on cellular and humoral immune responses. L. D. Loose and N. R. Di Luzio. 0. Reticuloendothelial Soc. 11:419, 1972 (abstract). ^ 300. Ultrastructural changes in the liver of subhuman primates following lead and endotoxin administration. E. Hoffmann, K. Holper, L. Brettschneider, N. R. Di Luzio and R. A. Trejo. Am. J. Pathol. 70:57a, 1973 (abstract). 301. Reticuloendothelial dysfunction and endotoxemia following portal vein occlusion. I. Olcay, A. Kitahama, R. H. Miller, T. Drapanas, R. A. Trejo, and N. R. Di Luzio. Surgery 75:64, 1973. 302. Phaaocvtosis in diseases. N. R. Di Luzio. Book Review. J. Histochem. Cytochem. 20, no. 12, 1972. 303. Enhancement of endotoxin shock in the lead sensitized subhuman primate. K. Holper, R. A. Trejo, L. Brettschneider, and N. R. Di Luzio. Surgery. Gynecol. Obstet. 136:593-601, 1973. 304. Suppression of P. berghei parasitemia and enhancement in survival by RE stimulation. L. D. Loose and N. R. Di Luzio. Comparative Biochem. Physiol. 4:201-207, 1973. i^ n m m e a lt .. 305. Environmental presence of endotoxin. N.R. 0i l.uzio and T. J. Friedmann. Nature 244:49, 1973. 306. Hepato-splenic detoxification of endotoxin: a macrophage function. R. A. Trejo and N. R. Di Luzio. Gastroenterology 64:200, 1973 (abstract). 307. Protective influence of pyrazol.e on ally! formate-induced injury. N. R. Di Luzio and E. 0. Hoffmann. Gastroenterology 64:158, 1973 (abstract). "" 303. Hepatic functional alterations during lead-endotoxin interaction in;the subhuman primate. L. Brettschneider, K. Holper, R. Trejo and N. R. Di Luzio. Gastroenterology 64:17/, 1973 (abstract). 309. Comparative status of hepatic cellular function following hepatic ischemia i-n the subhuman primate. K. Holper, I. Olcay, R. Trejo, R. Miller, A. Kitahama, L. Brettschneider and N. R. Di Luzio. Gastroenterology. 64-: 156, 1973 (abstract). 310. Light and electron microscopic changes in the liver of subhuman primates after endotoxin and lead administration. E. 0. Hoffmann, K. Holper, L. Brettschneider, N. R. Di Luzio and R. A.Trejo. J_. Reticuloendothel. Soc. 13:392-393, 1973 (abstract). 311. Comparative evaluation of particulate and bacterial opsonization by plasma of normal and neoplastic individuals. J. C. Pisano, J. P. Jackson and N. R. pi Luzio. Proc. Soc Exp. Biol. Med. 142:1355, 1973. 312. Functional alterations in alveolar macrophages exposed to cigarette smoko in vitro and in vivo. P. E. Lentz and N. R. Di Luzio. J_. Reticuloendothel. Soc. 13:350, 1973 (abstract). 313. Cyclic AMP as a possible regulator of the immune responses. E. F. Miller, J. C. Pisano and N. R. Di Luzio. 13:363, 1973 (abstract). J. Reticuloendothel. Soc. 314. Mechanism of protective effect of methyl prednisolone and cysteine in lead-acetate endotoxin induced shock. J. Cook, R. Trejo, E. Marconi and N. R. Di Luzio. J_. Reticuloendothel Soc. 13:384, 1973 (abstract). 315. Inactivation of S', enteritidis endotoxin by diverse macrophage populations, R. A. Trejo and N. R. Di Luzio. J_. Reticuloendothel. Soc. 13:385, 1973 (abstract). 316. Macrophage-mediated malarial immunosuppression. L. D. Loose, J. A. Cook and N. R. Di Luzio. J_. Reticuloendothel. Soc. 13:392, 1973 (abstract). 317. Deficiency of humoral recognition factor in thermal burn. R. McNamee, A. S. Goldman, N. R. Di Luzio, L. Loose and B. Rudloff. 0. Reticulo endothel . Soc. 13:394, 1973 (abstract). ^318. Protective influence of diphenyl-p-phenylenediamine (DPPD) on hydrazine induced lipid peroxidation and hepatic injury. T. E. Stege, E. 0. Hoffmann, and N. R. Di Luzio. Gastroenterology 64:A208/894, .1973. VRD 0002013259 319. Protective effect of cysteine and methyl prednisolone in lead acetate- endotoxin induced shock. J. A. Cook and N. R. Di Luzio. Exp. Mol. Pathol. 19:127-138, 1973. ' 320. Protective influence of DPPD on hydrazine induced lipid peroxidation and hepatic injury. N. R. Di Luzio, T. E. Stege and E. 0. Hoffmann. Exp. Mol. Pathol. 19:284-292, 1973. 321. Influence of macrophage activation and recognition factor administration on tumor growth. Fed. Proc., 1973 (abstract). 322. Autoimmunity in P. berghei malaria. L. D. Loose, and N. R. Di Luzio. Microbios 8:111, 1973. 323. Endotoxin sensitivity in cadmium acetate and lead acetate treated rats. J. A. Cook and N. R. Di Luzio. The Physiologist. 16:287, 1973 (abstract). 324. Reticuloendothelial (RE) dysfunction and enaotoxemia following portal vein occlusion (PVO). I. Olcay, A. Kitahama, R. H. Miller, R. A. Trejo, and N. R. Di Luzio. The Physiologist 16:412, 1973 (abstract). 325. Tumor development as influenced by humoral recognition factors. N. R. Di Luzio, R. McNamee, I. Olcay, A. Kitahama, R. Miller, and E. 0. Hoffmann. The Physiologist 16:296, 1973 (abstract). 326. Deficiency of plasma humoral recognition factor activity following burn injury. A. S. Goldman, H. B. Rudloff, R. McNamee, L. D. Loose and N. R. Di Luzio. J. Reticuloendothel. Soc. 15:193-198, 1974. 327. 'Inhibition of tumor growth by humoral recognition factors. N. R. Di Luzio, R. McNamee, I. Olcay, A. Kitaham, R. H. Miller. Proc. Soc. Exp. Biol. Med. 145:311-315, 1974. 328. Influence of portal vein occlusion on RE function and endotoxemia. I. Olcay, A. Kitahama, R. Miller, R. A. Trejo, T. Drapanas, and N. R. Di Luzio. Gastroenterology 65(3):A38/562, 1974. 329. Hepatic functional and ultrastructural changes due to lead or cadmium interaction with endotoxin. J. Cook, E. Hoffmann, and N. R. Di Luzio. Gastroenterology 65(3):A-10/534, 1974. 330. Recognition factors and cancer. N. R. Di Luzio. Guidelines to Metabolic Therapy. 2:2, 1973. 331. Peroxidation of lipids in alveolar macrophages and pulmonary protective factor by aqueous extracts of cigarette smoke. Arch. Environ. Health. P. E. Lentz and N. R. Di Luzio. 28:279, 1974. 332. Transport of alpha aminoisobutyric acid by alveolar macrophages incubated with cigarette smoke and nicotine. P. E. Lentz and N. R. Di Luzio. Arch Environ. Health 28:333-335, 1974. 333. Ultrastructural changes in the liver of baboons following lead and endotoxin administration. E. 0. Hoffmann, N. R. Di Luzio, K. Holper, L. Brettschneider and J. Coover* Lab. Invest. 30:311-319, 1974. 0 0 ltI0 l0 0 0 .J lW j/334. Pyrazole inhibition of ethanol, ally! alcohol and ally! formated induced hepatic injury. N. R. Di Luzio, T. Stege, and E. 0. Hoffmann. Biochemical, Epidemiological and Clinical Aspects of the Etiology of Alcoholic Liver Pathology. Internatl. Symp. Alcohol and Drug Research, 1973. ^'335. Lead, cadmium endotoxin interaction: effect on mortality and hepatic function. J. A. Cook, E. A. Marconi and N. R. Di Luzio. Toxicol. Appl. Pharmacol. 28:292-302, 1974. r*' 336. RE function: determinant for survival following hepatic ischemia in the baboon. I. Olcay, K. Holper, A. Kitahama, R. Miller, T. Drapanas, R. A. Trejo and N. R. Di Luzio. Surgery 76:643-653, 1974. v-337. Effect of ischemia on hepatic parenchymal and RE function in the baboon. K. Holper, I. Olcay, A. Kitahama, R. Miller, L. Brettschneider, T. Drapanase, R. A. Trejo and N. R.Di Luzio. Surgery 76:423-432, 1974. 338. Comparative evaluation of macrophage inactivation of endotoxin. Trejo, R. A. and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 144:901-905, 1973. 339. Macrophage recognition factors and neoplasia. N. R. Di Luzio. International Academy of Pathology Monograph. The Reticuloendothelial System, vol. 14, 1974. 340. Surgery induced alterations in plasma recognition factor activity in normal and renal donors and renal recipients. N. R. Di Luzio and E. S. Lindsey. Proc. Soc. Exp. Biol. Med. 143:715-718, 1973. 34.1. Vergleich von hepatocellularen funktionen nach akuter ieberischamie in uberlebenden und nicht uberlebenden Pavianen. K.' Holper, I. Olcay, R. Trejo, R. Miller, A. Kitaham, N. R. Di Luzio, L. Brettschneider and T. Drapanas. German Forum, 1974. ^ 342. Reticuloendothelial function and endotoxemia following hepatic ischemia in the primate. K. Holper, I.-Olcay, A. Kitaham, R, A. Trejo, R. Miller, L. Brettschneider, N. R. Di Luzio and T. Drapanas. Europ. Soc. Exp. Surgery, May, 1974, Salzburg. 343. Role of macrophages arrd recognition factors in tumor cell recognition and inhibition: an experimental and clinical study. .P.W.A. Mansell, E. T. Krementz, N. R. Di Luzio, I. Olcay, R. McNamee, and E. Hoffmann. Xlth Internatl. Cancer Congress,1974 (abstract). ^ 344. ^345. Alcohol and teh Liver. N. R. Di Luzio. 2nd Special Report to the U. S. Congress on Alcohol and Health, 1974. Prevention of hydrazine induced lipid peroxidation and hepatic injury by DPPD. T. E. Stege, E. 0. Hoffmann, and N. R. Di Luzio. Fed. Proc. (abstract), 1974. 346. Clinical Experiences with immunotherapy .of melanoma. Mansell, P. W. A., Krementz, E.'T. and Di Luzio, N. R. Symp. Immunological Responses to . Melanoma Antigen. Hanover, April 1974. (in press). V U U IB IB B B rflM 347. Comparative evaluation of immunogenic RNA of liver* splenic and peritoneal macrophages. P. E. Lentz and N, R. Di Luzio. J. Reticulo.endothel. Soc. (submitted, 1974). 348. Isolation of adult rat liver macrophages (von Kupffer cells) in .Biomembranes (cells, organelles and membraneous components). A volume of Methods in Enzymology. eds. S. P. Colowick and N. 0. Kaplan. Academic Press, New York, 1974. 349. Isolation of immunogenic RNA from liver, splenic and peritoneal macrophages. P. E. Lentz and N. R. Di Luzio. J. Reticuloendothel. Soc. (submitted, 1974). 350. Antibody-induced alterations of macrophage immunogenic activity. J. C. Pisano, E. F. Miller and N. R. Di Luzio. J. Reticuloendothel. Soc. (submitted), 1974. . 351. Cadmium acetate and endotoxin interaction: effect on hepatic parenchymal and Kupffer cell function and morphology. 0. A. Cook, E. 0. Hoffmann and N. R. Di Luzio. APS, 1974 (submitted) (Abstract). - 352. Functional- characteristics of isolated rat hepatic Kupffer and parenchymal cells. L. D. Loose, T. Stege, and N. R. Di Luzio, Gastroenterology (submitted), 1974. 353. Effect of cadmium on antibody production. L. D. Loose, J. A. Cook, N. R. Di Luzio. Clin. Res. (in press), 1974, 354. Comparative uptake of BSP by isolated Kupffer and parenchymal cells. T. Stege, L. D. Loose, and N. R. Di Luzio. APS, 1974 (submitted) abstract. 355. Rol de los macrofagos y factores de reconocimiento en la neoplasia clinica y experimental. N. R. Di Luzio and E. 0. Hoffmann.. XI Congreso Lateinoamericano de Patologia (abstract), no. 7, 1973. ^3S6. The effect of acute cadmium administration in the liver and kidney of the rat. E. 0. Hoffmann, J. A. Cook, N. R. Di Luzio and J. A. Coover, Lab; Invest. 1974 (submitted). 357.. Comparative endotoxin_susceptibility of newborn and adult rats following lead acetate or cadmium acetate administration. J. A. Cook, E. 0. Hoffmann, E. A. Marconi and N. R. Di Luzio. Proc. Soc. Exp. Biol. Med. 1974 (submitted). 358. Macrophage mediated destruction of human malignant cells in vivo. Mansell, P. W. A., Ichinose, H., Reed, R. 0,, Krementz, E. T. McNamee, R. and Di Luzio, N. R. J. Natl. Cancer Inst, (submitted), 1974. X 359. Factors modifying susceptibility to bacterial endotoxin: the effect of lead and cadmium. J. A. Cook* N. R. Oi Luzio and E. 0. Hoffmann. CRC Critical Review Journal (in press). ^ 360. Glucan mediated macrophage-induced necrosis of human malignant cells. N. R. Di Luzio, P, W. A. Mansell, R. McPlamee, E. T. Krementz, H. Ichinose and R. J. Reed. Federation Proc. (abstract) (submitted), 1974.