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Lorillard

Federation of American Societies for Experimental Biology, Dallas, 790401 - 790410

Date: 07 May 1979
Length: 6 pages
03732248-03732253
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Author
Zahn, L.S.
Type
MEMO, MEMORANDUM
LIST, LIST
Area
LEGAL DEPT FILE ROOM
Request
R1-004
Alias
03732248/03732253
Master ID
03732159/2629

Related Documents:
Document File
03732159/03732629/S and H Re Smoking and Health General Volume 3 780901790605.
Named Organization
Federation of American Societies Fo
Intl Academy of Pathology
Leonard Zahn + Associates
Tobacco + Health Lab
Usda, U.S. Dept of Agriculture
Ctr, Council for Tobacco Research
Copied
Y, A.
G, W.U.
H, R.C.
Stevens, A.J.
Litigation
Stmn/Produced
Recipient
Hoyt, W.T.
Date Loaded
05 Jun 1998
Named Person
Shelburne, J.D.
Brody
Carp, H.
Craighead
Harel, S.
Hawkins, H.K.
Hitchcock, D.R.
Janoff, A.
Louis, T.M.
Maron, M.B.
Penney, D.
Schepartz, A.I.
Shamberger, R.J.
Site
N14
Author (Organization)
Leonard Zahn + Associates
Characteristic
MARG, MARGINALIA
UCSF Legacy ID
ukz61e00

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Page 1: ukz61e00
C May 7, 1979 W..."T~. Hoyt ~ ~ CC: AY WtTCx. Leonard S. Zahn RCHi SUBJECT: Federation of American Societies for Experimental Biology, Dallas, April 1-10, 1979 The Federation tried a r'stretch" appr©ach~ to its meeting usual five-day meeting has resulted in a tremendous crush of people and papers. It's anybody''s guess what will be done about the stretch-out. On the other hand, the Federation's were p.Veased with the aarrange.uzent. Many scientists complainedi peared that only the'hotels,,'restaurants and taxi companies` five days,'the other three for the second five days: It ap- this year: three constituent societies met during the first next year. At any rate, 'attendance throughout totaled about 2'0„ 0!00,, lkeeping,intact the Federation's claimita holding the world's largest,aaanual scientifiic session. More than 7,000! papers were presented, yet press coverage and attendance were quite limited. Indeed,, the local newspapers covered the meeting sporadically and no major lay media from elsewhere were rep- ~resented. Only two reporters remained for the full 10idays ' and they were from foreigncountries. 'Snmking, was the sub jlec of se leral reports„ but only one (ozone treatment of tobacco -- see b!elow) attracted'some slight press attentiion, and that was because it came early . inithe meeting and was written up in a Federation press re- Thus,, when the tobacco is burned, lower amounts of PAH aree found~. The ozone treatment also leads to lowered levels of' The high]lights : 1. "'Removal of PAH precursors from tobacco by treatment with ozone,"-- A. I. Schepartz, Athens„ Ga. (Tobaicco and! Health Laboratory, U!.S. Dept. of Agriculture). Previous work inihis laboratory has shown that most of the polycyclic aromatic hydrocarbons (,PAHs) in ciigarette smoke tar come from the com- bustion of'lipids in the tobacco. He and his associates have devised a method that decomposes these lipids and'„ therefore, s leadsto: a signif'icantd'ecreaseinPAHs when the tobacco is,burned'.~ ,. ~:- The method consists of treating the tobacco with ozone which results in oxidation and decomposition of the lipids. eonard (P. OL BOX 223), 13 LINCOLN'ROAD • GREAT NECK„N.Y'. 11021 •(212) 695-7445' lease.. ~~~~ PUBLIC RELAT'ION~SCOUNSEL l:(/~(Y andAssaeiateslnc
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nicotine and phenolic compounds. "These ffhdingS indicate that it `should be feasible to of'lung cancer," Schepartz said. Hbwever„ he addied, more re- search is needed to compare the health effects of ozone-treated tobacco with those of untreated tobacco. treat tobacco with ozone on a large scale, thus producing sa- fer cigarettes and resusting,in a redh,iction in the incidence literature on the presence of respirable inorganic particles in 'cigarette `smoke,, Shelburne said only a single report (by'',: smoken' -- J. D. Shelburne, Durham~,. N.C. Reviewing, the brief 2. "Respirable siilicon-positive particles in cigarette (3' filtered, I unfiltered), showed abo ut 8 times more Si than Shelburne said, his study of four popular brandis of.oiigarettes amounts by weight of aluminumi(Al) and silicon (Si)!. 'However~,' thydrat~ed aluminum dis~~ilicate~)~'~., Kaolinit~e~ has about ~eiqua~l 't'-' .Bro,dy-Craighead) had a one-sentence reference to kaolinite `' .A1 by weight ` Some of' the Si particles in smoke are not of' respirabl'e tained from the lungs of smokers showed large amounts of Si. In smok-~;,`.47%9 of the particles he has looked at are positive for Si.'Si-containing particlies also have been found on green size, he said. Electron microscopic study of macrophages ob- , tobacco leaves. The Si could be h,armful,; `b ut the' particl:es `cou]1d easily be re- moved during,processing,, if they are on the leaf. However,, if'they are part of the leaf,, they could not be washed out. During Q and A, Shelburne 'speculated, the.inroganic particless i emy of Pathology.) similar report at the recent meeting, of the International Acad- be dangerou:s." . . - . . _ _; . __ . . . . (One olf She7.burne"s associates, Hal K. Hawkins,delivered a or be related to the development of emphysema. However, the role of the particles really is vnknowni; they may 'r'possibly could be carriers for carcinogens in smoke such ais blenao(a)!Py- rene. If the particles are of quartz, they could cause fibrosis 3- rnL'ung, in jiury induced byc leukocytic proteases" -- Aaron Janoff, Stony Brook, N.Y. ][n what was mostly a'''state-of-the- artn' lecture, C1R' grantee J'anoff reviewed recent research on enzyme injury of the lung. He also discussed what mig]ht be calledi his I"new'"i beliefs concez-ning, two different proteases that damage lung connective -6ssue, -resulting in emphyserna. Cigarette smoking was mentionedifrequently. pulmonary alveolar macroph~ages~~ (~PAMs~~)! .~ The~~se~ are the~ main candidates damaging~ proteas~es --~~ polymorphonucle~ar~ leukocytes (~,PMN~s): and ~ O W W A There probably are two majior sources in the body for tissue-~ ~;
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for consideration in any discussion of lung, injury induced zyme. by leukocytke proteases. Each secretes a different type of en- 'the disease seems to be correlated'with environmental risk tims are genetically normal for Al Pi, and in these:persons ~ small percentage of affected individuals. Most emphysema vic- physema associated with inhibitor deficiency represents a:'very 'leased from neutrophils. In humans, centroacinar type of em.- Janoff'''s current view is that emphysema may be produced by an imbalance between the major inhibitor of protease -- alpha-1 antiprotease inhibitor (Al Pi)i -- and enzymes re- __.,r j . : . ,. . . . ,... . . . ...,: . ant °.: -~~ 4 ~ , . ,,.; . :,.:< .r~ .~.. .. , x: iactors,, 01- which cigarette smoking, is one of the_most 'impor- ~,,.~ ~'; . .. , . , Tobacco smoke may contain substances that suppress the lung,''s elastase-inhibiting capacity, thus upsetting the "'delicate" balance between proteases and antiproteases. '--'•'r' activity of neutrophilic elastase. ' There are several pathways of protease-mediated lung in- jury in emphysema. He currently feels thatt panacinar'emphysema of the Al Pi deficient person results from the n'unrestricted,1° resistant to inhibitory action. :..:. i. , . . ::.. On the ©ther hand, centroacinar emphysemai of the cigarette smoker may result from either of two, pathways :(1) the same en- zyme may be the determiinant..of"lung injury by suppressing the inhibitor through oxidiating, activi.ty of tobacco smoke;, (,2'), en- zymes fr.Qm the PAMs may augment secretion of elastase that is. Elastase released by PAMs is "'trivial" in amount compared to that released by PMNs„ but these small amounts "may be a potent mediator" of lung injury. :~'These enzymes are radically different,'Inhibitors of one do not affect the other.,'" tissues.. those provided by Janoiff. He said that oxidative inactivation of Al Pi in the "miicroenviromment'r of' PMNI may permit proteases, released from these cells to inore readily damage inflamed lung acity by oxidants from PMN, "1 giving more detailed data than Two other papers dealing with emphysema were presented by members of Janoff's group. : H. Carp spoke on "'Suppression of elastase inhibitory cap- S. Harel, speaking on "Immunologic assay of'li.ung elastin degradation,"' noted that degradation of connective tissue
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elastin leads to an increased urinary excretion of desmosine, an ami.no acid unique to elastin. She described work aimed at developing,alradlioimmunoassay for urinary desmosine. the gas and oil fields of west Texas. ;.. wetlands . and' als.o _:occupati:onal. exposure_ to . the gas occurs in f.ide,, he said. The research provides a tentative explanation ~ f_,or,thee]levat.ed lung cancer rates in whitema~les found in manynon-industrialized rural counties in south Atl'antic- and Gulf' Coast states. Hydrogen sulfide is found in coastal and inland tween lung,cancer mortality and the presence of hydrogen sul- His preliminary study has found evidence of an association be- Both Carp and Harel credited CTR with support for their work. 4. "Lung cancer mortality and hydrogen sulfide sources in •%l ... 1I, ~,r~. southeastern coastal states" -- D. R. Hitchcock, Farmington, C'onn.. producedlin the atmosphere from hydrogen sulfide, which is a natural.produc~t~o~~f bacteral mietabol'ism!in wet soilds. ~ Hitchcock undertook his study because of'evidence that sul- furic acid mist, a common constituent of'polluted air, can be - .Texas . ,~ Speculating that the factor linking lung I cancer in cities and in some rural locations might be the common presence of sulfuric_acid mist, he analyzed the relationship between white male lung,cancer.mortality,.iniall rural counties in Maryland, Virginia, North and South Carolina, Georgia,, Louisiana and Rural counties in tholse states were classified in terms of the presence or absence of industries entailing,a high lung cancer risk and/or those entailing hydrogenisulfide exposure, and also in terms of the presence of'wetlands (salt water and fresh water).. . A hig#h ranking of lung cancer mortality was found more fre- quently in counties with wetlands than those without wetlands. -.Thiis was true regardless of whether the counties had high lung cancer risk industries or with hydrogenisu!lfid!e exposures.. Hiitchcock noted'that his study was not conclusive proof that hydrogen sulfide exposure or sulfuric acid mist increasess the risk of'getting lung cancer. However,, he said his findings "'confirmithe very strong,possibility of a causal link that should be explored further. t' Some industries that havebeern associated withevidence, of an increased lug g cancer risk (chemical, rubber, nickel re.- fining, coak coking) alsolentail hydrogen sulfide exposure, andi the gals is also a constituent of cigarette smoke. ""The sig- nificance of these associations remains to be determiined.r'
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5. Hitchcock said that last year, scientists in Louisiana had reported'tha_t lung cancer mortality rates in males in that state varied significantly with the proportion of' wetlands in the county of residence. 5. "Cardiac effects of pre- and postnatal carbon monoxide (,CO)i exposure"' -- D. Penney, Detroit. In a poster presentation, Penney briefly d'es ribed results of'experiments in which~groups of rats were exposed to C0. One group was exposed to 200ippm for 15 days. Another group of pre-natally CO-exposed newborn was removed to CO-AIR while another group was exposed' to 50!0 Ppm CO for 28 more days. A third group of rats served as contlrols with no C0O r exposure. : Litter sizes and birth weights from C0-exposed mothers were smaller than in the AIR group. Cardiomegaly developed in the CO group witihiheart weight/body weight ratios being twice that of the AIR' group at 14' days of age. After 1051 days the rats were killed and their hearts dissected andi examined. Heart weight/body weight ratios of the CO group were significantly higher thanithose of the AIR and!C0-AIR gro ups .The dataisuggest no permanent gross morphological change results from chronical prenatal CO exposure, Penney„concluded,, but changes are seen in early prenatal exposure. 6. "Progesterone, prostaglandin (PG) F2alpha, " a7e.d fetal and placental weights after chronic administration of'nicotine in near term guinea pigs'n' -- T. M. Louis, Greenville, N.C. Ex- periments were done to study the effects of nicotine on certain aspects related tolpregnancy. Guinea pigs were used because r their responses are in many ways similar to those of pregnant women. :Sixty female guinea pigs were assigned at random either to nicotine or saline treatment. Nicotine at_the rate of 3 mg/kg/ day or'saline was given twiced'aiily throughoutthe:entire g,es- -tational perio!dl. Maternal weightt'and' food-water intake were mea- sured' daily. The nicotine-treated animals consumedy essentially the same amout of food as the controls. Crown rump lengths of the neonates did not vary at birth,, andi gestati;on times were the same for both groups„ as were the number of live births. However, nicotinized neonates weighed less than control neo- nates. Also, there was a decrease in transverse head dia- meter in the former. There were no signs of malformation. Progesterone and P'C F2a wEre not affected by the chronic ad- N ministration of the relatively high d'osage"of nicotine. Fetal N- weights and placental weights were lower in the nicotine- ~ treated animals.
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6. vented from reaching the lungs, the pressure increases were virtuallyelim~ina~ted. Fu]lmonaryvasocons:triction occurred ini both nificantly elevated. When the adrenal venous blood was pre- constant flow and outflow pressure withiblood from the left pu]- monaryartery. When adrenal venous blood wasd~iverted (,intotheo vena cava) andinicotine injected into the left ventricle or as- cending aorta,, pulmonary arterial-left atrial pressure was sig- in anesthetized dogs was isolated; the LLL was.perfused at a scribed research in wnichithe lower left lung lobe ('LLL)! perfusion 7~.~ "Adrenal c~ompon~ent~ tothe~ pulmo~~nary~~ hypertension elicited by nicotine~-in the dog" -- M. Bi. M'aron,i Milwaukee. Maron de- LLL andlthe right lung in response to the nicotine, hypertension. neural reflex„ wais the majior factor in eliciting the pulmonary as,a resUt _of the nicotine injection, rather .than a direct Maron concluded that the release of adrenal catecholamiines,, 8. I'Blood selenium and human heart mortality in 19 states", geographic inverse_correlation between four kinds of heart dis- ease and selenium in blood bank blood from 1i9 states. The epi- , demiolog;ic studyshowed that in states~whiereselenium!is found in high concentrations, the coronary heart disease rate, high blood pressure rate, cerebrotirascu!lar death rate, and car- diovascular renal.death rate were significantly lower than in. _.states where selenium is found in-lesser bloodlconcentrations. ,, - - . S!elenium is a heavy, metal-like substance that is essential Raymond J. Shamberger, Cleveland. He has fow:ndia significant unknown, Shamberger said. . ,, ., to well-being but its precise action inhuman heart disease is water consumption. Inisplite of' a good food distri:bution net- work„-regionall blood blood selenium differences do occur. Zthis leads us to believe that other factors may be involved. Perhaps selenium could be inhaled as part of airborne matter. Other scientists have shown that lead is present in the dust of'the lead belt areas around Missouri and that people living there have high lead levels in their blood. The same could be true for seleni.um.'1 ' body, n1' he said. WMost selenium is takenlin through food and "We do not know entirely how selenium is taken in by the Shamberger also cited evidence linking selenium to a re- duction in the frequency of deaths from certain cancers, par- ticularly cancers of the breast and colon. SN'3.ti 6Z6j ~ ~ A VYq -- Qh I ~ ~, ~ ~I

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