Document gDmnQv7RyOrp2woQ4ZbwYxBne

460.0902 - Asbestos PLS. FY1 -Wc HNDL/ v GAY C/ufffid )j /0-<y SOUTHWESTERN BELL RECORD COPY Docunert review date_____ __________ _ (Red stamp denotes office Be copy.) Houston, March 7 > 1990 QUIROGA WARRICK WHITE [/ /rruuou DISTRICT MANAGER-ARCHITECTURE-Dallas: -^DISTRICT MANAGER-ARCHITECTURE-San Antonio: This letter is to confirm our previous telephone conversation concerning air sampling in the various 'locations wfere^rtable or potentially friable asbestos has been identified. As you know, Mr. Shaffer has requested that this be done in those buildings in order to assure the continued health and safety of SWBT employees. Therefore, please, review all buildings known to contain friable or potentially Triable jiabestos and establish! an air samp 1 ing?P rogram Tor each. The testing sKould Ibe"conducted at least semiannually, and should comply with all OSHA standards as welJTas dlT ulO-100-904. Samples should be analyzed by Phase Contrast Microscopy. If the sample results are at or exceed the OSHA action level of 0.1 fiber/cc, then the sample should be re-analyzed using Transmission Electron Microscopy to confirm the presence of asbestos. Please advise me in writing, by March 21, of your schedule for implementation. I am also requesting that test rpsiii.ts IS)e provided tome f or review as they are obtained?" A form will be provided to you for this purpose. Please address any questions you or your staff may have to me on 713-521-8976. irea ManagerEnvironmental Regulations Operations Staff AVP-Support Services Attachment CC: Assistant Vice President-Support Services-Dallas Division Manager-Real Estate Management-Houston: 004804 460.0902 - Asbestos S0UTnrtf.STE3U BELL RECORD COPY Document review date (Red stamp denotes official file copy.)' St. Louis, January , 1990 MR. FOSTER: Attached is a copy of the asbestos study that appeared in the January 19 edition of the Science journal. The study focuses on the health hazards associated with asbestos exposure and the Environmental Protection Agency's (EPA) rule that requires schools to establish plans for managing asbestos. It should be pointed out that Southwestern Bell is not legally required to. ^comply with this EPA rule and our asbestos program is not based on 'the EPA regulations' The Company's building management program on asbestos was developed to comply with our legal requirements under regulations established by the Occupational Safety and Health Administration (OSHA). The OSHA requirements are not addressed in the attached study. Of particular significance is the study's challenge to that part of the EPA's school rule that requires visual inspection of asbestos as a means of determining the need for abatement. As an alternative to visual inspection, the study recommends taking air samples to determine the amount of asbestos in the air. This is the method recommended by OSHA and is the approach outlined in the Company's building management program. Under the Company's current instructions, the state Safety representatives are responsible for conducting periodic air sampling as a means of detecting deterioration of asbestos in Company buildings that contain potentially friable (i.e., blown-on) asbestos. Abatement would be recommended in those cases in which the air sample results indicated that the asbestos was deteriorating and was approaching QSHA's regulated limit of 0.1 fibers per cubic centimeter of air on an eight hour time-weighted average. To date, no abatement has been required under these circumstances. I will be available to discuss this matter with you at your convenience. Procurement Vice President-Procurement Attachment John WHemswi 004805 Asbestos: Scientific Developments and Implications for Public Policy B. T. Mossmax, J. Bignon, M. Corn, A. Seaton. J. B. L. Gee Asbestos is i commercial term for t group of fibrous Physico-Chemical Characteristics of Asbestos minerals often associated with the development ofpolmo* "Asbestos* is a broad commercial term tor a group of naxursiiy asrv incersxzsai fibrosis (ssbatosis), lung cancer, and occurring hydrated silicates that crystallize in a fibrous habit. The maftcpnanr mesothelioma in occapaannaily exposed indi- legal definition ofa fiber aa promulgates by the EPA and other C.5. viduais. The pathogenicity of diifigcnt forms of asbestos regulatory agenaes is one that possesses a 23:1 aspect rata. varies long, thin amphiboie fibers are most pathogenic, However, this definition ha been crinexed by mmerticgists id). particularly in the inaucaon of mesothelioma. Available Asbestos fiben in ores are not respuioie unni released and made data do not support the concept that low-level exposure airborne during mining and processing. The family of isbeams to asbestos is a health hazard'in buildings and schools. mmcrais can be subdivided mm serpentine and amphiboie libera The concentration of asbestos fibers in air, type of asbes (Fig. 1). Chrysoolc, which accounts tor over 90% of me worid's tos, and size of fibers must be considered in evaluation of producson of asbestos, is the most common fibrous serpesnne. potential health risks. whereas the amphiboies. a chemically diverse group of less incusrr.- aily important minerals, mriude the fibrous mmcrais and crcecoiits. amosire. anmophvllis asbestos. aennoiite abeams, and treswiite asbestos. Tremoutr, aennoiite and anrnophyilite, whicn occur in SSZStOS EXGSXDEIS 30TX FSA1 AKS PAXtC IX U.S. bath fibrous and nonnbtous harms, have been oniy tareiv mined for Asocstv. Observation out asbestos-containing materals use is commercial ubeasos. Both the fibrous and noisferous terms .'ACM', have oesn uses x. schools, bminings, and hosptous, of these amphiboie mmcrais are somenms tcund u conamauna ana the Ascestas Hazard Emergmcv Reapatue Act (AHERAo)f, caommercial depones of chrysccie. tarn. vemuemite. ms otner manoate hem the Environmental. Prctesson Agency (EPA, that mmcrais (4). The Bonfibroua sums of croadoiire and amente are requires inspection or" the nzusn'i puoiic and pnvtte schoais for refered to u rieoedore and gruaerte. respectrmr. asbestos, have rcsuiiea in the ecpicuve growth at asbestos idcszmcx- The vanous types of ubesnas fibers differ m their chesscal non and removal companies. 3v EPA essmaxm, cirenuon of EPA compoaeon. morphology, and durabiiitY. Therefore. Pre etoiogic reauiremena to apprrsnmatciv 733,000 public and commcrcal sfeca ihnuid be considered individually for each fiber type. Ideana- buildings containing asbestos wiii cost $53 billion, discounted at anon at speeds types of asbestos in air samples requires septum- 10% over 30 yean (1). Because of uscerainoei regarding the cited technology sues as transmission electron microscopy, z-rey amount of ubescos and its conaiaon m dese buildings, esnmaro difihenon. or energy dispersive x-ray spectroscopy. The rod-like for removal of asbestos are as high as $100 to $1S0 bdlion (2). ampniboles appear to penetrate the penpnerai lung more resdilv Asbestos wu shown to cause asocsnrars as the turn ofthe century. Its aviogannn with the ransanm of bug sad pleural tumors in asbestos minen and wonten was demooeenad in the 1950s and 1960a, respecavdy (J). An igseront issue is whether mese diseases ire aiao hazarss to the general pooutaoon << m airbome levels of asbestos in tchoois and other auiidingi. Does avaiiehic evidence support the concept that asbestos causes disease m tbs nonoccupa- donsi BmuBHffwirt What are ms mechanised of asbestos-induced Table 1. Summary sonsen ear avenge airborne fiber eonctssssecs m UA. yhras (II) ana buildings (ID. The asm asm in the akaisnen ct ucs static are the average cnnmigmaBa(rrpmsartsBuabgabets gresag (ha I me m ieegut per cubie aramrm ur) in a bedding {(at odoor nmam) or me eaecrastrsoen ouxsxk ads buiidieg (for ouaooer massa (ID]. By visual inspemm. wixgory 1 buildings corounca no nowres- CBROlBRg n--wl (ACM)- my'y 3 fnimworf ACM IB ORSBar* Uv foou coauoon. and buddisfe a category I dsewva it tease mc'am of fibrogenesa and ORussfacsu.1 Mos unporoniy, have tecent data ACM. la the study on public buildings, 387 Indoor been idnauieety in m tfa United Surra for regulation ana banning of aibeaaoat In this trade, we summarize devciopmcns their for sod 41 aadoor air saaeta were evahuad. No uoe fibers wm deseed a 13% of the 317 sstapis. The sense* mm ia givai u pureauu oeow cash haedmy. public peiicv. j ' , YT QS40C. I. iT( . M. Com anr of t DMmi f ' Kveaat me ?iauc Hamm. Mae Estonian. MO 1UOS.A. S<vxaar<xM Incan ac Oca Madwgn. Sohm SHI MC 1.1. - Gn Scheois -- (71) sir ( Median 0.00000 Mm 0.00024* a00039 SD 0.00033 0.00090 Public bmidis^s Csagorv 1 !0) Cteasry 2 (61 <7ST 0.00010 0.00099 0.00191 0.00040 0.00039 0.00032 0.000U QJX073 0.00072 004806 Flj. 1. Cuusncsr. ina morcr-ciosy cr iscestcs iibr3. The insertcs mcmzncii ire isacnir.g acerrors rrsereznem ot Union incerr.innnut eoorre ic Cir-ar etcererxe iimcta or enmoute A i*ft' irx croeioouse uoatos tflgnt) (beia ct view u -12 wn in bora pnotognomi. The un* piuDotes ire eepictto ta oraer si car rtunve industrial imocrtance. =ro*non* I Cifyscm* Mg.S.O^iCHl, Aibattos America* Croeicait* Ntjtfe1 j.F** !;Sif2jy3H1j Amosit* iF*. Anmeonytme Trtmail* Acitnem* iMg.raUSigCjgiCHIj Ca,M54Sl,03IlCHI, Cl,iMg.s#i5S.,S,,:CHi- cun chryscaie fibers. which ire curhr, can ocas in bundles, and ean be intercepted a: urwav oifiirscciu (Fig. 1). The chnrucai makeup at each fiber type is complex, ana fibers may conns at a vinery of trace mesas and organic camseunna acquired in ores or during processing. Asbestos is artraenve to indusov oecause of its resistance to heat ann cnemicais. hign tenslie strenzm. and lower cost compares co man-mine rrurer.m. Aithougn -as: of tpray-on asbeseos as a fire proofing macenai or tnsuiason nas seen banned in this counov, aa well as in several European ccunm.es, ubeseos is incorporates currently into cement conscrucoon materials (roofing, shingles, and cement pipm, meson isateuu 'brass linings and dutch pad*), jotnong ana gaskets. asphait esaa ana seaisnts, and other similar proauen. As a result of these appiicacons. an estimated 20% of buddings including nospiois. sermon. and other puhiie and private strucrures contain ACM (I). Aicestos ui buddings does not ipoma* neousiv sneo fibers, but pnysicai damage to ACM by deeav, rtswvancn. or oemsunon can cause rexasr of airborne fibers (i). Diseases Associated with Occupational Exposure to Asbestos Occupational exposure to ucores can cause tour types of disar- das: asocstosia; lung cancer, ssetnciiemaa ofthe pleura, pencami- um. and pensneum: and bemgn cnanga in the ptaxm (J). Aabato- ns, a puimotury intrrnanal fibmns with cmciiiv* deposition of collagen, mused progressive rung impaired gas ccehange, disability, ana dean us many worsen etprmd betbre the cnrbru- mas at acespanonai sancarca. Lung cancers. that is, tumors rasing in gacneooroncuai eptceiiai or alveolar tpitheiiai cak. have occurred in asbestos worsen in most eases 20 or men years ana rhea first exposure a asbestos. In general, lung cancers have been found in aaocseos worsen wno ire and only rarchr m nemmoem itf). A nuoscr of cpidcruoiogic studies have indicated chat the reason cetwmi ens aweiepment of hug caneera and cumulative exposure to asbestos 11 appranmarchr linear, but wide varanona in nope of tbs line occur apparently related co fiber type ana mauarrui usage (7). Dears nas ns hag canccn in aaboeos worsen, aa measured by stanaard momlity raaoa (SMRsh the oosenrad mereautv of a cohort ehnded by the mortality of a control population, are lowest a cnrvsonie mitten and worsen mamriac- curing mcnon mazoiais. In ccnsait, lung m Mg*** m those minin* and wonoot with asbestos. Tcmie exnibited a sending increase in lung cancers with duraccn of exposure when compared to Canadian enrysode miners mummers. Solvents and oils in texoic producon might act as ccearemczens in the development of these lung tumors (7). Diffuse malignant mesotneiioma is a fatal tumor truing from mesothedai ceils or underiving meserxavraai ceds in me pieura. pericardium. and peritoneum i3). The nme between siagnosts and inmal occupanonai exposure to asbestos commomy exceeds 30 yean. Smoking evidently dues not enhance nsk of mesomedoma in ubetoa worsen (J). Althougn mesotneiiomaa are curemeiy rare malignances, mat is, onlv 1648 wen rtcorrirri from 1973 co 1984 in one survey covering approximately 10% of the U.5. population (F), they may account tor as ouch is 18% of the proporccnai mortality in crogdoiitt worsen (20). Mcsocnciiamai also have been observed ate household exposure of family meacen of asocnoa workers and in individuals living in dose prenrmtv to asbeseos mines (11). Although mesotneiioma has beta ccniidered bv some as a disrate pathognomonic of apesure to asbestos, appreamatsiy 20 co 30% a mesotneiiomaa occur in me geneni population in adults not ctpmud occupanonailv to asbestos 112). Mesomedomas art raresY found in children. Diagnosis a memrhriinmas ia a challenge as the tumor mav resembk mcnanacs of ocher tumor types occurring in the pieura. or penseneum and assume a wide vinery of nucro*copic appearances. Thus, death >** m*y ether underesdmate (because these turnon are asnbuted to cancers of the gainomtemnai tract and aster organs) (II) or ovcresaznace the innrimee of meaomedomaa. In France, mesoeheiiomaa are nwginmimi by a ricror of 3 on deans cemficaiea m companion to the mesothelioma registry (24). A at pieuni changes ***** fircHr cmw runcsaoai impamneat have bees obaervea us asbestos worsen. These tnehide picini effusiaai. pieuni fibrosas, piruni plaques, that is. tccumuia- ucni of acdlular collagen ots mm ym chest waiL and paeudocumoea or of the iuag orea asaocimt wim plaques. The* pieuni changes any refiea exposure a asaestos but have no demonacarcd relation oo the dcvxiuumcnt ofmewtneiioraa. Turnon of the garausaosai net. iarvnx. and other organs mending the kidser, ovarv, pancreas, penoudhus. eye. and iym- 004807 '.vorxers : 13. IT.. In ecneru. me enhanced SMRs sbr these anon are not stansncaiiv disongutinioie from norma; fiMRs ir.c have not beer, confirmed a most tenons. Bom iarvngcai ana 5ajtrou1tescr.11 rumors nave otner ec0i05-.es acn as smoxing, uennou diet, me intestinal poivposu that ccrrcuna me mterpretaaon of cpioemnlogic data. The Amphiboie Hypothesis TI\e association of mesomcuoma with asbestos croarure wu ant describes in i960 in the normwest Case area ot'Saum Africa where long, dun croadolire r.ben svert mined (16). Since them an increases incidence at mesemeiisma has been reported in a number of occupational settings incusing aetories that presunubiy used oniy chrysoak. Within me past decade, sophisticated technology has aiiowes examination of e types of libers in the lung tissue of these worsen. Resuin reveaud mat many ehryscak-cxposed work ers snowea an aporedabk lung burden of amphibeie fiben, which were used tor bnefperiods in the workpiace (17). The perusecoca of ampruooies in human hangs may be aareburea to dieir menses ability to penetrate the perepneni lung, lack of clearance, or durabilizv. In contrast ehrnonk has been found post-mortem in imailer amounts tnan cxpcces a die lungs of asbestos workers (13). It disappear] with cme most ukeiv because magnesium and silica, are leached com che fibers (IF . Recently, the lung content of asbestos and nonasbestos fiber* has been compared in diagnosed cases of mesotneiioma. lung cancer, and cardiovascular disease (controls') from the western coast of France, a region containing shipyards (20). The number of amphibeie nbes (croadoiite and amosne; was sigmficannv higher in lungs from mesotneiioma patients, whereas numbers of ehrysc'tiie ana nonasbestos libers were similar in ail groups. These dan suggest mat me lung burden of chrysaoie and nonasoestos libers bean no reason to die occurrence of these cancers. Severn recent studies incicax mar die r.sk of pleural mesomeliama is tower wnere chrysoak u used witnout admixture or coizaminanon oy ampniboics (21). :s: sample a gradation of death rates from mesotneiioma has beer. observed in both male and femaie asoesms-exposed cohorts. Mesothelioma has bees responsible tor approximately 6 to 8% or' is prepomonai mortality in men womng witn mixtures cnrirm-ifg errairiniirr or araphibok (crockolite or amesite: in companjos to less than 1% of tie prepomonai mortality in men working witn amcok (10). In fianak cohorts, die proportional mortaiirv from mesothelioma wu highest tor amphibok exposure (10.6S': and lowest tax rfcry"wi expewre (0.2%1. Thus, these data suggest that amphibnkl are the major cause of mssomeiiomu m aseestss workers. Chrysoak miners and mr.kn in Quebec who wee supposedly exposed oniy to chrvsnnk have aevcioped Sew maochejinmu (22). However, recent fiber analyses on the tuagi of both there workers and chrysebk factory woexers snowed the presence of tremotits (2J). This amphibok in the ahraui form hu been rnmijrami as the causanve ages of maomeunmaa and lug cancan in miners exposcu to verm-.cuiitg heavuv coataminattd with tremoiae (24). Although semoiue composes teas than 1% of the asbestos dux in the Quebec mines and suds, the reiatrve ratio of tranoha so chrysoak abets m the lungs of Canadian miners and sullen d related directly rs their risk of developing mesothelioma (25). For the reasons above me few aeeothciiomaa observed in Canadian chrysoak worsen appear to be ..... . b fibrous tremolire. an Obscrvaoon compaabk with other evidence that amphiboies are me sox pamegense ubunrorm mmeraia. Likewise, recent data on London assesses ftcrory worses show due the levenv of asbestosu anc carcnama of ms :ung (as weu as mesotnelicmai correlates witn ms .ung surcen of trecdsiis inn imoaitc usesccs and chat me proportions of chrcoak ana nonasbestos fibers are cccrcasea in comparison to masses ccmrei pscents i2fi). A British cohort ccposco since 1970 to csrysoak at airsorse ieveis not exseesiing 0.5 to i.O fiber per cubic censmeter m me manufac ture of frisson matenais snowea no excess of deams from lung oncer, other isDeltas-rentes rumors, or chrouc respnterv disease (27). These and other data (7, 17, 21. 23) suggest that ampniboics are more potent than chrysoak in the incucaon of fibrecc lung disease and asaoaaced lung cancers. Experimental Models of Asbestos-Induced Long Disease Several studies have shown that mesotheliomas are induced in a dosage-dependent fashion after istrapieurai and intraperacceai in jection of asbestos and Other asbestos-like fibers into reaests (29). Girvsonic wu u carcinogenic is the amphiboies by these routes of administration. However, differences have been observed between the eareisogemcisy of fibrous and nonnbrous matenais. For exam ple. in one study, fibrous tremoiia wu caremogemc after mtrapleurai injection, whereas nonsbrous tremoiite wu noeearemogeuc at idendeai concenmaona (30). Aithoum the natural reus of exposure m fibers by inhalation wu circumvented is these expenmesa, they were usdui in indicanng mat fibers longer than 8 iun and leu than 0.25 pm in diaaieeer save the most marxed caronogenie potential. that is. the "Stanton hypothesis." These sata have been supported by the eesuio of inhaiaaon studies ta nts m which short (S3 am in icngtn) and long fiber preparasona of amesite and chrysonie asbestos have oeea compared (31). In contrast to the busies of amoute ana chrysoak asbestos containing manv long fibers, short fibers of amosits produced neither asbestosu nor pulmonary tumors. Short chrysonie produced a smaii amount of ueeitosu and malignances, 'cut mese were atmcured s cantaminaeon of the short cnrvsonie prtparacon oy longer seen. Fewer long dun shore fibers of beta r/pes were present in the lungs of ill ran at the termination of exposure, bun regardiesi of size, rtwer ehrvsenk fibers remained in the lung. These resuia support me observations char chrysooie fibers, in comparison to amphibok fibers, are cleared more rapidly from human uings (17). This pnesomenor. and limiced aiveoiu penetracon of curiy chrysonie bundle* (rasher dun mar inherent abacnce of carcnogemdtyj may account tor the apparent lack of asaocanon of chrysoak fiben with the development of mesotneiioma in human cohort!. The exorbitant costs of inhaiaaon expenmenn with animais preclude long-term studies to determine die arenogeme wwimij ofaabexa at iaw-lcvd exposures. The development of malignancies in rodents approaches me 2* re 3-year life-span of these animals (32), a period of too brief re reflect the consequences of the long term nubility of chrysoak in the human lung. Mechanisms of Asbestos-Induced Inflammation and. FSbrogenesis Both cpidcmioiogk and ctperimentai daa support the concept of a threshold for chtyaodk-indueed puiraosary fibrosis, la a sheep modd of aabeaeoiu, inflammation ana hismaxhoiegu evidence of disease were aoc observed after leas than lOOmg of ehryaook were iajacted into the trachea of the sheep (33). After breed intense inhaiaaon of chrrsock. the sheep accumulated alveolar macrophagea (AMs) acareasofdceanaca offiben (4). These ceil orpes are 004808 viewed u '`cfrbstnr-' eeiis or disease as they produce 2 manure a: tibrooiuc growm factors, chemstacsc facron. ana Sbrenecsn. Prosragiandins. pjsminogm icuvztor. a heat-mole near unfair to piareist-denven growm factor . PDGFi, iysoaoms: enzymes. and acsve oxygen metabolites. one or more of which any cause proiiroranon or funcaonai impairment of neighboring cpiaidial eeiii and dbrobiasn m the lung, were reared after exposure ofAMs co asoestos in vtcro i J3). These suostuces might nvgiaee boa acute ana chronic incammarary reacnonj in man and snimtls ateer inhalation of ubaros. In support of this hypothesis. AM-derived growth factor (AMDGFi, PDGr. mccroxidc (Of), and HjO? were sDontaneously released son: AMi recovered by bronchoaivco* lar iavage scan paoents with osoesssu (id). Similarly, AMs lavages from ootn mice ana sheep that nab an earlier intratracheal injection of chrysouie released enhances amousa of a growth factor that inmuiarrd praitrersnon of a human embryonic lung ceil line (WI- 381 (37). In one study, AMi from oots sonnal individuals and pasertts with idiopathic pulmonary fibrosa engrossed a 4.2-ldlobase mesren- get &NA compiementary.to c-<u. a proto-oncogene coding n; the B ehxrn of PDG? (38). The amounts were approximately fourfold higher from AMi of oaneno '.nth pulmonary Sbtotu. Because PDGF is mitogenic to mcssnoivmai eeiis, which possess junctionsi PDG? receptors, cevated Icvca of FDGF in iung tissue or Suios cornd induce lung dbrobiascs to oivide or to produce exotsast soousts of collagen, die haiimarx of the fibrooc lesion. Quiescent human mesodaiiai eeiis alio uncargo DNA synthesis liter exposure to PDG? and a bread spectrum c: othg growth facsors (39). Within the out few vein. Severn laboratories have focused on aenve oxygen species (AOS) as causaove agents of both asbeseosu and asbestos-related malignances. Increased amounts of niperccude (Of) have been produced after recent AMs were exposed in vitro to long isc3cos doers, whereas gmerxdon was minimal after shorter doers and nondbrous oarncss were incoduced <40). Smaller f.ben ana parsecs are incorporates xto phagolysosomes by AMs. whereas longer f.ben are mcsmpieteiT phagocytnseo. a process liberating more AOS. The csservtson mat exogenous administration of scavengers of AOS prevents asoestca-induccn rod death to cultures of tncaeal epimeiiai ceils ana iung dbroo.asn (41) suggests mat AOS are intimately routes to tsoeseoa ccxititv even in me ahrence of AMs. Fibers may incuce genenson e: AOS arte; phigocytoia or oy gxtracsiiuiar mrmanures. For example, roeent studies with asoatos m rod-tree systems have deaonscrtd by eleeaon spin romance that chrvsccie. ertxiaoiite. ana monte generate AOS in toe presence ot' HjQj or payuoicgsi saiins (42). Under mere erream* stances. St** on me surface of fas doer appears a drive a mrwiifiwS Haber-Won (fensoaj reason mat retuha in pmducnnci of die toxic hvdruryi rsaicai (OH") from KjO) and Of. There reasons result in lipid pereandason. wnten is prevented by incubation of asbestos with the iron cneiator. enfanssamme (43). Ac high concentrations. AOS arc cytotoxic so ceils ofthe respira tory tract, but at low . cner induce fuscscmai dunga in recent lung fisrocina that mxv se ended to the pexsogcncu of fibfqflg liiwy pgf ITUS tddiSOS of xanthine and xanmme osease ta efeemicai system ptoduong Of), rat lung abomasa in mo produced inaasea amounts of codigtn in a j--bo ri+*r observed sizer then exposure a aataereae (40, 44). In a iruitianisn modes of nptd-ossee uocsceia. pumps ing ooivedrykne giyeni (PEG'.-caspuyarrd canine, the caeviue scavenging HjG*, were -mpiamte jubeuaceoushr mto rata before they were exposed to croedoiize far 20 days (43j. This procedure hoosma levels of catalase in the sera ana of there smmiis sod imeucratea bam the girfammaenn ar.a fa.: sevenrr ma cam of fbrosc lesions mat normaiiv develop afrer in.iaianrm of aioasos. This scusv wu tne ant mccessrui cxscnmsaai apptcacn :c cne prevention of asbestoa-sssocarea iung auease. Moreover, tne results support tne concept of a cause and enec: reiaoon between AOS ana die development of asbestos*. Mechanisms of Asbestos-Induced Carcinogenesis Carcinogenesis is a multistage process that classically has been described in two stages (48). The "initatien3 stage corresponds to a henobie gsiede change (point muaccni induced in a ceil by a carcinogenic mhmnee- It ij followed by the `*promotama stage, a series of events m which the iniaitec rod undergoes proiifaranve and genotypic cnznges conferring the mangrant phmorype. During the past ftw years, the idendaaaon of t number of protooncogenes has resuited in s new taiccrsnnding of the successive geseac evena involved in the process of malignant transformation. Increased expression of there genre may cause the production of growth facEors or growth-factor receptors. Lou ofother genre i inn- oncogenes! also appears a conmbuee to the eatdnogesie process. There fadings indicate that the diadnceoa between geneoe and epigenesc evens in eardnogenesis is not staple, espeoailv because chromosomai reatrangemena or driesota swocsmi wim point mutation and aesvadea or losa of genre can happen at any nap m the process of ceil transformation. Whether the muissage model is direcuv ipphcabie to asbestosstaoc.sted carcinogenesis is undear. Uniiice most caroncgens. asbes tos does not cause base subsntuson and framrehift mutznons in bactenai-mctaaon asuys (47). Of use 23 agents dwigratca u group 1 human cardnogena by the Inteznxcotui Agency for Roearcn on Cancer (IAB.C), only ubestoa ana ccmugazea estrogens were ncngesataxic as defined by born the Ames test and roacm centmarrow assays for dcacaon of chrcmcscnui abezrenons or micro- aucearod erythrocytes (48). Althcugn usestos was weaxhr mua- genie in Ciinese hamster lung ceils (4$\ it was not mutagenic in Ever epttheiiai eril or in Svriaa hm<rw esorya (SHE) fibrocusts (30). Asbestos did act cause morphoiegte transformacoa of C3K iOTI/3 ceils (31), but gmiformiiti bom 3AL2/c#3T3 ana SHE Sbrcbiisa (32). Glare frbers and nondbrous silica (albeit it muea higher mnesn gallons) also were aaxve m the SHE bicamv. In mis system, longer, thizmar dben were more potent in the aducron ot' gmsfonnition and chromneomai T.rrui._ an obsemson consist- est with the inemred maiignanr porenr.ai ofthese dben in compar ison to thong dben or parade* afrer aids idrninatrinon menpieuzaiiy, intrtpertasneaiiy, or by inhsinion to rodena (29, 30). In three sad osar in vmo studies, the biofogie cea at bre types have been amwed enmpanervaty on a mare (ouliigrama of dben per dish) ratfagthanamantncsi imanbcsofSbtncfagwm sixe per dish) basis. Cytctpurity and eyeogeaede eften of dsysodie. ctoddaBte. and crionae (an ausasoadicue fiber) recersBy were comsarad in Chiarea hm.--, hag dbroaksa (V79 aib) (S3). Numbrn of dimocie dbos recared to proosci cyimcsa: cr evtoge- neoc enegre ware savani otden afaupasda higher a companton a anexua. dw more poeres dbar, or oostsise, a &ar ofsresseoan poancy. There (aoies are arena wua the higbar tumongBiie pnwnnel of adoeire in rodeos mvivmim (34). In aoree atadiea, reberen pp--n bo ^sd cummguuc effinos of *--" > cuosoges and nrtiidon. fat eampk, both ereddoiire and ehmotxie ieoared fas frequency of ^.IIHWW.' tmi tl IM'WIIWWW IQ wrmimmr adk llld dfatO- bissts creowd a bmto(]prrcsc (Be?) (30) aadrsdisdenornaan 004809 .Wl l= ` ?Q L?:T- c-HEIICE f'A>: jiaha oaracks i31). However, jvaeganc eseca os asbestos tea BaP wen not oosavee in two truss with SHE ana ratmesemeisi cedi, respectively (52. 55). The oaracuiase nature of aacestos and its capacity oo bind nucleic iriA* has prompted transressan studies in which asbestos was used as a vehicle nor insroduong DNA or RNA ism a number ofcall lines (Si). Under these arcunutanees, ubeams wu intentieeiatt in tan* in comparison to a number or ether insoluble Acilitamrs mending niaum phospnate. oic ana kaolin, none of which have been uiocaatcn with die mducacr. or* cancer. After sdHiwrm to human o; rat meseoieiiai cells, both chrysocie .'in rats) (57) and amosite (in humans) {!!) have caused tceupioidy and altered growth charaeterancs after rcpcacca passaging. Iajccbon of rat mesotneiial ceils into nude mice after a single exposure so chrvsooie did not cause tumors in animals, but muhieie exposures (36 nmei) m chrvsctik and repeated passaging resulted la turned* gone ceil populations (57). In contrast, human mesotneiial ceils displaying chromosomal abnormalities and growth aicciBons after duplicate exposures to cytotoxic canctr.saeani of aments were not cumongeme in nude mice (52'. Atbates promoted the proii&rxaca of mesotneiial ceils both in organ cultures of human mcsothrihim exposed to asbestos in vice and in mice given inmpeatoaeti injections of asbestos (59). Asbestos fibers come in contact with the chromosomes of rat mesotneiial ceils (60) and hi sumac apparatus of V79 (53) and SHE (61) ceils in vitro'. These tnrtnctons might induce chroma* lomsi muaggrcgar.cn or abnennaiihes. Several invengason have cammed chromosomal aberrxsetu in human mesotheliomas, but changes appeared inconsistent from turner a turner. The most common abnormalities involved inversions, truuiookons, and de* lenons of chromosomes 1, 3. 7, 9,17, and 22 (62). Consdtuaveiy enhanced eeprewon ofthe PS G?-3 gene, die proto-oncogene c-itr, was observed in human mesomeiioma ceil lines when compared to normal human mesatnriiai ecus (65). In comparison to human mesothelial cells, human bronchial epmdiai ceils in vitro are rtjoveiy reasons to aibesscs. In ant stuav, concentration* of ehr.icoie, crocidolite. or amesia asbcaroi approximately tea arses as mzr. as that required tor mesomeiisl cdis were required to achieve t cornparable increaM in eoscay (as meiiurea by t 30% decrease it. coiocy-fcnnsng emcencr of human bronchud cpttheiiai ceils) (*' In mother study, ancaploidy was not increased significantly over a range of ccaammena of either crocdolia or chrywole assesms (65). This lams obscrvsaos and the demonssranon that mserass of asbestos inn rat tracheal grass can eausc the devdopmess c caronomas Mewing insertion of lubaronogemc ameuna of the poiyqnaic aromatic hydrocarbon, dimetsylbensoiejaxahncesa :6S), suggest due ubesros is a prometer in tns dereiapmet sf hang *****>. In support of this concept, beta croddaiist sis duysook ssbeseos i"**---*^ a ct biocheateai prodressre sistradooi is rodent and human reaches! sprtheiiai ecu indorse cultures that were stmiiar to those observed in mouse *" h--w fyr*A tdxh the tumor promoter 12-O-ccsadeanovrohorool* 13-acemc (T?A) (67). The repeitons of then prciiicTcv* which wen masked in sachet! escssdsi cells in a high-mum contusing msainm or by adriirinn o: '**g growth kcor-cyps B (TG?-3i) (fill, tndudrd ernanerri tooarponooa of `H-tfaysnidioe, increases m coiopr-tbcming sxBdmer, aad the devdopmesx of squamous maraptMis. thee is, coeveixuoa o difitressazad tmaeod- liary esiis to kennmang ecus teasmhiiog epidermis. Inda-hra of ornithine dscarbesyisss .CDO, a nse-iiedesg " in the biosynihcUa of poiyami&cs that a incxcasad io moos akin ttea exposure to TPA bis sot after of nomamor promooag "**' J fitg oeeumed m * etrmmw JJJ aacnesi cpitheiiai ceils exposed a tens. cun. asoesss and gius fibers. In contrast, nonabrous paraces and ihctts assn mi not increase OOC activity at nsuiar concsnmasoas (69). Unci quits recently, it wu unccar how ubesttu enggered proliferation in tracheal cpitheiiai ceils. However, severe: axes of daa suggest rhat mechanisms ofceii signaling oy ubcstci ire suniiar s those observed with TPA, a soluble tumor promoeg tear binds direcay to proten kinase C (PKC, a caiaum* and ahesotiniipid- dtpmdent enzyme that aesvata a limb of the phospntssosmde signeirframoumnn padtwiv (70). Misogsmc esnceasxcstis of CO- cidoiitc asbestos crated increased accumaiation of diacyiglyoerot in gachtai cpitheiiai cdii (72) and fubscuuenc acmunan of PKC (72), presumably by aedvadoa of membrane phosphdioasea. The in* geased procucnon of inesaoi gia* sea rtaaiuiphospnitg appeared responsible for the generinoa of dlacyiglyeerDl, which preceded isoeased ceil diviaioa Abrogadca of crocidoiitt-induced OOC aedvity in tracheal epithelial cdii by inhibisors of PKC and oioum rhannet ujtagonisa (69) suggests that PKC is related causally to iib*. ifw**Tt"`*'*rw^ ***11 proliferasoa. Mcchaniams other than turner promotion by asbestos also may explain inttncscni between smoking and Mbiotor. there mechs* niisti could be in the development of iuttg cancers in asbestos workers (7, 73). For example, smoking impaired clearance of amesrta asbestos dam rodent lungs and increased rnsntion of fiben in ainrsy epithelial ceils (74). Both dgarets smoke and asbestos induced AOS in a synergisdc fashion in vitro and damaged isolated bacaeaophsge DNA (73). AOS liberated asm asbestos fibes siw catalysed the nridasen of 6-hydroxybeszo(s:pytene to a more mutagenic and carcinogenic radieai (76). Beams aoeidoUts and chrysooie asbestos adsorbed BaP and acted as vehicles to increase both upcske of dune lipophilic carewogens ana &tmaaon of DNA addurn in tracheal epithelial ceils (77), ;en might faaliate the mioxsioa of lung tumors by BtP. Public Policy The tvuiabk apenmsntai and epidessologkai data indiare chat both fiber type and me are assartanr dearaunana of the pathoge nicity of asbeatoa. Although uhesma has caused discus in the workplace (7ff) sod such occurrence has rauked in ails Sor reguia* dons to protect workers (79), reseat epkenuoioga daa tre cpgccr- dans wn the suggesoon dtat gpesure to chrysouis at careen: occasssosai standards does not ineresse the risk of asbestos* assorumri diseases (27, 21, 27, 2S\. Unlike most otaer samara, patttenisrir in the European communiry, which have sore stringent tequiiemena ibr reguitBon and imponaaon at ampmboiea, federal policy in Unified Scaces n"** not Hiftwnww henmn nUfermr types of asbestos. Dots tirboxBC asbucot prescat a risk to the health of indivtdaals in fir"1' sad other buddings! The xveiiabk dssi do not mciicarr tHo aibcxos-usoosted ssui^nocia or Bmc&sssl isnaumenr will oecar as a result of gpesure to most airborne coasenazsoa of abesaos in buMags. Ftm and foremost, the kvea of subotne ssbueos in buddings, even with ri*m*p*4 ACM, arc msgntmrin lower than coocnannoos in the unregulated workplace a the past and approximately 1/100 of the pcasussMe eposure of 02 Bbers per cubic centimeter of air in the U.S. workplace :4fl). Before the mearewneta ofoceupuronai studatss. workplace concensmu of 100 or more Ebon per cable ctsmntcocr of sir were not uncommon (ft). In concur, surreys of ssbueos in idtooia and pubtic btaidiags show thee me men airborne wi rhanuwo- foldlower (Table 1). With new the type ofalbums fiber found prtdomaudy in buddings is chrysooie. Accasaiaong rvt- 004810 :sr.ce indicates cut cus asocsros is procaoiv not usoaatso vim ms occurrence of mesomeicrjs it .ow levels of measure. ror rxampie. recent anaivses on me tier ecncentnnans in lungs of isoestos worsen rnowen that enrvsooie women with mesothelioma ,iad 400 tunes the mecian urns irer bureen in comparison to workers exooseo to amoniboles. Data indicate that mesotheliomas n chryiocie worses appeared a: rung bureau comparable so that required for me development of isscssoiu. a disease awnciarcd with jccuoanonai exposure os asbestos m me cast unregulated workplace 82).' Transmission electron mierosccev of air sample is essential for me idessscation and quansasen of finer asbestos fibers. In the Tmtee State and United Xingucm. me direct transmission electron microscopy method is ldvoorea to dcermine airborne asbestos riser concentrations in buildings, in France, the indirect traumas- non electron microscopy technique it used, and concentrations are ecoreseb on a mass ; milligram: resu. The limit for detection of fibers by poise-contrast micruscoev u approximateiy 0.01 fibers per cubic centimeter of air. a conger-noon higher than that repotted in most schools and buildings (Tib-s l). Moreover, phase-contrast microscopy cannot be used to iccnuiy types of fibers (asbestos or nonasbeseos) or to detect does tess man 0.5 ism in diameter, twice the diameter offibers assocatec -f.tr. the greasst biologicai activity and ir.ducnon of tumors in roctsa : diameters sO.23 um, that is, Staruon abeni (29, 30). Such .eng. thin asbeseos fibers are rareiv found in air sampia of buildings 33). As shown in Table 1, fiber concenmanons from recent sruaies in buddings ire comparable to ieveis in outooor air. a point sureiv relevant to assessing the health risks of asbestos in ouiidihgs. Airrume cancencanons at asbessoa in buddings reportca m me 1970s were somewhat higher, presumably beause of earlier, less sopnuticass sampling and analytical tech- nioues. Recenr epidemiologic studies c: bssfos foam mesothelioma in the general population aiso suggest r.:: nut from asbestos in buildings is mutuale: 9, IQ, 41. In comrir.:cn to lung cancan (an average of 130.000 cases per vear in die Unites Stairs, largely attributed to imowngi, an estimated 1.500 cues of mesotaeiioma per year occur in me U.5. population iiS). The ton on death rates foom pleural or peritoneal mesotneiiomas over me past 10 to 20 yean indicate that mesotheliomas are increasing m maies over 65 years ofage who have a past occupational historv of exposure to asbestos (84). By contrast, dcatr. rates from mesotneiioma m females of ail ages haw siighdv or remainea constant. These results support me concept mac asbestos in buildings is not an important risk factor, u one would expect increased cnesatseiiomas som mala and in fou ease. A recant trenoi stuov did r.o: show increased risks ofasbestos- moastsa malignances, pleura, r.iques. or ftincaonti impairment of die lung (eftea dearhr present in asbestos worsen) is penons exposea for 10 yean to airborne asbestos la buildings (id). Ai- diougn thu survey u soli in promas. no mesotheliomas have bees observed to date among apprexusatehr 15,000 permanent occu pants. Althougs the validity of >ii-i.|.niiriwj from high to low Ieveis has never bees confirmee tmsiricattv is die evaiuatson of ubeseos. calcniarra lifenme ri from mcsocheiiomae and lung cancm sigtbuiaaie s n a scsoois sad other oufidiafs have appeared m recastyean 183.87. Tie linear dose-response equations in these tnoaeu have been uses wrfo die usuroooon that mere is no threshold for disease, a hypotnau wtuch is open to quesccn. Moreover, the range at rja vmnes from study to seedy. With me excepssn of one ana.vsu (U). difiertacts between die pamogemc patenoai of ehrysonits and smphiholra have not bees coraiders! in these aucasmess. and the mnnm of fiber toe has bees ignored. Elcgirokss. crammnion or mrmkwmti daea oca Tibia 2. or nsk acre ubesros exposure in senoois ie ceseinscn is otner risu m U.S. sooetv. Dies tram six cusuanee me anrnts i7. n wntch tom beams uung canca ana oaotnacusasi smsuaas to uoerea jiooiutc over * lifetime were esomaced per i irniion itueesa eepoua to 0.00024 aben per cubic eeasmstcr sir (foe man urooroe arecneafion ut scnooiL Tibia i) for five school vein, beonssg it in 10. Eiomires inttore ant me antuai rare is 0.003 ea J.093iiwait per rmiiinn naacna ibr in avenge ufe gpeengey of 75 >ean. Modified wimscrmisueo som VVedl ua Kugnas ttO). Cause Asbestos exposure m schools Whooping cough vaowtaea 11970 to 19801 Aircraft accidents (1979) High mod football (1970 to 1980) Drowning (ages 3 to 14) Mocsr venide undent. pedcstnan (ages 5 to 141 Home accidents (ages 1 to 14) Leaf-term looking Arena rm (drams per muiioni 0.005 to 0.093 1 to 6 4 10 27 32 40 1200 published risk eadmarea shews that nsks of asbestos-rented tool deaths (both lung cancers and macmchomas) due to exposure in schools are aagmtudn lower than commonplace nsks in modernday society (Table 2). The AHEJLA ruiing of 1986 brought asbestos to the attention of the U.S. public and insniied fears m parents that msr children wouid contract asbescos-reiatea malignancies because at high ieveis of airbotne asbestos fibers in schools. Panic his been fueled by unsupported concepts such as- the "one fiber theory*/ whin main tains that one fiber of jwhaivd asbestos will cause cancer. As a resuit of public pressure, asbestos often is removed hapnazardv from schoois and public buildings eves, tnough most damages ACM is m boiler roams and other areas which are inaccessible to students or resides* (2). The removal of previously undamaged or encapsulates asbestos can lead to increase in airborne concentrations offibers in buildings, somenmes for months afterwarcs (83), acd an resuit in problems with safe removal and disposal. Asbestos acarcmer.: also has led to the exposure of a large new cohort of reiaeveiy young asbestos removal workers. While these people snauia be protected by careful regulation of the arcumstances or removal. :nr.* are odes etpnrri under subopnaial wonting coacissns. As a resuit of the AKERA ruling, public and pnvace schools are required to inspect for asbestos and inform parents if ACM are present. Although the law docs not require or set snesards for me removal of asbestos, schools, often with iirric expert asvice. must submit a management plan detahieg how ther will deal with damaged asbnrcs and can be fined a maximum of 55000 per day for lack of compliance to deadlines. The ?A has recommended bulk sampling of ACM to derermine foe pretence of asbestos ano visual inapeennn to dceeame the course of arton, rather than measurementor* airborne ievtia offibres data that are ar more impotoaam determining the seed, if any, for removal of ACM. The xvmikbic data and comparative nsk ueeamena (Table 2) indicate dot chryiocie asbestos, die type of fiber found precoma- naraiy m U.S. whooit and buddings, is not a heahh rak m the nonocnipauonai environment. Geariy, the asbestos panic in the U'J. must be curtailed, espeoallv because unwamntea snd poorty asiiBoiled asbestos abatement results in innrc.nmv nsks to young removal workers who may develop asoama-reiatea ranters in later rlrrvin The caoeurve removal asbestos hu occxned less Bequendy m Europe. grerennon (espeoaily in arinlocvmsi of cbirm smoking, the pnneipai cause of hug oncer in the general population, is both a raoea promising sad rational apptoacata riiirnnanag lung turnon 004811 1 1^^* 9 than uoeatos abatement. Ever. icxncwicdgmg that one. intense txposms to aiocsto* might ccr- is custoaiara inn service women in buildings wtm scvermy diauaed ACM, wcnter ctnacation ana buiidinj maintenance will prove far more esessYe in hak orevennon tor sick worker*. aifzuncii ams Nona 1. AtsoIt to OK Cor.gra. iedv : Ilium Ciimum Mamma a Adik SmUmm (L'.S. Snvwonmaiai Ptuacoan -Vccacv. Wtma&aa. DC February 191*1, p. A 2. M Corn. new iiiiBin it T-t 2Ltd Inarawocai Cungma as Qffjgaanim HeakS. SuW. Auiaim Septarroar. 19*6. 3. B. T. Msaraas td /. S. L Gee. .V Sal. / MM. 330. 1722 (19*91. V K. C. W. Skioner. M. Ac*. C ?:onad. Sic, AMatm mi Qtkm POnm `intuit (Oxlmd Uv. Fran. New Van. i**). 1 M. COR. Aw. Ini. H. Am*. *7.31* (1916). 6. A. Stncn. Said. Xi*. 9,171 (1917) 7. I. C McDcnnM nUO. iUCosnlA in /bkanwrUmd Mdfrmny, Z. K. Amman ana I. Ainanr. Sia. lCr~ ine Jtncxcex. Orlando. 1917). pp. 37-79. |. j. Oman. i. Bipeo. A Htae. Eu ~m Plan m Horn m* Ota tDtkku, New Yak. 1915). 9.JL K Carnal*. JL Seam. M. K. Marat. C L. Pcrcr, J. t. hoan. J. Sal. Cam but. 79, 31 (1917). 10. A. D. MrDoneid m I. C MOaouA n Aanm Xiiim Maiipiam*. A H. Asuan tod I. Aunar. dk <Csa iaa Smmn. Orlando. 19*7). pp. 31-4A 11. H. A. Andean. JL Uia. A M. Sun. A t Pttta. I J. 5akho Aw. S.Y. Aad. Sd. 371. Ill (1976). 12. A. Hind n *1., Am. J. In. Urn. 3.413 (1913). 13. L Odd led I. fen, a AiwmwiliLma Military, K. H. Asesan oti I. Aiaur. Edc. (Craw an Season. Or.mao. 1917). pp. 11--96. 14. J. Sipnon. F. SiBmnai L OiMc-a. K. Ptyan. Ajm. N Y. And. 3d. 338.4(3 (1979). 13. O. A. Udraao. Or. }.ln.ii*i. 43. 71 (19**): C A Chin ani I. A L. On, J. Ocap, MM. VI. 33 (19*11. 16. f. C. Wan*. C A. Scfp, 9. MwauUL M J to. MM. 17.260 (I960); a JL 9)iiid Tpanrr. Am. iV.F. Aua. Ac. 133. 213 (1961). 17. J. C Wipner. a Berry, ?. 0. loom. *.MM. J.Uk 403 (1912): M. J. Ganimr. P. 0. Wins. 3. Tinas. C A Pam. *. /. Zed AM. 43.724 (19*6); A Csucf, Qua 9a. 631 (191*1: AM. Uata an A P. Moan, m Nm Hwaieni Ermmn a tilmm Firm. J. Bipmr. f. 7'ss. A Straak Edt. (laagninaai A*xacr ror Fx--ren aa Oncer. Lyon. 19*9'. ip. 330-333. 15. T. C Wtsoar d.. Am. Oa nrf. 26. 423 (190. 19. M. C Inifina. 1. Bifnan. P. Searsat. J. Cora. Swum. Mm. 14. 245 (1977); A. Menu an A Holm*, me. 39. 473 (19(6). 10. A flindirrar a a., did. 33 (KSl. 213 (19U). 21. r Demon SL t_ Hara. M. I ivmora. C M. Star. Aw. ; M A6d. 4. 431 (19*3)1 M. fiontawa. Aw. aw acww. Co. 139. 7S4 (1914); I- M. Kusna a a.,. /. iW. MW. 66.161 (1957., A. D. McOoudd. 1.1 Fry, A. I. WooOdd. j. C McDobul da. 40.366 (19ir. p 361; C C. Chieoi an C HipM. me. 43,397(19(3). U. A Cusp Oaa 93. 631 U9M'- 1. to.it P Scaaaom. C McDonald. A. 2. MrOeari, *. Can. JL Kasrv, Mr j. Sit*. 46. ISO f!9(9). 24. r. C .'.(cDonUd a a., did. 4X 4J6 [ 19(6). 25. ACnr*. 1. Wi|p.L. Cesaou.1. Xaiapa. AStenoa. Aw. Xiv. Jtapw- Bit. 130. 1043 (19(41. 26. C Wipe. AC L- Newnouw. j. Damn. C A AI naiwr, D. M. Otafcsa. B. to. Um. 46. 303 (19(0. 27. M. L. Nownouaa aid S. L Slums, did. 46, 176 (1999). 23. a Serrr an M.U.NeMdaac.xt.4& 1(19*31; a I.TlHBd(.LLBaaaaadkP. C Ilwood. P. M. iwoonan. * /. (ad. Mad. 19,373 (19(2). 29. I. M. C Dana, a .......... yi / M Jaannaad Ciffipma Om Kama Tilimaii a .fmpy (Aabaaa la--! Adaaaaacd. (ohaa--oa*. 19*3), pp. 23-43; F. Fas and X.H.TnU'W Mia wnaaaddla *9.31* (19711; M.F. Sanaa an C Wranak Jr. /. O-wd*. m (1973); M. C Taaaat. I. Tlaar. Q. Mnamiua. M. Naha. I. Slfnas. /. NW. Cam Iaa. 79,797(19*7). 3a W.L3ma.aO.)UK.l!.lMl.liaaaenOiedana.L Laraa an!. M. Danaat XdL tana Pak fame. 0.1979), pp. 331-339. 31. I. SL G. Dam a m.. *. J. o Pant 67.41S (199*U I. M. C. Dana a .Vn> Oapwd toi a M-aw Ana. f. l|naa. }. Pan. A iaa Ida. (Inamanaai Amer far l--im an Cuaw. Lyon. 19*9), pp. J3-U. 33. r. C Wapas. a Bear, I. W Sarim. V. TlaftML . ;. Caaw 29. 312 (1974). 33. A lcfa. 3. Maaaa. M. tun "laianiii M. taw a Onpran. is tat r-wy. a. A Pta and M. A Dai*. Ida. (Data. Naa Ycrik 19*7), pp. *7107. 34. A A Iraar. A M. H2A A Adana. A W. O'Cdnaw Aw. A*. laps. Otk 12A 479 ami. 33. (. T. Mnaanaa^A Befan. Ad-BJfcw.eYBdfandOnaw Cdt. (Mown Atlane VaS* tap. ' ri"nr T1 1*"" ^ ^ ^ (1rnn*r 36. W.N. Aan.F.A*laarnia 1.1 laatiP. A Caana. A C. Oyak Aw. Bey. Xflpa Cb. UA 1634 (1997) 37. L T H. leaaan. 3. Mum 3.--------- Am. J. MnmL U3.20* 09*61. 3*. 1.1. Maaaa a*L.J. Cm. tom 7*. 61 <19*61. 39. AW Cebnanoo n a.. FVi.?3 Li.ZT'.T 191*1; AM. LuwokAN \5aaan. L. L. Moon. A1. Qswm. J. lasao. ;.i . > Cw Dev tot. 24.1077 ;19U1. 40. A Haw im A t. Mourns. Cant at:. 4r, 1611119*7); S. t. (Lamas. A Kinaas. i- P. Marat. SL A Brew. I. Praiaaa. a ArwOrrnmwii eiaw. a Vtiwrw riww, (. lifooo. i. Pea. A Sues. &. tlnxtrexaocii Afocr far &tacana as Cantac. Lvoa 19*9). pp. il-92. 41. A T. Mnaamas. /. P. Mend. M. A Shame. La. Aiwa. 54. 204 119*41; .VL A Shaaan }. P. Mtnft. *. T. Monona, hw da. 44.103 (19*71. 42. 1 A Wobsm an P. Oman. An. Aamn. Otar. 23A 17} (19*4): A 7lira. A Saancaa. M. C Jaunna. [. Gtueurd. M Pear*. Co. J. Cum. ok 233* (19*7). 43. IA Wa--s ins A I. Watber*. tam. /. 22A 2S9 (191*5. 44. *. T. Mdaanan a Oar 19.160 (1916'. 44. I. T. Moaanun r d, ]. ftt* Bed. M. Mrd. A 33S (19*61; S. T. Moaaiwi a a.. Am. An. jirptr. Dii,, ia proa. 46. L SenonesB. Cnaar da. A 44 (1941). 47. M. Oinnmin an A M.Tronv. Minw. 2u. 43.139(1977);W.C.U(btsttlA T. Wo. n TSr 3a {(in* niter a Minna Dun. A C Brown. L ?. Caosirr. SL Oumnmem. A Daman. d>. lAadcnae Pna. Lanaoa, 19*01. pp, 139-143. 4*. 3L 0. Suibv, Mam. Mtt. 204.3 (19*1). 49. S. AHu**,iMi*A2*lll979). ja A torn. C Too*; A Tdany. C. M. WiUisa. tan. At. 31.100 (19*3): M. Odhisun, T. W. HanriMcy, T. Tiuain. I. C Sum. C*m da. 44. 5017 (1914);). A OiPiaio. A l DeMaraua. I. Doetyee. Jtaani.ff 27. OS (19S31. 51. A C. Srown. a Pooin. G. T. A Flams*. Cwr La. IS. 231 (19(0: T. A Htt. C A Gta A1 Oaaak M. Imam Sr. /. Oaor *A 391 (19S31; T. A Kak is Sfn *f Manw Dam an Cdlk B. T. Manmas and A Bcps. Ida. (Nona Adana Tran* Orpnranm Advances Seanct tnrannr San H. vek 30) (SpnwpVdris*. Sesns. 1999). SA T. W. Human* aidl.C Buns. Cam Mm. 44.2170 (19141: U.UC Luna. A Lowy, L Onaravunnov. MsMtmma A 3SS {1911); 10. Mitaaw A S/vaail T. Saisur. Qraiaei 9, *91 (191*). 3A L D. Make. A M. Moo. 0. L CoAl Sanaa, to. 46. 142 (19<SI: L 0. Paiakar.!. T. tvx*. A 3L Moat. D. L CMBa Ct*mttwmmt A 5S3 (19171. 34. F- C Wifnar a a., *r. j. Cam 4A 727 (19U). SI. M. J. Piuraur. ]. llcaon. M. C Itucand. Cadmtamm A 323 (19SS). SA I.D.AppakT.M.Fiav,D.AXdtas.3. D. KattB.AM. JaSenod. Par. MaL Acad. So. U.S.A. U. 7670 (19(9); C. A Cuba sal L A Max tit vm CM. Dm. Aid. 24.173 (191*1. 37. M. C Tamandk L. taif, L. Mifcn. I. Bipnon. Mna. So. 169. 141 (19*61; Sc Ibdrws a a., is tfMtom Dun m Oik. A T. Mounts ana A Ssps. Edc (Kara Asasce rrcarr Oryauasan. Advuns Seianct isisnn* ienai (SoaBB^Vciic. in om), SI. iPLmsnoaa.. Pm. StoAto. Si. VS. A. IA 3334 (1913). 39. A T. loan. I. C Wansar. P. H. vina. Sam* 23A 346 (1973); P. A Moaili. I. L. McDonald. L. A A--A S. Kean. Am. }. Pttot. 12A 426 U9*7). 60. N. A Waif n a.. Am. J. Stto. 12A 343 (19*7). 61. T.W.HoutostsmI.CButm.CarinapmnA473(19151. 6A N. C Poecaca. A P. Cubnan. ). A DiPdolo. Cwar iu. 4A 142 il9*I): A Cibaa a el., Cner Qam. Cyaynwi. 20. 190 (19(6); M. Tinned. L. Tanmnewn. A Muodr. A Kniassa, da. 3A 231 (1911). 63. A Ceram m a.. Caaar in. 47.61*0 (19*71; M. A Venod. A Huaeneaer. M. I. Soon. T. K. van dcr Kwaae. H. C HasmiBrn. Cnayiva A 601119111. 6A A Kadfan a i.. to. J. Cam SA 265 i 1952). 6A Y. Kodam. C I. Sarmao. A C Maseaa. T. W. KamcOert, a drenwieao. 6A D. C Toppaif aid ?. Neanums. J. .Ved. Ctwar toe 61. 627 (19101. 47. A T. Mnaanen. C. A Ciwrmn, L. Yam. is Cwnv A Qwiivwawrt iw Cwnr aw Iiwiimi . 7m, Paanaam Frowi. M. I. Mow. 0. G. Kiubnai I. M. SiamaA V. A Sawn A Naeow. ida. tAiveo. New Yor*. 19131. pp. 2L7-230. 6*. A M. SaaUd and A T. Manaus. Cum Htt. 49.2743 (19(9). 69. T.P.Maufeand A T. Mamas. i*d. 4A 709 (19**1. 70. Y. NIUiaui Siam 23A 304 (19161. 71. A 3A Setae. M. Ciboc A T. Moaanas. m pripartaon. 72. M. Ptdaran. I. P. Man. A T. Mouoan. is preptuoak 73. A C Hammcwd. L J, SckkoC H. Sadnaw, dot. N.Y. Asti. So. 330. 473 (1979); I. C McDoauA Om 7* (rappel, 374 (19*0); C. Bary, M. L Mu hum. P. Auook Jr. J. iad Mad. 43. U (19*1). 7A D.I(r9iddnAl. A Wrinra. A Wap. A Qua*, An. to. tar. Pit. UA373 (1966); D. Mrfata.I. U Wriahc A Wifp, A OasA Am. J. Pant. 12*. 91 (19*6). 7L I. H. JukMd a d.. /. Cta. bvoc *0.1090 (19*7). 7A P. Gdta and A A Woman. An. tann. Uudyc U7.411 (19*7). 77. A Iiwuia. A T. Mraia au A Srmax Cnntr Mm. 4A 13*1 (19*3). 7A L SakbadL A C Haunsak H. ScUraan. Cnoa4A 3736 riMO). 79. ). B. U Cm mi A tam, .V top. J. MU. 2SA U17 (1971). ta Is 1971. du OtnpMuw Sa&tr an Hate* Atanaomon (C3HA) piaan i is unammlamu fcaabara proanaus i LMl ttt r at aw ai Akaar aawwauma tvansa la to Mai m <L2 fibtR sv i II. J. M. C. Dana tnd I. C MeOanwx Jr. ] to. hUi. 4A101 (191*1. CL ACkntfmdt.A Wrimo.u.Nu Qranaw ii Sian arnMiam Ww.1.1 J. Pam. A Tiwnm. Eda. ilsauaauanai Aancy fat Aomen on Cmob Lyon. 1P97). pp. J14-11A *A C. I. Bnaasom A A M.T. liAnr. Aw. Oma. Myf *a 111 (IPMhM. Coen, in Awmnwa Symdmmi m Hamm Aipaa tfSaaaan a Adma w SwUWfk J. a liapir H. OUniiMA P. MeCaoa. JA Laa, Aid. IHum UaU. Pma. CsaandpcMAinyrtui; D. G. Mamv >&Femtmr amtv.Ne--n Afad. /. 4A 1*3 (19*7); A IA Snow. A 2fc IdU, A. M. Lanpu, tam. Ba. JA 46 0 04R12 anr.i. vot. let : 1985;. 54. V Haiansoa ana P. Scnrem. '.Ji. Cjvm lau. 79. 31 !S. i -L Hu^nei ana H. WVtii. .i- rn Hamr. On. 133. 3 ;t9lt). 16. S. Gsidicr inn. Envwm -rrum 42.303 (1937). 17. Ntoonai Rawn Ceunei. Cr.*Ba on .Nonocoicjoann Hcutfl i-ua at AibtMubrRi ribm. /timaon* ran .Smuom Httiik KuOr I Njoonat Aud- . eirr Prtu. Waamit^Bs. 2C 193* areonwaw UA Corewar Proausaarior Caamauoa a* tna Gratia Kisre Advuorr Pins an Attma (Comuokt Praihus Safety CanORBuaiv Wussjra. DC 1933); Aabmm Mm Hmm Auru--i L>Mir (Eninronflw.ti. 7-..ja.jun Ajmer, Wubut|tea. DC 1933): . D. Aenaan ana M. (. Catrinr. .-`.mm. ft* Cm lass ar Am (Her Mjbmv5nnoor Otflo*. f,<..-SiT i9Ml: lUgoct on manator OeaOfi ana utter mint tfom tna uac or uoenot c. -anrm lOtiono Horn Ceammau Onano Minuay at me Attorney ueitn. Lireem. i984)i 3. DnU tna!. Pm Aimhc sAnt w Amur w rrmiir a .ismm , Her Maam inocnen Giit. .jiymn 191*1. Si. M. Com, *. . Crests. D. Mcfaa. ,v Lee; is snwwan, 9. iarrrac i.ninmma Gtvnwa. Poet mio>tih, Aiiunte fechnawy wrauwnnn. Energy imaaogy Oyjuirx,Ta ana Mjawot iaoroi unman. Auuum ***** m Adiu ButUmtt iPA Cam. ,V. tmtBMM. amt boor bt xe Sipmme Eniimnn Dmaae. 1939). 90. K. Weill mt}. M. KujSaa. .4m. Xt. hUt Hmm 7. 171 (WSil. 91. IVethinsL 11Oaiii, V. Keikcer. maM. Beacon. Haamame eacnmrrat B.T.M. ht* been tugganoa by pins ran aw .Njaaou Cases xjmia i Ml CA32301). Mituott iaretua stlsrumaoBau Hans teanaa i U1C30317I), Naaeott Heat. Liany, and ileed Inaeona (Ml HU9449 mo. iCCX. pm 14212). innAmencanCtnor joettr i3C 413) WcalnmmH. C X Stismr feeber nepns granana. Priming and Human Memory Systems Endel Tulving and Daniel L. Schacter. Priming ii a nonconsciouj funs of human memory, which ia concerned with perceptual idenrifianon of words and objeca and wmefa haa only recently been recognized aa separate from other fonxu of memory or memory systems. It is currtndy under intense experiment tai scrutiny. Evidence is converging for the propoeizion that priming is an expression oi a perceptual repreaenta* don system that operates at a prt-aemanric lcvei; it emerges early in development, ana access to is lacks the kind offlexibility charactensdc of other cognitive memo* ry systems. Conceptual aiming-, however, teems to be based on the operations o: semantic memory. Memoay was txabttzzxxllxthouohtto aa a uxttaxy faculty ot the mine. ?.ecmgy, however, many researchers have adoptee me .-r.pomeus char mommy cocnisa of a number of nitons ana suonisss wnh Hiffufewr operating charae* rensna. The probiom ofwhat mssc svsteau and their properties are. and how they ate reiatra to ene another, now ocupio the center stage in research on memory One broad, a yet tentative, orgmaaneoai scheme disdnguiiha pfocedutaL semantic, and eaaeeismcnccy (lyPtocedotai memory unaeriia changes in skillful cmaratincs and appropriate respond ing to stimuli: scnunmi tnemotv hu a do with acqussitian and use of factual knowledge in the :madcst sense; and episodic memory enables people to tememser tcrscnailv caperiencod events. The domain of smeadurai meamr.* ts behavior, whereas that ofsemantic sod episodic ateotory is cesroon or thought. Cognitive memory systems have tire capability m modriing me <*" wood--that ia. of storing repressnranoaa of ebieea. evena. tad rriaeona among them whereas procedural memory docs not have this capability. Evidence is aceumuiaaag scout yet anodser category of E. Tuivuie u uonwi MSS ui: 2. L Stka 7voarn.Ai.Um. aueanr m pmmamtr it res UaowMr m AAm. and memory, one that is net procedural, seaunne or episode. It hsi come a be known as priming {Z). la function is to improve idenadcaaon of perceptual objeca. Pruning ia a type of implicit memory; tt docs not involve explicit or conscious recoiicccon ofany previous experiences. It has trinities to born procedural and seman* tic memory. Priming resembles proceoirai memory m that it enhancer perceptual skills. It also resembles semanne memory in that it involves cognitive represeactcons of the worid and expresses itself in mgnman tamer thin behavior. The prototypical priming experiment esnsists of two rages. In die ant (stuov) stage; the luojea is pteaemes with a snmutus oojec (target). Target stimuli may comprise words, line cnwings of objeca. drawings of rices, and the like. In the second ireni stage, which may fellow the fen trier an uucrvai that can vary from Ksonaa m months, the xubiect u given reduced perceptual informs* dan about the object and aaked name or categona n. Reduced cues may consist of initial lesrrs or grapoeauc ttagirxnn of words, parrislly obiitenced worss or figures, originally presentee aces in t more highly schcmsdzad form, or raciaioscopic prrjennnrio of wunuli. Priming it said to have been demonstrated if fee probabiiiry of the tdeatriaaoa of the previously cneoumered targea is in* creased, or the latency of the idenrmcarien response ts rtourro. in comparison vim liariiar measures nar nonstudled conoot nans. The djffuenct beeweets pcffeimarirr on the argg aems and sa noon* died itena provides a manure ox the of fee priming Although priming and other ends of implicit memory hive been reposted from erne to rinre. syseemaoe ttreapo to coiore it began about 10 yean ago (J). One of the tr.ggca fer fee scunv of pruning turned out to be esperimena by Wamagson and Wcuksasset (4) showing fes densely imnns oarieno. wno were severely impaired in feeir aaiiey to renumber recently seen information, txrubiroa aearenotmai ieatreng when drey were reared by mefeeda feat tapped wrin we now know ia priming. A neona for me seudsr of priaung lay in naearcn oooccmea wnh the nioae of arc teem m lexical represenrenora (S). A thud source of hriiaanee was the growmg unerase in die riuuficsnon of ssemsxy mm discssmnre casegrriei such at epbodic and semamc memory andptoeedani ami dedxrenvc nremnay (7). 004813