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R'ORKSHOP: CARBON MONOXIDE AvD CVD N. S. The prnalencc of coronary hean diccasc associaled factors in an Auslralian rvnl com- munily. Arntr. i. Epidrmiol. 89, 521 (1968 1. <S. Zciner-HcnriAacn. T. Cardio.asculardiseasc. s)mptoms in Korway-A study ofprc~alcnce and monalily follo,up. J. Chronic Dis. 24. i57 /19711. a = H i~.. . W _.__ ._.. _ . N N ~/ N ~ N

CARL ZENZ . - I volume map range from an averaFe of 10liters per rninute to as high as 66 liters per I . minute (19). In determining significant levels of CO exposure in %srorkers, the metabolic Icvcl of uork has a great bearing on the intake of a potentially toxic (respirable) material into the human organ systems. Other concomitant stresses may be present such as radiant-heat stress. hicher humidity, psychic stress, dehydration, and other poten- - . tially toxic substances. - , . In 1972- 1975. almost even. foundry in Finland %~as surveyed extensivelc for dust and other dangerous materials; at the same time, the health aspects of the foundry uorkcrs u'ere also investigated (17). Evcn though Finland has a popula- . ; tion of about 4.5 million. close to that of Wisconsin, the scope of such an immense project, probably the first of its type, deserves praise and much of the results have i , a bearing on CO exposures applicable in other countries. Under the direction of . . The Institute of Occupational Health in Helsinki, a comprchensive plan tk as de- signed to survey the vs'ork environment in all Finnish foundries. althouch the practical problems of carrying out such a study %sere recognized. Various statisti- , eal samplinc procedures Nrould be used to concentrate on typical hazards such as ~ silica dust. certain ehemicals- metal fumes, and carbon nrono.iide and their ef- i fects. In terms of manposser and funds, this project became the most extensive single research project ever carried out by that institute. This im'estigation in- I volved about 25 researchh workers and assistants, hso employer organizations. i The Ministn' of Commerce and Industry, The )tfinistry of Social AfTain and ' Health. and The National Pensions Fund. It is worth noting that this project ssas _ ; : i not undertaken for scientific reasons alone, but that labor organizations regarded it as equally important to determine hygienic data and instructions for the im- provemcnt of the individual foundries. The total number of workers in this project : i numbered slightlc over 4300 in 68 different foundries-iron, steel. and nonferrous. j In 1976. \'irtamo and Tossacaincn reported their results on carbon monoxide in foundry air. having measured the CO concentration in the air of 67 von. steel, or copper alloy foundries, making -1100 CO determinations (41). Thec mea~ured , blood carboxyhemoglobin levels of 145 workers from iron foundries. finding that . the carbozy'hemoglobin level of 67c uas exceeded in 26Sr of tlre nonsrnol.ers and in 71 /i orrhe snrokers. As is typical in foundry µ'ork, CO concentrations exceed- ' ing the TLV v`'ere found around cupolas and in the casting areas, again relating that a worker's exposure to CO depends on length of stay in these areas. A i • suu:ma-n- of their recommendations will be stated later. Hernberg et oC. (18) reported their investigative findings based on a prevalence • study of !^00 foundry workers. This focused on angina pectoris, ECG changes. and blood pressure from a statistical sample from 20 foundries with longest ssnrk- _ . exposurc times. Angina history was obtained from a questionnaire recommended by the Health Organization and the ECG's coded according to the Afin- ~/~~~~~~! nesota code 21 (18)- Based on uorkplace air CO, workers were divided into three _ . ~ occupational exposure groups: one .cith definite CO exposure, one «ith slight or occasional CO exposure, and one without CO exposure. Allouance .cas also - made for present and past smoking habits. All comparisons .+ere made on an • intrastudy basis between the different subcate€ories. The prevalence of angina C

\\ORASHOP: CARBO\ MONOXIDE AND CVD long periods in the blast furnace areas, were stressed by Silk. Davies (13) discussed the problems of continuous CO exposure in totally en- closed environments such as a nuclear submarine, wilh reference to nonsmokers and smokers and to the effects on individual and overalLsystem performance and on health. Reference is made to his excellent presentation on tbe increasing number of workers "entrained" in sealed or "closed environments." There is eoncern for the health of these persons even though the majority are of the younger categorv of the work force. With the development of under-~.ater aa tivities. particularly for obtaining- under-sea mineral and oil supplies, oc- eupational-environmental factors %cill gain importance. - Davies states that "smoking- COHb and cardiovascular disease is now %%ell established, and there is probably no abore-endogenous COHb level at i~hich there is no increase in the risk of disease. A le%el perhaps could be found. how- ever, from e\perimental and epidemiolocic evidence, at which the increased risk is so loxthat it can be ignored.".Wald cr ol. (43) showed that smokers \~-ith COHb levels greater than-5`,"r \sere 21 times more likely to be affected by atherosclerotic disease than those tihose IeLas>:aI less than 3c7c, and Astrup (9) quoted figures shou-ing that nonatherosclerotic smokers generally had COHb levels less than 4.5 7c. .rhile atherosclerotics had levels of more than 6`7. Knelson (24) demon- strated acute cardiody namic changes in healthy persons, and further elcctrocar- -:-iraphic changes in persons with a prior abnormal ECG. at COHb levels of 5°7 and ~ho\e; and Adams,/er al. (I) also demonstrated cardiodynamic chanees in dogs at 4% COHb. Nevertheless, Eckhardt-er aL (15) found no abnormal cardiac or brain pathological changess in cynomolgus monkeys carning COHb loads of 6-8 r continuously for 2 years. In humans, honever, the evidence points to a substantial increase in disease risk associated with continuous COHb loads above 37c.-7Trcrefore, allot.ing for the concurrent presence of other health hazards Within the submarine atmosphere- a maximum COHb burden of 2.5Sr, cquivalent to an ambient carbon monoxide-level of approximately 15 ppm, is again recom- mended. Jones and Sinclair (19) studied blast furnace \~orkers at a large ironmaking plant, demonstrating Ihat these morkersabsorbed CO at k•ork irrespective of their smok- ine habits. Studies in 1962 and 1974 showed similar results with mean increases during k nrking shifts of 2.0-2.6 ccarboxphemoglobin. The prevalence of car- diovascular disease in this group and a matched control group shoued no signifi- cant difference. The number of deaths of blast furnace Norkers from coronary thrombosis ..as not significantly higher than for other uorkers at the iron and steelxorks. On the evidence available to date, blast furnace workers are no more likely to develop arterial disease than other steeltsorkers, despite shouing raised earboxyhemoglobin levels of this order. . Jones and Sinclaireoncluded that, on the evidence available to them at the time, the blast furnace workers \%-ere no more likely than other steelworkers to develop arterial disease. Not only does the occupational exposure of the blast furnace- \corker to CO vary from day to day, but even from minute to minute throughout a u-orking shift and the ph}si.^al levels of %Nork cr energy espenditurc required can vary from mild to more than moderate levels. The increase in ventilatory minute - - - --- ---- -- Y - I -- i

CARL2Er.Z hanges, nor the extremely important aspects of effects on intrauterine develop- nent and the netvbom. Howeser, certain aspects must be reiterated concerning both sexes working vith potential CO exposure. Carboxyhemoglobin is incapable of carrying oxygen. kt any Fiven level of CO in the air breathed, the rate at which blood becomes ;aturated ~ith CO is directl% proportional to cardiac output. Thus, a vigorous )enon wzll note the onset of s% mptoms and signs much more quickl} than will one Ahci is sedentaq• or at rest. From a practical standpoint, a "orker driving a forklift ruck (a common job assigned women) will have a much lots'er level of CO in the )loodstrcam than .cill one uho is loading heavy barrels onto a pallet in the same cnvironment (21). In dealing with this facet of occupational health, that is, CO exposure, the following questions appear. (al Can occupational CO exposure produce heart disease? (b) What methods are there to detect and quantify this relationship, if- true? (c) Is prevention possible for those with such occupationaLrisk? However, funher research has shown that formation of carboxyhemoglobin is not the main mechanism of CO toxicity. In 1975, Goldbaum et al. produced a definitive paper demonsuztinc that carbox%hemoelobinemia was of onle minor or secondarv importance in CO poisoning (15a). In their experiments at-the Armed Forces Institute of Pathology, three groups of five dogs each were used. Group I was given lli r CO by-inhalation and Group I_I was bled to an anemic state, reducing the hemoglobin content of the blood by an average of 6Wr and then had blood volumes restored to normal udth_saline and Dextran. Group III %.as bled to the same anemic state as Group II but then transfused with packed red cells which contained SD-.r earboxyhemoclobin. All the does in Group I died isithin an hour with earbozy'hemoglobin les-els rancineg behseen 54 and 90%. Group 11 dogs sur- %ived indefinitely. Most important was that Group Il] dogs survived indefinitely with determined carbox}hemoglobin levels of 607 (57-6A9). From the foregoing. it is clear that even extensive combination of the hemoglo- bin With CO is not verv dancerous. Other Ncorkers have demonstrated that the true _site_of toxicity is the cytochrome a, oxidase in the mitochond_ria (10a, 1]a, I8a). _ The clinical condition of the patient is therefore determined byy the amount of evtochrame a, oxidase that is blocked. This is the same enzyme that is affected in cyanide poisoning and hydrogen sulfide poisoning. Fortunately, ox%gen competes with CO for binding to cXtochrome oxid-ase-and, therefore, oxygen treatment is eEectne. Because it is not clinically possible to measure the level of impairment of the evtochrome system, our only-laboraton' index is the carboxyhemoglobin. It must be borne in mind that all of the published literature relates various degrees of incapacitation to the carboxchemoglobin level. These must be interpreted as av- erages dependingon ahetherthe exposure is acute, chronic, or prolonged. The actual clinical •tatus of patients varies widely w'ith any given level of car- box.hemoclobin , 1l'hen t;,e tissu-,s of the bod% become hrpoxic due to e}'tochrome blockade, the heart must supply more blood by increasing both its rate and its output. Thus, the eoronanarteries must supphmore oxygen to the heart. The mrocardium nor- mallx extracts 75% of the ox%gen supplied to it via the coronar~ arteries, which is 1 ---- - ~------ I-- ~~. - = ~- _ , w

'~_.___.. .. _. CARI.ZEifZ probability from a statistical point of view. The authors' reminder of the associa.lion betsreen caposure to hcat and exposure Io CO is a key factor. With this in mind, these results do not allow any conclusions as to the cause of the slight elevation of the blood pressure found in groups wilh CO cxposure from smoking azd occupation. I According to Koskela and coinvestigalors (25), when CO exposure is consid- ered a causative factor for coronary disease, the failure to f~nd excess mortality among those exposed may be due to too small exposure differences between the "exDosed" and the "unexposed," i.e., the gneral population or other categories of foundnworkers. First, all categories contain about the same proportion of smokers,Oend, therefore. the reference cale6oq' is b)' no means "clean" with regard to CO exposua; second, CO exposure is inlermiuent in foundries and only . part of the "exposed" worAers actnallv have higher carboxyhemoglobin values Ithan from smoking alone (<q, Health selection may have contribmed also to the Inegatire finding: its possible impact has been discussed elsewhere (26). For these ~aasons. Koekela rr a1. concluded that their study must be regarded as rather noninformative with respect to a possible effect of CO exposure upon coronary mortalilx'. The ideal stodr vwtid be resrrinrd lo noaso+oRers +cith e.+robGshrd CO uponvr and uardd require a prospecli,e design (?5). With regard to my three questions, the state of the " rt o occupationnl medicine;" -industrial hcci[ne," and "environmental medicine" are not sufri- cienOy adcanced, nor cohesive, that any deGoiti,e solutions mzy be offered- An inference can be drawn from epidemiologic im"esticatior.s to auempt to showthal an environmentzl cavsc has a medical effect,.but it is especially difficult to relale environmental or occupational ecidence to diseases with multicauses, such as certain ezrdio,ascular dlseases- seell recognized to hace underlying predi=_posing factors in many subjects and multiple etiolocic possibilities. Perhaps experimental epidemiologR utilizing large animal models such as monkevs or baboons under simulated conditions oP-'S hr work` Itreadmill + CO 4 heat + adcquale ["humati J die0. might pro.ide some ans.vers. Ho.recer, based on my background and viewpoinls. I concur ssholcheanedlc with the recommendations made by % 'inzmo avd Tosaacainen fSl)' i Aln order to prevcnt the health hazard created by the presence of carbon r~ monoxide in the air, foundries should reduce the carbon monoxide concentrations in the air xith technical means and provide for the re€ular monitonng of both the _ carbon monoxide concentralions in the air and the carbox,rhemuglobin levels of the workers. Insulating the furnaces acainsl leaks and installing efficient local and /gcneralexhausfsSystemslo.%erthecarbonmonoxide-In'elsinthezirofwo+Asitcs. ~~ In addition. foundnes can reduce carbon monoxide concenlrations in the casting areas bc installing local exhaust syslems) enclosing the conveyors, and by blowing clean air into the work sitcs. _ AA good ventilation system inn the casting area is also important because other ~ Iharmful gases, such as those formed from ~he psrulysis of resin binders, can be _fpresent. ,properly choosing the qualiry' and quantity of the molding sand zddiiives ma)~ , Dreduce the amounl of carbon monoxide formed during castin6A .'~ J, ~ L i

._/ . /tL 1 _ `..-t T4• fJ.. ,1 ..2 l. _ " si6- ParrrnE MEDicr•1 B~n q/,19 9 Thls Se( CJ p or Querie s. kul;. ,r r , hdicate all cnrrectioas The Epidemiology of Carbon Monoxide in Cardiovascular Disease in Industrial Environments7g,~ A Review' CARL ZENZ L/ X 2416 Ronr Rlirr Per4r.es, R'esr AfGs, Il~sransin 53227 Carbon meeoside ICOI. uhich is encountered in man, industries, processes. and Sarious places of uort:,;s or.e of the most common industria) poisons. This article re•'iews Anown factors concernir.g tSc role of CO in card_io+ascular diseases along ui;h imponani occupa- tional aspecu. such as uork iniecsil) (encrF) requirement of a job and'or degree of metabolie acCi.iic ofz uorker) and influence of CO production resulting from occupational exposure to me:h%L•r.e chloride, a..idef.' used soktnt which. in man, is mnaMlized panty to CO. Reasons for threshold limit alues 1"TL%'s") are given and hnu' they are derived from the feuepidemiologic studies a%ailaNe. Ihau'ing from Briiish. Finnish, and selecicd U.S. insestiFations. the difficulties in conducting epidemiolopic-suneys from different working groups are sel forth as are 1he major conelating Gndings of Ihe potential influence of CO on the ea:dio,ascular slatus of chronically exposed unrkers. Carbon monoxide poisoning is thought to be the most common industrial poisoning, mainly because it is odorless and.tasteless, giving no %.'arning of its presence under most circumstances. and because thP-early symptoms can resem- ble other diseases. Almost any industrial item manufactured today involves the use of heat, fire, combustion, or oxidation at some point during its processing. For these reasons, the possibilities of carbon monozide (CO) poisoning are ubiquitous. Certain industries have been long recoenized to be particularlv hazardous in rela- tion to CO exposures. These industries are the iron and steel foundries, pulp paper mills, petroleum refining. sintering mills, and the manufacture of formaldehyde and coke. Within tose industries. the main sources of CO have been identified as emanating from the cupolas in the foundries. catalytic cracking units in petroleum refineries, lime kilns. and the kraft recovery furnaces in kraft paper mills, and the siniering of blast furnace feed. There are many other obvious but less well- documented sources known to produce large quantities of CO, with the greatest hazards found in automotive and garaF work, forklift truck operations, ete. Be- cause the amounts of CO produced usually do not create problems, poisoning may occur with little warning if either the production of CO increases or ventilation is decreased as mayy occur during cold weather. . This presentation will not consider details of acute and severe general effects from CO exposures. the pathoph}'siology% specific and specialized treatment, the vexing and compounding influences of tobacco smoking. behavioral-psychomotor ' Presented at a Wod.shop on Czrbon Monoxide and Cardiovascular Disease, sponsored b)' the American Health Foundation and the Federal Health Office, Federal Republic of Germany, Berlin, October 10-12- 1978. I -'--- -- - - 0091, i435,'79A300040050?.00'o C,>rpAi L IY%9GI Ac.Crm.r Prn-Irc A4 ~hia or m-t re,m, rrarneG. ~ tfii; se~ G

1 •-r N'OFASHOP:C.xhtiO\'LtONOLiOExsDC\'O much more than the brain uses. Therefore, as anyone •,lth coronzn' heart discase soon n'iIl suffer from hypoxia of the nyocardium, the heart should be considered the first target organ in carbon monoxide poisoning because of the necessity for ~ increased cardiac oulput Ihe mpocardium extracts?pyruxate and - 1:ormally . , Iaelale from the coronaq circulation for oxidation. R'hen the carho.chemoplohin reaches a mean of 8.7ry, the mpocardium fails to eurzcl cilher of these two substances and actuall)^ poduces both (10). Obviously. an $J i anemia is not the cause, but the mito:hondrial ectochrome failure is the c\planation.The acute effects of CO on myocardial function in hezllhq adulrs, in palients xcith coronan. anen, disease, and in patients with noncoronaqhean disease have been amply descrn3ed by inGestigators (4, 5, 12, 16), There is general acreemenl that the most culnerahle tarFet organ for low-Ievei CO exposme is the heart. In 1979, Sjostrand. milizing inupro• ed methods of ineasurements. demonslraled that the human body scas a net producer of CO, identifying the source as the alpha- methene bridge betxeen the four porphyrin units in the heme malecule (36). During Ihe "req'clin" of the heme molecule reclaiminc iron, four molecu CO are released (or c.eqmolecule of hemc catabolized (31). At this !ime,~jos) (Tpf ` ' S P - Irznd and his colleacucs also suggested a vep' practical means for eslimating ,/-- body's level of carboxchemoglohin, through analy'sis of expired air. Ningold rt nl.\ _'~~~ ~YI}/d1 (31) extensively applied these techniques fur expired air-sample analyscs for esli- malion of carboxphemoelobin in epidemiolocic studies of larce populations and in f''P ' screening studies in Callfornia. Amon_c these many nome•ronhy fndings ..erc the multiple complicatine zspects im'ol.ing smokers and nonsmokers. a topic bcyond the scope and time of this presentation. Astnp,tl8). Kjcldsen (_'2), Thomsen (40), and Wald and Hov:ard (4'_I had hecn observinB the possible role of CO in the patho8enesis o(atherosderosis. Kjeldsen . ('_3) demonstrated that in choleste ol fed rahhits, exposure to c rbnn rro ex-de or I to iow oxypen trnson uould _ crease the amount of I p d A posrt'o the ane -al +essds Da msern! st,rd-cdCOandexycnmentalathe nsclerosis rahbtssclh conflicting fnd- es (141. Irrvestigators have concluded that there are se~eral svavs in ~rhich CO at the most commoolc found Ievels can dinicallc affect czrdiac function_ or ir.fluence the occurrence and severin- of coronaq' hcan disease. These are: aSgrncation of . angina pectoris: aeeravation of intermittent claudication: aheretions of elec- [rocardiographic responses in normal suhjects /these effects hace been observed - in certain occupations uhere exposure to CO is very hich. i.e. as in firemen) (38, 39): production or ageravatiun o(athermrlerosis associated v, ith the CO in smok- ing: and, possibly, a decrement_pP^:.urviral in patients \~ith zcme myocatdial infarctions. There is abwidant documenlation that an elevaGon of carboxphentoglohin levels greater than 5% can affect adversely patients ..ith anginz pectoris and certain other cardiovxsaular diseases (2, 3, 71, and that exercise tolerznce is ' _drereased and ancinal pains are of longer duralion. ~ ~ Not onl musv endoeenous CO (ormation in the human bodybe consideted, but I ti~ M~ other exmrnal contanir.ants mz} funhcr;^ mpound the~.•rob]er.A. Most commonly encountered, especially in the vnalmr ustnal estabhshmems. as xell zs t In e se_ ese contain a carietp of hydrocrrbon i homrs, is exposure to paint r°movcrs Th ~

i}-=_ - CARL ZEVZ i----- ---- Au - ~ U ngredients. a major one being mcth)lene chloride (dichloromcthane, CFif~Clr) ~-(~~1'~ ,,~~!I~. +hichhasbeensboxcntobemetabo!izedrapidlymCOt79.37).Undercondiuons f~ 1 ~ \~ l Z-1 !- ~ f il i h i ffi i i i h b ~ .. c ~ poor.ent at on,suc as nsu enta rmovemcnt na omeBaraSe, asement. ~ , x small s.orkplace, concentations of inethy!ene chloride vapors can accumulate • quioklp. Smvan (37) has shoRn that ihe use of such paint remover for a period of 1 hr easily ean produce carboxchemoglobin saturation of 5-10 7- Src.re" ds=-..r.A tharaprnraACn>-!+aukcc-heslvtal-mirtNcccQ-painl~.tuppinp,.-+a.--•-~ i i f^rTl e ef '.k rg-as-part~Fa~cupa+ienz!ihetapY forpnrnm: including operat:~s-ccuaner~parsriie:.:c-ia-iAu: e.,r!)r vzlest.enl-peri[akVIt is noti possible to determine Ihe extent of paint remover use in the U.S. pricate sector ~ and perhaps equally difficult to determinc occupational exposure to maih)trne ' hl In terms oride in the thousands of workp!aces uhere solvents are in daily use_ c of potential worker exposure. methiicn.e chloride. although not the most hazard- ; I , ous chlorinated hcdroearbon. is sometvhat unique in th<coniext of CO sources. In ~r"4 addition t0 its common use as a plnt or Varnish remOr'er, it is trldCi)' used in d:greasing. as-an aerosol propei!am~as a solvent for paint; in plastic uxtile /~ - ; making, in producing photo Glns.fin preparing cer.am oils and-srexes-e,nn&- t - Th KIOSHimf i US ib 70C'J0 -e estate o exposuren the..s aout. i I w'orkers. but this estimate does not include home use. - ~ In addition to nicotine and CO, tobacco smoke is knor.n to contain numerous ! other respirabie components such as nickel oxides, oxides of nitrogen, hcdroe^_n eyanide,cadmiumoxides.andotherpro!)ticproductsoforeanicmam[ialsinthe ~ I tobacco binders and papers. Silk (35) presented suFstamial insight into Ihe dif- fculties of assessment and measurement of exposures in re9ationship to the de- vdopmem of threshold limit calues ("TI_V") nming that in the United Kingdom. . the-mosl hazardous p:ants associ3lyd , ith CO exposure are the blast furnaces and coke ovens. panico!arly in the steel industries •rhich. in 1972, uere responsible i for about 6tr< of the total reportab!c cases of CO eaposnre in his muntrc. He referred toU.S. NIOSH Cntena Document fnr Carbon hlanoxide. emphasizin ~/g that compliance with the recommended lrccl of CO exposure to 35 ppm "-ould ' '. mean that the maximum zccepiable level for carbox.hemoglobin in the blood v.-ould be S~-The main features of the NIOSH document are .conhy of restate- menL (al to present acute CO poisoning. (b) to protect the employec frnm delcte- - rious aherations associated acith carboxphemoelobin in excess of 57r,~c) lo pro- side the emp!o)ee.rirh protection from adverse behaviorel manifestations resnlt- . ine from prolonged exposure to IB++- CO lecels. Taking into account the ..ell-defined relationship betrseen smoking and con- - __ .---- -- ` comitant CO exposure in inhaled smoAe. the criteria document may not provide yr'.41: the same protection for smokers as for nonsmo:ers. The document did not com sider the fertile or prcgnant--thrs standard needs to he loscered to compem sate for loss of ozycemcarrpinc capaciqof the blood zl hicher ahitudes such as !i - C'~ 1500 tn ?46J m above sea lerel to 8(L'`0 f)_ Silk apdc pointed out the preblems oferrvrsion rclrers s, hich vwill make fumre epidemio!oFic studies extreme!g difficult from the standpoint of knoscledge of the ronri~unas (rrr8 of true ezposure to CO. The marn' difGcu!t technical aspects of accurate assessment of CO content of the air in the riorkplace, particularly ortr / .'

N'ORI(SHOP: CeRROS sIO~OSIDE nND Cx'D shoued a clear dose-response relationship a'ith regard to CO exposure from occupalion. smol.ing, or both, but no such trcnd scas found for ECG Gndings svggesdie ofcoronaq hean disease. Thes< resulls may suggest a greater sens6i•- ity in delectinc coronary haart diseasc on the part of the angina questionnaire. The systolic and diastolic blood pressnre^of CO-exposed uorkers wcre sfightfy higher than thoso of other worAers .chen age and smoking habits uere ialen into consid- tration. Houcs-er. eaposure to heat •cas intermixed.$Ih esposure to CO. It could be sho.crt that seleclion based nn health had operzted in Ihc foundri[s. Hence.lhe prevalence found can be considered to be underestimates of Ihe `tru<' occur- rence of cardiac disorderx. Ke,enheless, both angina and "corooap'ECG findings u'ere more precxlent than in other methodologically comparable studies on the general population or industrial s.orkers u'ilhout tosic exposure. HernberF and co-v.od.ers reponed thatexposure to CO secmed to emerce as a significznt linA beiu een cororary heart disease and foundq uorkers. As reponed elsewhere (dq. quite high CO concentlzlions do occur in the furnace and casting areas offoundries, espedallr in iron foundries. Although exposurc is intermittent. it ma, cause clearly elevaled concentrations ofcarboxphemoclobin (up ro'OS) in casters and furnzcemen. and Iheir exposure may u'ell constitute a haazard (18). When the combined elTect of smoking and occupational CO esposure nes studied. it zppeared that nonexposed nonsmokers had the lo,est s.'slolic pres- sure: and CO0.exposed smokers and exsmoL.ers, the hlghesl. These imesticators pro-rted critical statistical data In delineate reasons for certain succested find- ines. Both the ECG and the histon' of aneina obtained uith the standardized ques lionnaire used in this snrvey are uell-documented epidemiologric methods. 7be - authors state. horse.'eq that their diaenostic ac_curaep cannot, of coursr, be that of a thorough czrdiolopluiexaminauon, but in population svudics, both mcthods --- - giee useful results. This stalerneru has been documented often (Il, 20. 28, 30, J2_}<. _..5). - Howeserv cressseainnal studies of coronarv hean disease most be iolerpreted ,cilh caution since the zcu[e narure and high fatalily rle of its more secere man ifestations re.ult in underestimates of the lrue occurrence. This is e.en more true for occupational groups wilh phcsicallv demanding uork- because selection be" ~ comes as added factor. It is quite conceivable that poor health fa:xc-:.-Ye~ted?~ ~/[,t.~Z0./ persons to Ieave uork, either voluntarilc or because of a doctor's decision. As a 1~ result of such selection, fit and healthy uorAers are usually overrcpresented in / J ph)'sica117hheas?uorA in fdr~wel~i~(2d). C44',t~ The reason for the apparent relationship betueedblood pressue and CO eapu ~ / sure is b} no means clear- Several studies have shoun that buth scstolic and S diastolic presstursnse irnmediately after smoking (6). and the rise can be demom slrated ex en 30 min after Ihe smoking of hvo cigarettes. This occurrrnce is usually attributed. hnu e.'rr. to the nicotine in the cigarettes rather than to the CO expo- ; ~ sur<. Pan of thc smoAeri results in this stud)' can probably be eaplained by recent A~ ae- smeAinF. since abstinence could not be achieved, but the diRerences bn~r ten the occupalionalgroupscanrtotbeexplaineA_akw~_Oe.posurefromtheamldentzir ~ ^ app<aredtobzveanefTect.esnnthoughicoul d notbeveriGedailhah!cI)Knough MUNIVititt

o VC_ - CARL ZLNZ ILa. InFenim. A. l., Fedler. P. C..ind fton a. L. 1:cFal outrnpic aclion of carbon m aidr on IAe isobmd Lnaolumic bean vhh a hemoplebimfrcr pcrfusz:e. Frd. P•nr. 33. 501 114>a). 19, Jonrs, l. G.. a nd Sir.dair. A. Anerial dieras< amonpt b!asl fumace •. erAcn. Ann. Ora r:y. H, . 16, 1!-I0119'S). :0. Kr1s, A.. Arn.nis. C.. Bhdburn, H. a'.- ran Buahem, F. S. P_ euaiv, R., DJOrdjeaie, B. 5.. Donm. A. S_ FCaov. F., Kanon<n, 3.f.1.. Kimma, N_ 1<LOS. D.. Afonll. bt, Puddu. tl., andTa.IUr.H LEpidemidnfiasluGl< rdalydloeor0nar.bondlseas<C6araaeruu.snd men aFed aD-t9 in seren couoldes. Arra }1e1. Srnnd_ suppl. J60 (196)I. 21. Kind.a9. E. P. Caha.r mnno.id:, in "QcuCaeional \ICdidn JPrineiples and Pac:ical App6o- aioni - /C. 2<0[. Ed.) ) pp- 60a-61?. 1'ear Book Dled. Pub-. OikaFo, I9]5. 13. Kjeldsrn. R. "Smolinp and Alhnesderovis;' Thesis. CoprnhaFrn. blunAaFazrd, 19t9. J. Kjeldsen.K-Seolinpandcarbanrnmdudvup,a4easarlsAfacmrlnavhnroaclemllecardin.aarular dnram. Ad.. Erp I1eE. ffinl. 63. 31>-3'_I (19]5) . - 24. Kndson l. H Lc!uqca:i~iulri¢rien u>d icmissiensFCnz.ene for Lohlenmono.id {o den t'cr- inipmn5m:mSmuE32 180-IS?1197J1 - -- , ~ + ..- 1_r. KmLtla. R-S. H-1<rP S_ Ka•iai. R_ Janinrn. E.. and t`l.+mincn. \(. A monalm s:udp of foundr).oden.Seand.l.R'or4E- Lns.Elcoirh;suppl.l~l3-fl9119'61. IrLY•r f-L.LfA(1 yz onrn. Srcrd.l~ Po•t En• . Nrr'rh ; suppl. I,90-1o5119:6J ?n ' ?l.anl<LH..andHacsul.M A! .SU nicafaspecsoflheanal_siso(CauSmmrerre;pe<n resludin ofdisrue.J.lacCcnrnhnr.2;i19-.:6(19.9L 1 W ~If / 25. Pumu, S_and Kanonen. f.L 1. AnFina Froern and FCG abnnrmaTniee in reta:ion lo preFnosi ls n/1 of corenarc bra.-s di,nase In {..pulntlon swdles in Fin:and. Ad. . C-dnl. 8, 1<9-16111r,A- • 29. Ramey. R S.. N eFn~~n D H, and EIAim. H. \ . In di n co. sion or merMiene <Moride io ac n n . Arrh. En•vun. Hc!rA ]L, `_3-2'6 (19'a) 30. Reld.uDM. D_CornfidC.) . alarl.ush. R. F., S<ICd.I•.. Pedencn. E_ and HaemreL M'. Swdies of dis among T'~Fn zndn e peru ,mGrealBrinin.For-a. andrheCnueESime. IH[Paesalen of eardln espjraop s n:plomn a onF miFra.u. and nzn•e br:rn m Ihe l,'nned Slaqf. 3ur. Crcrrrlmr/11nnoFr. 19,331119fL1 11. Rinyold. W.. Go:dsn:rh.l. R_ Hd.iF R.. Fr,IR_ and Schurnel,F. Evimaiinp rerem <arM1Or' o.ide esFo'urn- A rapid meih.d. Ar.h. Envenn. Hrclrh 5. 149-3 19 119R'_IL 32. Rose.G-A Ivchem~:bcand,sra•emn:ddleacedmenPSe.alenceaompznsonsinEurope B.dl RH03B,Ms/IW.FI. . 33. Rose. G. A. P:eLza ine < onn bea e Lom minor -, mv and decnoczrde, ,; h'c fndinps. B.n. l. P.n. S^Alyd. 25, 9: 119tI1. 14. Rose. G. A.. and Blac4urn. H. "CGrdimzacular sur.n mohods:' H'odd Healih qeanua•,~un. Orncca. 19fE. 3S Silk. S. l. The Ilmahold Ilmii talue fin earMn monovide. A- _ (1reee- HrF. 18, !9- Js 119'9. ' I )f. SjCasrand. T. EnCOFenous formanon of ealor. mnon.idr in man under nnrmal and pzl6elop;+J ~ .lkid- laruf'' - mndmmns Snced. l. CLn. In6. Jmnr 1.2014Ja (1949, . ~ ~ ojUl - QJ~ 3!. Le.an, R. D.. ar! Hale. C. L. Paieo remnaxr hazard IAVA 235, 39E-a01 (19"/61. )8. Stc.an, R. D.. PnrnuaJ. E. Fishn. L\.. Hml.o. )f. l.. Barnu. F D_ Dodd. H. C_. and " Hen n. A. A. Eenrim ul bum espoaur< lu hiFh eoncemnnam or cmbon mono.ide. Arrh. EnaJrn.n Hrcl:h 26. I^ )119%31 - 39. Sreun.R.D.Sir.artR 5_SUmm.K..aadSedco.R.P.Rapidruimmionofcarbonhemn k llobinloclin6rcGFhmnJAAIA235.)(/390-39If19%61 0 Tbom , H. K CAL•on monoaide.InGUeed ameruselerovis in Frin.ales. Ad,eeo,drroed 3., 13} 'aD / 19-ai. ' al. Yrnamo, M_ and Tosvwren, A G_ .tce vionsalde in foundr. au. Srnnd. l. NTS( En,,,rn. ~ lfec.'rh 2, suppl L a%--1119%6L I a'_. Nald.6_.ndHa.arGS 5n•.oArnFCarNr.monmidrandznerialtlneaa<.A~~n.Oru:p H, r 16, - 1-la 11~ J) . a3. Wald. IJ., Ho.ord. 5.. Smi@. P. O.. acd ICjeldvrn. K. Anwrlarion bernren aihrrusJe•oric ' drsea.n a-.C or1•a..[aemeploSL~ l<.<I, in IoTr.re smeArn.B- . sfrd l. l, )41-J65119%cl. ' u. w elbom. T. A_ Cunpian. G. 6_ Cu1hn. K. l_ Cumo.. U. H.. V cCall, !.L G. and 5, -hou- a. NNOW