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na" or "Alonda` morninc dcath." The noniatal cases zre attaa6• o hi,h ~r•emhie angzna pe~:ori,. but ~khich are nrt pr,.?, .tl.td hk :~rra.e ur pcti;hi. arousal. The O:,ur I'•1 d,3tie- e.pewre to nnroalveenn sth~;enr _,i:..ji Jtnitrace tr,.!';onscqutnt{y the Jrwrnataon -n ;ra:r ~~:;h rc al -rmPtom..' has been u•r.7. THi• es;*rr-+on,a,a• ~ar:ru• onijittons- ;uch .t..anginu. ,uronar~ •pa•m.,m~o:ardial sntar;tion, ar- rh~thmia, ancJ uJden death. Ini tho.e instances in autop,+ %va, performed. normal coronarN ar- terit• t%tre tound Simar :a,e reports ra%e been published in other ,:ountne. t.61-266t. and tlorton', :omprehensive re- ti tt%+ trom 19-- t.6"1 ;ontatns an excellent review of' the literature .:onrerning %,rrhdra%%al hazards related to occupataonal habituation to aliphatic nttrates (7-t reterencest:.Ir,appears from %(orton's re+ic%% that. dur- tng the period 195:-19'=. articles %%ere published about %londa> mormmne attacks rn,German>. ltalv. Ja- pan. France. S,ktd'en. Czechosto%al.ia. the So%iet Lnion.and theLnned Sta^.es. It appears turrhermorc that the first fimen,can des:rnption %% as not Carmichael & Lteben"s article from 1963 (_6a9, as formerlti be- lietied.,but an article fiomi 19a'3'by Foulaer (2681'. Foul- ger's article on "e\posure to toxic chemtcals- did not mention. ho%ce%er,. that it concerned nttroglycertn: ethylenc gl\ col, dinirrate. [See. in additton. the cor- respondence between Fouieer and Mt7rton (269)land%torton's article omthe ethtcal problems oficonceal- rne medical kno%% ledge %%tthtn ocrupattonal medicine (:"0)i. Half a.ear after %iorton's re~ieK. Hogstedt & Asrlson,t.'1 t introduced a nerr era in this research by publishing the first truly epidemologic study. it was a case-referent study .~hicti~ «as later supplemented kk ith a prospecti%e study (.'2) and with hygienic mea- surements (2"3). µhich together with two additionali articles formed part of Hogstedt's thesis (27.t), In these %torks of highepidemiologic quality„it is documented :n a:on% immng' Nay that, exposure to nitroglycerin/ cth.lene g(.cot dinitrate not only causes symptoms, dis- eases. and deaths due to nitrate wuhdrawal, but also raises the risik for CVD many ycars after the cessation of erposure. Hotastedr's results ha\,r beemconfirmed during the 1980s by two other investigations (275. 276)t both of .khich are historical' prospective studies. In these studies. more CVD deaths were found than expected among the erposed' workers despite preemplbyment screening and%or medical m,.nworing of the employees. Thus it is now clt;ar that nitroglycerin and, especial- (y; ethylene glycol dinitrate increase the risk for,CVD in, the following two ways: partly via the specific "tilonday morning attacks" due to nitrate withdraw- al and partly sia an increased'risk for CVD which per- sists long after the cessation of exposure. This double effect, is described in a few of the reviews, such as Fine's (,I ) and Kurppa et al's (6), while reviews on the topic were still'being published during the i980s which only or almost ecclhsi%ely describe nitrate Ktthdtawali and'-4fonday morntng attacks" (2. 3. 5. 2'")'. Other chemical sUb'srances and compounds This section brie(l~ re~icNS canous studiesconcerntng C% D and other chemical substances - areas in which onh• a fcµ studies ha%e been cond'ucted or in uhic.h se%eral' "competmg" exposures occur in the same itud+. Om(rroroliwne_ (n 1986. Levine ct al (2'8)publtshed a historical prospeeti.e study of,Workers in, two fac- tories in,which the emplotiecs had been exposed to dinurotoluenc (27$). As in so many other instances. it was a susptcion.of carc.tnogenicitv w htch mottrated the studj, but' no tncreased', incidence of cancer was found amone these .corkers. Hoµe.er, an increased, incid'ence of IHD IS51R 1511 appeared when the data firomiboth factories uere combined. with a relatton- ship between the duration and'the intenstty of the er- posure and the incidence of IHD Accordtng to the authors, only s er} few of' the workers had' been er- posed to nitroglycerin or ethylene glircol diniuate. Organoph'osphares. Two cross-sectional studies - one Danish (279) and one Indian (2801 - have shown an increased pre~alence of "ischemic" electroeardio- graphic changes among workers exposed to or ganophosphates. The Indian study included 155 ex- posed persons and 60 referents, while the Danish in- vestigation included 446 workers. of whom 114 were classified as heavily exposed'. fn the Danish study, the higher prevalence of electrocardiographic changes among the heavily exposed'individuals remained after control for age and smoking. Anrimon-v rrist,lfide. fn the work by Brieger et al from 19541(281/, a factory was mentioned in which 125 men were exposed to antimony trisulfide for eight months to twoyears. During this period, eight of the workers died suddenly. Two,of the deaths were due to chronic heart disease. Four of the deceased were under 45 years of age. Because of this finding, the workers were ex- amined. and elbctrocardiographic changes were found in 37 of the 75 examined. A review of the literature on animal experiments with antimony trnsulfide seemed to show that the substance is cardiotoxic. At, the fac- tory studied, the use of antimony trisulfide was stopped, and no further sudden deaths were observed. In 12 of 56 reexamined workers, the observed elec- trocardiographic changes persisted. No other studies on antimony trisu(fide were found in the literature. Beryllium. Im a historical prospective study by. Wagoner et al (282), mortality was investigated in a cohort of 3055 workers who had been exposed to be- ryllium. Despite an assumed healthy worker effect, an SMR of 113 (P'<0.05) was found for heart disease in comparison with the mortality of American white 255

males. The highest value (SMR 129) was recorded for those exposed for at least fiwe years. Polvcvchc aromarrc compounds. In a ease-referent stud% (383) of 6000 men employed by a primary alu- minum smeiter}, there were 306 new cases of IHD dur. ing the period 197t- i983. The persons concerned were compared with 5'9 matched referents. Among the bl'ue-tolliir workers. a relanve risk for IHD of 2J was found. The risk aas particularly elevated among workers emplo)ed' in the reduction divisions. These workers had a relative risk of 1.7 for IHD when com- pared with the remaining blue-collar workers. Unfor.- tunately, the referents were matched for duration of employment- and this type of matching prevented the researchers from uncovering a possible relationship with the duration of the exposure. Both a Danish (284) and a Swedish (285) mortality study of chimney sweeps found an excess frequency of' IHD. The Danish, studyy cohort consisted' of 713 chimney sweeps, and the SMR for, IHD was 222when employed men were used as the reference. The Swed- ish, study cohort consisted of more than 5000 chim- ney sweeps, and the SMR' for IHD was found to be 135 when all Swedish men were used as the reference group. In both instances, the excess was significant at the 5 Ma level. In a historical prospective study of gas workers, Gustavsson & Reuterwall (286) found excess mortali- ty due to IHD (SMR 125) and stroke (SMR 152): In this study;,occupationally active persons in Stockholhn were used as the reference group. Due to the small numbers, these results were not statuticallysignifiunt. Common for aluminum reduction workers„chim- ney sweeps, and gas workers is that they are exposed to combustion products. According to several authors (6, 284, 286), it can be hypothesized that polycyclic aromatic hydrocarbons or other polycyclic aromatic compounds are not only carcinogenic, but also increase the risk'for IHD: This assumption is in accordance with the monoclonal'hypothesis of atherosclerosis proposed by Bendirt & Benditt (287);, according to which atherosclerotic lesions might be derived from the proliferation of a single cell and could be considered to be benign tumors. The excess frequency of both IHD and lung cancer among, Danish cooks and bakers (288) in the national Danish, mortality study further supports this theory, as it must be assumed that many working in these trades are exposed to polycyclic aro• matic hydrocarbons. Concluding r.marhs During my collection of the material for this review of the literature, 1 found no additional'studies that could be judged as sufficiently relevant for inclusion. Since, of course, the judgment of which studies are to be regarded as relevant is inevitably sub)ective, the reader may wish to supplement this review with other comprehensive ones dealing with CVD and chemtcal exposure (1, 2, 5, 6, 9, 10). In a recently published' article (283) concerning chemical exposures at work and the risk for IHD. the authors wrote: "Several personal risk factors are known to contribute to the development of IHD, but the effects of adverse working conditions have re- mained almost unexplored [p 659)," (283). This is a very widespread conception, but both the present review of the literature concerning chemical occupational fac- tors and CVD and the previous article concerning non- chemical factors (14) have shown that the conception is not completely correct. Hundreds of studies, in fact, have been carried out in this fieid, and, in several areas, knowledge today is considerable. The present review has, inisome areas. confirmed other reviews of the literature, while in others the con- clustons reached'are contrary to the currenrvieM_ For carbon disulfide and nitroglycenn;',ethylene glycol dini- trate. the general opinion is confirmed. Ih these areas, studies have been conducted which have convineed vir- tually everybody about the causal relauonship between these substances and'CM It should be emphasized', that what has convinced'the scientific community is not the number of'studies - as a matter of fact, there are very few - but the high methodological quality of' the studies. For lead and passive smoking, this review concludes more positively than others. The research concerning lead and CVD is very old, but not until recently has in been "discovered" in earnesn. This phenomenon is, to a large extent, due to the remarkable results con- cerning low-kvelllead exposure and blood pressure from the National Health and Nutrition Examination Survey 11, which were published in highly esteemed journals (70, 72). The research eoncerning passive smoking is new, and there are still relatively few studies, but they have a high quality and the results are consistent. In other areas, the conclusions are more negative than usual; especially for cadmium and carbon monox- ide. The research concerning cadmium and CVD is genenlly of poor quality, but the few good ~ studies, together with the fact that tobacco smoking is not a risk factor for hypertension, makes it reasonable to conclude tbat cadmium is not a CVD risk factor. For carbon monoxide, the situation is more complicated, since there might be acute, short-term, and long-term effects. it is concluded'that there are acute effects and possibly short-term„revenibie effects, but that carbon monoxide does not increase the risk foratherosciero- sts in occupationally exposed individuals. In table 5, an attempt has been made to classify the possible cardiovascular risk factors which have been reviewed in this and the previous article. The basis for this classification is the view tharempirical relation- shtps are not "proved" once and for all. Hypotheses 256

are :onformed or invalidated through the collecti.e and cumulaweMork which researchers carra out, and s%s- temanc :rmcal re~le+ts oi the literature constttute an exer more Important~ pan of this process. Se%eral oi the factors mentioned under "~erc defi- ntte" and "quite deitnna" in table i' are Ntdespread in tndustrtalized countries This is true for physical inaati% it at ttorl.. noise. shttt ttork. µork stratn: lead. and~pass+,e;mokins- Even if the relato;e risk forCVD .onnected tttth e:;.:: of these factors is modest (from apprortmatel' y 1.1 to :.0)i the total'etiologic fraction tattrtbutablertski will be considerable. and therefore the potential pre+entl*e benefit' is great. Nott the classic question "ls enough known to use this kno%.ledee for pre%entive acti.itues' artses. This is naturalln not a scientific questionbut is stilllone with a hlch,researchers are often confronted and are e.r- pected to be able to answer. One ans%ker could be that enour:hiis known about the factors which have been mentioned under "ser% definlte" and "quite definne" in table S to initiate pretienuon, There could howeser be a risk, of making a mistake since one or more of the ei¢ht rtsk factors mentioned, at some point in the future, might prose not to be a risk factor (or CVD. With respect to this possibility, the fol)owing rwo points are worth making: (i/ if one chooses not to act until one has "100 °'s certain evidence," one is likel% to make mistakes whichihave serious consequences for the health and mortaliE,y of many people, and (ii) the factors wfiich~ha%e been mentioned in table S are alli risk factors for diseases other than CVD. If one or more should pro~e not to be a risk factor for CVD, there Nould'stiil be a positi.e effect from reducing or remo.tn¢ these factors. !n should be emphasized that table 5 only includes factors which,.ha%c been mentioned in the literature as possible risk factors for CVD. The absence of'evidence about a causal relationship should, of course, never be confused with evidence about an absent causal'rela- uonship. it should4urther be mentioned that the ta- ble deals with levels of exposure which occur "nor- mall% " au workplaces in Europe and North America. Marmot & Theorell (289) recentiy claimed that psy- chosocial strain at work is probably part of the expla- nation for the negative correlation between social class and CVD incidence which is seenn in industrialized countries. fnitheir review; they emphasize Karasek's job strain modetl The deliberations by Marmot & Theorell are an important: supplement and corrective to the prevailing explanations which virtually always have their starting point in individual risk factors. It should be stressed, however, that not only job strain, but also several of the other factors mentioned in ta- ble S, are more widespread in the lower social classes. Therefore changes in the work environment might con- tribute to the efforts to reduce the social,inequities in morbidity and'mortality which eonstitute an impor- tanr target in the program "Health for All by the Year :000" of the Vworld Health Organization and in the health policy of many tndi.tdual countrtes. Finally_ some remarks on~the form and content of' literature ret teKs Mtthtrnmedlcal researchi It is true for most re.iews that the eraterus for collecting the litera- ture and for esaluating the tnditi tdual studies are net~ ther explicit nor systematic. The most common mode is that the authors of the re; re>{ mention some posl- ti.e and nerratr.r studies, obser%e the evident lack of consensus. and conclude that further research is neces, san. This kind of resteN does not li;e up to elemen- tary sctentificc demands and'does not contribute to the development and claruficatton,of research. One ot the consequences of the steeply rising num- ber of scientific investigations all over the wortdis that researchers and other persons become ever more de- pendent on,reliable re.iews of the existing literature. Therefore re% iews musr, try to live up to the demands forvalidity, reliability, precision, and repooducibility which are in force for ,:^,: individual empirical studies. To the extent tharretu" 5 do live up tothese scienrif• ic demands, they will be able to ser.e two very noble purposes: (il the clarification of future research needs (one must northink only of stressing the ever present' "need'for moreresearch." but of a sharperclarifica- tton of hypotheses. method4nd design problems, mea- surement problems, etc> and (ii) to indicate those areas in which the evidence is so-certain" that preventive activities ought not be postponed further. In this con- nection, it should be pointed out that sottx uncmtatnty must alk•a,vs be accepted, as is the case in other hu- maniand social contexts. As is noted,in this and'the previous article (14), sev- eral reviews have been published in recent years in which.anempts have been made to live up to the men. tioned demands (S„27, 188, 29(}-296). One must hope that development in the direction of more systematic reviews will continue in the years to come. T.W. S. Ctass-t/eation of poss bta nak tactors for carolovas- cuWar 01s.as. tCVpt in tne roru env.lronmant. Cwsal rnal,on to Lvo NOnCMrn1CL Nr{ltactOr Ch.+n-sar v.rp e.hnmr aws,cN w+runtr Caroon msuwaoe nnm~ It .on plyc&nnrwnroplrco/ Ourlt ON,n,N won stqr/, tr,Qalaa& OMN,N oa~anps ano lo. 1narMr+nO bwnca. M,h sort was-bl. no,w Cowrt. ars.nK. can0u1110n .0.00uc,5 Sorn..nal, tiaa" . ,rrn,atwn Orqsnoonosonetta 0,. oosrel. oo.frlr.ou.ncrTaon0rotolu.n, a,t11+wRY. MI,C /yly /o.bIn'14.vA,. COOOrt /rpyNnCT "WM ,nono.qM ~OOaD,r no M.crora.H. CWO' Cao,Mwn: Mpan.C ., mas,onsnio aw..nts' ~ Inanws n,e ns. torCuD tnroupn.mc+as.o wooO waswn a Mpln.laral a.DOluta Inay 0e 44Y sso.uany n.n coMan.a .nn otn• ., „s.:tactons .aooslt,. ,na. Caus. cano%aC aHTylnrn,a anp fY04M o..fh 237

t 7 Acknowibdqments The stud% was supported b} the Dani;h lit ork Ensiron- ment Fund tgrant 198-t-::l and~b} the Danish Heart Foundaam References I. Fine L1 O..upatwna! heart disease. In- RomAi ``, ed. En,:r,nmrntalland oc:upattonal medictne. Boston: L ule. Bro•,r, and Co. 1981 359-65. _ GoidhaoerSZ Cardio~a~;ular erfeqs of'potenual haz- ards J im Coil Cardtol t983:'_:I'_10-5.. 3' Gonzales ER Vo proor of en,ironmemal ill effects on heart 1-kM-k 1980:_u?:I_ly-_01 1 Harlan %1'R. Sharret AR. K ei!! H. Turtno G%l. Borha- nt N.O. Resneiio, L. lmpa:t of the enstronmenron cardtosascularr dtsease. Circulation 1981:63:2z3A-6A. 5. Hopwtns P.%. Williams RR. .# >,ursey, of ]46 suggested coronan risk factors Atherosclerosis 198II:30:1-32. 6. Kurppa i:. Hietanen E. Klockars 1,11. erial. Chemical exposures at work and cardiotascuf4r morbtdity: atheros.-leros:ts: tscfiemic heart disease. hypenenston, ardtomyopaphy and arrh%thmtas. Scand J W ork En- .tron Health 198i:10:381-8. `fillar JD. Summary of ••Proposed national strategies for the prr%entton of Itadtnq kork-related diseases and injuries. part l' "Am 1 Ind' %ted 1988:13:.23-i0. 8 Monson RR. Occupation and urdio.ascular disease. In: Monson RR. ed. Occupational epidemiology. Boca Raton. FL: CRC Press Inc. 1980:_02-1: 9. Robinson CC. Kuller LH. Perper 1. An eptdemtologtc studs of sudden death a( work in an industrial coun- tl•. 19'79-1982. Am J Eptdemtol 1988':1.8:806-_0. 10, Rosenman KD. Cardiovascutarr disease and environ- mental',exposure. Bt J Ind S1ed 1979:36:85-97. 11. Rosenman KD. Cardtovascular disease and work place etposures. Arch Enaron Health 1984:39:218-24. 12. Tyroler HA.,Hyti:•nes S. Cobb LA, et al. Environmen- tal'nsk factors in coronary artery disease. Circulation 198' :76/ su p p l 1!1: l 39-s4. 13'. Warshaw LJ. Cardl asculareffectsoftoxicoceupa- ttonal exposure,. In: Warshaw LJ. ed. The heart in in- dustr>'. New ork. NY: Harper and'Brothers, 1960: 456-522. 14. Kristensen TS. Cardto•:.:rilar diseases and'the work environment: a cntical'review of the epidemrolbpc hter- ature on nonchemical factors. ScandU Work Environ Health 1969;151165-79. 15. Fischbetn A. Eevironmental and occupational]ead ex- posure. In::Rom WN, ed. Environmental and occupa- t onal medicine. Boston, MA: Little. Brown and Co, 1983:433--47. 16. %fastroni R. Trace elements and ardiovascular dis- eases. Bull WHO 1%9:r0i30S-12. I1. Schroeder HA. The role of trace elements in cardiovas- cular dtseases. Med Clin North Am 1974:58:381-%. 18. Anonymous. Traee elements and cardiovascular dis- eases, WHO Chron 1972:26:51-9. 19. Anonymous. Cadmium. lead, and hypertension. Lan- cer 1976:2:1230--I. 20. Borhani NO. Exposure to trace elements and nrdsOVas- cular disease. Circulation 1981:63:260A-3A,. 21. King E. Lead poisoning. Public Health Rev t982:10: 49-76. 22:Shaper AG. Pocock SJ. Blbod lead and blood pres- sure. Br Med'J! 1985:291:1147-9. 23. Shaper AG! Cardiovascular disease and trace metals. Proc R Soc Lond /Btol) 1979:203:135--43. 24. W'edetin RP. Blood lead levels. dietary ealcium, and hypertension. Ann Ihtern Med 1985:102403-4. 23. Telcky L.,A norc on blbod pressure in lead'possoning. 258 J Ind Hsg Tomco11193'.19 1-5 '_6. Stoftn D En.ironmental lead and the heart 1\l P C:III Cardtot 197.4:6:285-90 _. Sharp DS. Becker CE. Smith AH. Chron c lo -Ir d• lead exposure its role in the pathogenests utih pcrten- , on Med Toticoi 198":...10-3'_. =8. Po-k SJ. Shaper AG. Ashbl D: Delses HT. Cla- ron BE. The relationship ber«een blood lead. blood pressure. stroke and hean atta.ks, in middle-aged Bhtuh men. Ens,ron Hcalth Perspec.t I988:'8._3-30 '_9' 1'icters W. Ettdence ior effects of ,hrontc lead o\- posure on blood pressuretn ecpertmental antmai6 an otierntew En.tron Hkalth Perspecr 198d.~8'1-6 30 Chai S. lkebb RC. Eifects oi lead om~as,ular reac. usu>. Ens+ron Health Perspect 19M"8 85-9 3!. Kopp SJ. Barron JTi. Tow JA. Card o.as:ula- act ons 32.. oi lead and relationship to hypertensron a re,iew En, .tron Health Perspe.•t 1988:^8i91-9: Victery R, T% roler HA. % olpe R'. Grant LD Summarr of discussion sesstons, ssmpostum on lead-blood pres- sure relationships. En.tron Health,Perspe.: 1988:'S 139-53. 33. Rogan W'1. Hogan,MD. Chi PY. Co-am D Blbod pressure and lead le.els in enildren. J En,+ron Pa+nui Tovcoli I I9'8.::51'-20! 34 . Lilis R. Fischbern A. Eisinger J. et al Pre%altn,:e or lead'disease among secondan lead smelter..orkers and' biological indicators of lead exposure. Ensiron Res 197:14:255-85. 35. de Alhtetd'a aRP. Canalho F\1. Spinola -\G. Rocha H. Renal dysfunction in Brazilian lead workers im 1 Nephrol 1987:?:#55-8. 36. Boscolo P. Galli G., tannaccone A. Maruno F. Por- cetli G: Troncone L. Plasma rentn aemtt) and urrnan kallikrein.excretton,m ltad-exposed workers as related to h.pertenston and nephropathyLife Sct 1981:.8' 175-84. 37. Dreesen WC. Health of leadt%posed storage batrery workers. 1 Ind H>g Tosscoll 19.33t25t60-"0: 38. Elwood PC. Yarnell Jµ'G. Oldham PD. et al- Blood pressure and blood ltad in surseys in %%aies. Am 1 Eptdemiol 1985:127:942-5. 39. Elwood PC. Davey-Smith G.Oldham PD. Tioothil! C. Two Welsh sur.eys of blood lead and blood pressure. Environ Health Perspect 1988;78:119-21. 40:, Gerhardsson L. Lundstrom NG, Nordberg G. µall S. Monality and lead'exposure: a retrospective cohort study of Swedish smelter workers.,Br J Ihd Mecd 1986: 43:707-12. 41. Parkinson DK- Hodgson 10.1. Bromet E1. Dew 41.A. Connell SiM: Occupational lead exposure and blood pressure. Br J' Ind Med 1987;#:744-8. 42. Hodgson M. Parkinson D. Connell :\1, BromerE. Lead exposure and blood pressure: lrtick of an association. Am J Epidaniol 1985:122:540. 43. Hopper IL. Balderas A, %lathews JD:,Anali.sis of,sar- ianon in blood lead levels in Melbourne famtlies.%fed J Ausi 1982:2:373-6. 44. Jhaveri RC. Lavorgna L. Dube SK. Glass L, Khan F. EvansHE. Relationship of blood pressure to blood lead concentrations in small children. Pediatrics 1979:63:. 674-6. 45, de Kott WLAM. Verschoor NA. Wibowo AAE, van Hemmen JJ_,Occupauonal exposure ro lead and blood pressure: a study in 105 workers. Am J Ind yled1987: 1 1:145-56. 46. de Kort WLAM. 2:wennis WCM. Blood lead and blood s7. pressure: some implications for the situation in the Nethertands. Environ Health Perspect 1988:7g:67-70. Lilis R, Gavrilescu N, Nestorescu B. Dumuriu C. Roventa A. Nephropathy in chronic lead potsonrng.. Br J Ind'%7ed 1968:23:196-202. 48. Moreau T. Orssaud G. Juguet B, Busquet G'. Plom-

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