Cigarette smoking and ill health among black Americans

Cigarette smoking and ill health among black Americans

RICHARD COOPER, MD, BRIAN E. SIMMONS, MO

Clgarelle smoking might be equally rega rded as a symp­tom of a society a t odds with itself or as a ca use of disease per se~ at either level. it has earned the reputation of public health enemy number one. Smoking is also a crucial ex­ample of how the health of the black population has wors• ened under the guise of social adva ncement. Blacks now suffer the highest rates of coronary heart disease (CHO) and lung cancer of any population group in this country.1

Th is fact has been obscured by the tendency in medicine to focus attention on .,typical" black diseases such as he• moglob inopat hies and hypertension .

In 1977, there were 80,000 excess deaths among blacks, compared 10 the morta lity rate for t he rest of the popula­tion.' Yet the only clear -cut genetic disease of blacks known to contribute to this differential is sickle cell dis• ease, and, in I 977, only 277 dea ths among blacks were recorded as hcmoglobinopat hies, or 0.3% of the excess. 1

Environmental and social causes must be defined to ex­plain the reinaining 99.7%. The struct ure of the educa­tional system, a discri1ninatory job market, and residen­tial segregation have created a series of social relation­ships that confine blacks 10 a fixed position in society . The sum of these social institutions. reinforced by common at­titudes and prejudices, generates the invisible chains of rac ial oppression. Although the specific causes of black ill health may change over time, the fact of the disadvantage is a constant and wiU remain so until the intensity of racial discrimination is reduced.

The cigarette industry has exploited racial divisions in defining a profitab le black market. Spec ific brands, nota­bly Kool (Brown & \Villiamson) and, to a lesser extent , \Vinston, More, and Sa lem (RJ Reynolds), Newpo rt (Loews), and Virg inia Sl ims (P hilip Morris) have been promoted for maximum consumption in the black com• muni ty through the black-owned press and by mea ns of sponsorship of black c ivic organizations by tobacco com­panies. At the same time, black-oriented educational cam­paigns to discourage smoking have been limited.

PAl TE RNS OF CIGARETIE-REl.ATEO DISEASE Sources of data. It is difficult to arrive at precise esti­

mates or the disease burden imposed by smoking on blacks. Long-term prospective st udies of a sufficiently large and representat ive cohort would be requ ired for di­rect es1imates. Unfortunately, no such studies exist, and there are nonecurrently underway. The major prospective studies or cardiovascular disease have never enrolled ade­quate numbers of black part icipan ts. Of the origina l 5,000 persons in the Framingham cohort, only six were black,l

Fro11\ 1hc: OMMOn orCu diology. Ocpa111nen1 or Mtditine, Cook County HO$pi-111I, Cbk:igo.

Address cotresponcknce 10 Dr Cooper, AflOCiate Cbaltm1111. OividOn of Cnrdi• olo,gy. Ocpu tmtnl or Mcdi,cii,e, Cook Co11n1y f-lo,pit.il, Chicago, IL 60611.

)4 4 N EW YORK STATI! JO URNAL OF MF,DICINE/J ULY 198S

and industry- based stud ies that were initiated at the same time did not include meaningful numbers of minority par­ticipants. ' A prospective study of smok ing by the Ameri­can Ca ncer Society enrolled I million participants , only 22,000 of whom were black .' Two large ra ndomized car­diovascular disease trials which were recently complet­ed- the Multip le Risk Factor Intervention Trial (MRF IT) and the Hypertension Detection and Follow­Up Program (HDFP) - scree ncd large numbers of blacks in the recrui tment phase, and the follow-up data are now becoming availab le.5.6 All partic ipants in MRFIT were men, however, and recruitment was aimed primarily at e,nployed inembers of the middle class , result ing in a sam­ple that is not representat ive or the black population. The cohort being followed in a prospective study by the Na ­tiona l Health and Nutr it ion Exam ination Survey (or the Na tional Center for Health Statistics, Hyattsville, MD) includes a more representative black sample, but one that also is limited in size (on ly 528 black men and 635 black women over the age of 25).

In the absence of survey data, it is necessary to rely on vital statistics. There are import.ant limitations of the vital records system. In recent years, deaths have been coded by race, as opposed to the color system of .. white" and ·'non­white." Although this may improve present data sources, it introduces problems or comparabi lity when looking at trends over time. In addition, coding of death certificates is subject to misclassification in categories such as sudden coronary dea th. Last ly, as in all morta lity st udies, com­parisons between populations reflect survivor effects as well as selection by competing cause. The survivor effect is best seen in the black-whHe crossover in old age. 7 Thus, while fewer blacks live to the age of 80, those who do sur• vive are hea lthier and suffer lower age-specific death rates than do whiles. Since a larger proportion or the white pop­ulation survives into old age, t hey will be more like ly to die of the more common diseases of old age. The phenomenon of competing cause tends to eLiminate potential candi­dates for a specific disease through premature dea th from another, related d isease . Thus, if cigarettes contri bute 10 both CHD and lung ca ncer, a population with a high rate of exposure to other risk factors (such as hypertension or eleva ted cholestero l level in the case of CH D, or industrial occupations in the case of lung ea ncer) might selectively lose high-risk individuals a t a young age . A cigarette smoker dead of CH O at age 45 is no longer avai lable to die of lung cancer at 50. Given the higher overall mortality of blacks compared to whites some distortions of cause-spe­cific differentials will be observed . Unfortunate ly, there is no direct way to compensate for competing cause effects, and its true impact can only be a subject of speculation. One way to derive qualitative estimates of competing cause is to examine age-specific mortality patterns. \Vhile

age-adjustment compensates for the differences in the age structure between the black and white populations, it still exaggerates the relative importance of the diseases of the very elderly, since a higher proportion of the white popula­tion dies in this age category. The practical significance of these problems will become apparent in the analysis of cigarette-related disease that follows,

Blacks have a six year shorter life expectancy and high­er mortality rate from all but two of the 15 leading causes of death.1 While violence and stroke arc associated with higher relative rates among blacks, heart disease and can­cer make up by far the largest contributions to excess black mortality, accounting for 30% of the increase in all causes of mortality for men and 40% for women. As the two major causes of death in this country and the major health consequences of smoking, heart disease and cancer will serve as the primary focus of this analysis.

Smoking patterns. Although surveys of cigarette use are subject to the bias of under-reporting, findings in nu­merous studies over a period of 40 years yield consistent conclusions.8 Blacks generally took up the smoking habit IO to 20 years later than whites, in large part as a conse .. qucnce of the mass migration from the rural South to the urban North.• The first severely affected generation of blacks was that reaching young adulthood in the 1940s and 1950s. ln the mid-1950s smoking rates for blacks were still lower than those for whites.8 During the past 20 years the racial patterns of smoking have remained stat ic, with parallel changes in both groups. The percentages of adult smokers have leveled off at about 45% for black men and 30% for women (Table I) , Despite the higher preva-

TABLE I, Smoking Rales by Age, Sax, and Race; US, 1965 and 1980

Pcrttnfagc C..rrtnt SmokcrS 1%5 1980

White BIJitk White B1111ck

Mffl All ages i!: 20 52,1 S9.6 37.1 44,9

25-34 60.7 68.4 42.0 52.0 35-44 58,2 67.3 42.4 44.2 4S-64 5t. 9 S7.9 40 .0 48.8 ;, 65 28.5 36.4 16,6 27.9

Women All ages 2 20 34.5 32.7 30.0 30.6

2S-34 43.4 47,8 31.6 43.2 JS-44 43.9 42.8 35.6 36.5 4S•64 32.7 2S.7 30.6 34.3 ;, 65 9.8 7.1 17.4 9.4

Sour~: N9tiofl1l Hc,ihh ln1c,vicw Sci~ (IS, p J6S)

lance or cigarette users among black men, numerous re,. ports have shown that black smokers use fewer cigarettes per day. Thus, while 37% of white male smokers reported use of 25 or more cigarettes per day in 1980, only 11% of black men smoked that heavily. Among women, 26% of the white women smoked 25 or more cigarettes daily. compared 10 I 0% of black women. •0 Age patterns of smok:ing are similar in women in the two races, yet among young black men there is a higher prevalence of cigarette

use.10 ln sum, taking into account both the prevalence of smoking and the number of cigarettes consumed per smoker, it seems reasonable to conclude that as a popula­tion black women smoke 10% to 20%1css than white wom­en, while black and white men consume similar amounts of tobacco. These estimates do not take into consideration other factors such as differences in degree of inhalation, length to which the cigarette is smoked, the age at which smoking began, and brand preferences.

Coronary heart disease. There is a common miscon• ception among physicians that blacks arc relatively im­mune lo CHD. The reasons for this belief are complex, based on such divergent causes as the reputation of CHD as a disease of affluence and the higher levels of high den­sity lipoprotein cholesterol reported among blacks. 11 Al­though CHD rates appear 10 have been lower in blacks than whites for a decade or so after World \Var II,1l.13 they are slightly higher at the present t ime. Based on the 1981 vital statistics, age-adjusted mortality for CHO (both sexes combined) among blacks was 144 per I 00,000, versus 133 for whiles. 1 Two recent symposia have debated at length the epidemiology of CHO among blacks.14 The data arc inconsistent, particularly in rcla• tion to men, and additional population-based prospective studies are needed. The most reeettt age-sex-race specific data for CHO are presented in Table II. Age-adjusted

TABLE ti. Age-Speclf'lc: Death Rates from Coronary Heart Disease, by Sex and Race, US, 1978 (p&r 100,000)

M ffl Wonll?r1 Agt(y") Whitt Olntk Wl1i1e Bin ck

35-44 57.8 97,7 10.7 38.1 45-54 253.4 335.9 54.1 I 59.3 55-64 713.7 846.3 216.9 446.4 65-74 1,654.5 1,568.3 717.1 1,039.3 74- 85 3,939.5 3.341.2 2,505.2 2,608.3

85+ 7.597,7 4,024.6 6,246.0 3,463.1 All ages.

ag:o-o.djus.ted 257.8 260.6 117.l I 59,7

Sou~ II Nfrli: Ulflltrl Suuu. 1981. pp 124- 127.

rates are virtually the same for black men, compared 10 white, while they are 36% higber for black women. The phenomenon of an age crossover is apparent among men, with rates 50% higher in the age range 35 to 44 years for blacks, but higher for whites above 65. Only the much larger proportion of deaths among whites above age 80 make the age.adjusted rate similar in men. Among woin• en, a crossover is seen at age 80, with rates over 8S being twice as high for white women.

Why should a population with high rates of disease in middle age become resistant as it grows older? No intrin­sic biologic explanation for this phenomenon ex.ists. In a period of rapid secular trends, it is possible that rates could be going down for whites overall, while moving in the opposite direction for blacks. The younger generation would thus represent a new high risk group; as this genera­tion ages it would continue to experience higher rates, and, eventually, the differential would be consistent at all

J ULY 1985/NE.W YORK STATll JOURNAL OF MEDICINE 34S

ages. In fact, the racial crossover is not a transient phe­nomenon but one that has existed in some form for many years. In addition, secular trends in CHD have paralle led each other in the two racial groups for the last 15 years, declining rapid ly in both." The most likely explanat ion of the crossover is a combination of the healthy survivor ef­fect and competing cause. Blacks at high risk for CHD, namely those who smoke or have another, related disease. such as hypertension, are more likely to die before reach­ing the age of 80 than are whites.' Loos of t hese individ­uals from the cohort would falsely reduce the importa nce of the underlying process of coronary arterios5!lerosis.

Direct evidence exists to support the argument that compe ting cause reduces apparent CHD rates. In the fol­low-up data from MRFJT, blacks had slightly lower rates of CHD, yet, as expected, t hey experienced a proportion­ately higher mortality from stroke .s CHD death rates were 4.6/ I ,000 for black men, and 5.2/ I ,000 for whites, while stroke morta lity was 1.3/1·,000 for blacks and 0.5/ 1,000 for whites. More important, given the proopective nature of these data, it could be demonstrated that the deficit ofblaeks dying from CHD occurred exclusively in the hypertensive group. It was this group that contributed to the excess number of deaths from stro ke in blacks. 11 seems likely that many black men who are prone to coro­nary disease bee~use of hypertension as well as cigarette use, arc dying from stroke, renal disease, and heart failure before they have a chance to become a vict im of CHO .

There has long been concern that death certificat ion may be less reliab le for blacks than for wh.ites, and may have biased the vital statist ics. A new longitudinal study of cardiovascu lar disease (Commun ity and Cohort Sur­veillance Program) has been organiz.ed by the National Institutes of Health and will allow more prec ise study of mortality patterns." Data from the pilot phase of the st udy indicated the following age.adjus ted rates per 1,000 persons of fatal CHO: black men = 3.12, white men ~ 2.77; black women m 1.37, white women = 1.00.is Al ­though both incidence and morta lity appear to be higher at younger ages, the black disadvantage persists in t he agc,.adjustcd mortality data. However, these rates are based on relatively few events, and only after completion of this Sludy will there be definitive evidence .

In summary, CHD remains the most common cause of death in the black population, account ing for more than 20% of all mortality . Despite the popular misconcept ion, it

TABLE Ill. Respiratory Cancer Death Rates, Men, White and Non-While, US, 1930-1980 (per 100,000)

Age-Race % lncr~sc Group 1?30 t?◄O 1950 I?~ 1970 19114> 1950-198-0

Wl,ile 45- 54 8 20 35 54 6S 15 +t33 SS-64 13 41 Sl 152 199 214 +152

Non-White 45-54 3 IS 34 72 113 148 +335 55-64 6 20 6? tl? 232 34-0 +3?3

Source: US Vilal S1J1tis1ics YearboQb. &eloc1ed )'(3"" IJ.-aflh: U1d1"1 Sra1r.s. 1981. pp l.ll- Ul

346 NEW YORK STATE JOURNAL OP MEDICINE/JU LY t985

200

150

,/'/' ,, ,, ,

While, - - ---

llloek·--

1930 1940 1900 1960 1970 1980 Yeor

FIGURE 1. Death rates from lung cancc:,t tOt' ,non, black and white. ages 45 to 64, us, 1930-1980.

occurs more freque ntly among blacks lhan whites. The increase in risk of CHO associated with cigarette smoking is the same in blacks and whites.5 Cigarette smoking has been estimat ed to account for one third of all CHD deaths, 10 and doubles the relalive risk of CH D among in­dividua ls with hypertension . Widesp read smoking has ac­celerated the development of atheroocleroois in the black population.

Lung Cancer. When the rise in the incidence of prima~ ry lung tumors was first recognized in the 1930s, the death rates among blacks were about half of those of whites. Since then there has been an enormous increase in lung cancer in the black population (Table 11(, Fig I). Rales among both black and white women have accelerated since 1950. A racial age crossover in lung cancer is seen for both sexes (Table IV).

The rate of rise for men from 1950 has been three times greater for blacks than whites, and in the "1naxima1ly af­fected cohort" - the generat ion with the highest age-spe-

TABLE IV. Age-Speelflc Respirator, Caneer Death Rate by Sex and Race, US, 1978 (per 100,000)

Mtn Womt" Agc(y,) While 8bck While Black

)5 -44 11.7 26.8 7.0 8.6 45-S◄ 75.0 147.6 n .1 41.6 55-64 2 14.4 339.7 69.? 68.S 65-74 407.5 43?.S 90.5 70.3 75-84 510.7 493.6 91.4 ?2.0

85+ JS?.) 215,4 77.6 50.8 All age$,

nge.adjustcd 57.4 79,1 16.S 16.0

Sour<-« IIMM: u,,Itrd $tnltS, 1981. pp 132- 134,

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CiQarette ads account fOr In OXC0$$ o t 12% OI lott\l &(Nertlslng In ESS6008, "The magazine for today's blade. W()t'N'ln" (top !eh) . Apart from alcohol ad'Mtlslr'Q(20%). Clgl\(0110$ (t(O lhO IOacllngl)f'octuc:1 category In th& magazJoo, Among adv9rtl&ers tying In 10 8&ook Hl$lo,yMonth In February 1985 was RJ Reynolds . whiCh nwkOd lhO o«Mlon In £$$Once with a <lsCOlW)t coupon good for $1.50 o ff a carton 01 Sa lem (boftom left). The adv9rtisement also loat1.Kod thO heOOlino "A Sl'tk.110 to Bl&Ck Scientists and Inventors" encl a portJalt of Goorge w. Cnf'\<or. Otnot advortlsers In each ls.sue of EssMCtl, Jot, Et,ony 4tld other bll'tCk•Otiente<I l)U1)11c&Uons Include Brown & WIiiiamson's Kool (bottom contOf) tlfod t.oows' Newport (~tom ~I) . Since 1981 Phil ip Motri$ has ptA>UShOCS A Gutdo 108'8ck Orgsnlzatlons. replete with cigarette advortlsomenlS IOtiturlng b&&Ok models, which Is distributed to blaCk p0litielan$ ol'ld Other 1Ctldet$ (lop right) . In the lntroelJctlon to the 1983 editio n . Phil ip Morris etw'man Hi4' Cvllmt'ln WY'OIO that the "dhctory'$ P4,rp0$0 1$ lO illU$b'010 for e1ncks- ono 1or an Americans- how m.JCh can be dOfle when people wOrk to09th0r 11'1 tno nomo ol p(ogress and p(Osp«ity,"

JULY 1935/ NEW YORK STATE JOURNAL OF MllD ICINE 347

c ific rates-mortality is more than twice as high. Age­adjusted rates for men are now almost 40% higher among blacks. Although the ra te of increase has begun to slow for white men, the exponential increase continues among blacks, and the peak canno t be predicted.

The sharp upturn in lung cancer among blacks in the 1950s is consistent with the 20-year latency period expect­ed from other population studies of ci,garette use,, given the increase in smoking amo ng blacks dur ing World War II. As noted above-, however, blacks did not smoke more than whites overall at this time and certain ly not in the 20-year period before I 960. The higher lung ca ncer ra tes cannot therefore be explained entirely by smoking. On the other hand, if racial susceptibility were important, a higher rate among black women (as compared to white women) would be expected.16 It has also been noted that much of the black-white difference in lung cancer can be eliminat• ed with control for socia l class. 17 It is possible that this class and race difference is mediated in part by other known risk_ factors for lung cancer, such as occupational exposures, low vitamin A intake, and inner-city residence. At the present time no direct data arc available to assess the relat.ive impact of these various causative factors. Whatever the mix of risk factors, it is clear that the intro ­duct ion of smoking into this population has created a pub­lic healt h crisis.

Bronchitis and emphysema. Little has been written on t he quest ion or chronic obst ructive pulmonary d isease (COPD) in the black population. Based on vita l statis tics, blacks of both sexes have lower rates than whites.1 Classi­fication of deaths under this code began only recen tly, however, and adequate time trends are not available. Be­cause COPD is a less freq uent ca use of deatl1 and is relat­ed to CH D and ca ncer by virtue of the com.mon cause of smoking, interpretation of these data is further complicat• ed by the problem of competing ca use.

CAUSE AN O Cl.IRE In a disease-based analys is, t he foregoing discussion has

attempted to outl ine the impact of t he cigarc llc on the health of the black populatio n in the United States . Al ­though the health conseque nces of smoking extend well beyond CHD and lung cancer, these disease catego ries subsume the majority of cigare lle, related deat hs and demonstrate the epidemiologic patterns. As noted at the outset, however, from the point of view of the etiology of this epidemic, smoking should be conceived of as a medi­ating factor- a proximate, not an ultimate, cause. Tobac• co use is a social phenomenon and can be best understood only through an analys is of the relationships between peo­ple and institutions within that society. Approximate ly $30 billion per year is currently spent on tobacco prod ucts; about S6 billion in profits return to the cigarette industry, S6 billion to the governme nt in taxes, and varying lesser amounts to a host of advertising agencies, retail stores, and farming interests. It is no secret that maintaining the flow of these profits has been the social purpose for which 360,000 persons a yea r die due to cigarclle-related disease in this country. Cigarette smoking now displays a sha rp class gradient, being concentrated among the working class and the poor of both races (Ta ble V). Extracting profit by this means has proven to be an effective adj unct

J48 NEW YORK STATE JOUR NAL Of MEDI CIN E/ JULY l98S

TABLE V. Age-adJusted Percentages 01 Current Smokers by Education, While and Black M• n,

1970-1975 and 1975 - 19B1

White Black Yta, High Sehool Coll~e High S.hool Collete

1970- 7S 48'.I> J6 S9 S6 1976- 8 1 J7'.I> 24 S1 4S

Source: Wynder El, (i.oodm11n MT: Smotio& and lung cancer: $0t'IIC u.nra oh'<'d lu-ua. b'pidtmlol Rm 1934; S:190.

to the overall process of exploitation at work in con tempo• rary American society. The basic causes of the cigarette• disease epidemic among blacks are, therefore, the same as the causes in the rest of the population.

There is no likelihood of effec tive cures for smoking­related diseases. Prevention requires the removal of tobac­co, obstacles to which arc too difficult to surmount in an economic system based on production for profit. The only realistic hope for prevention. under these circumstances, lies in broadening the gains made against smoking among the educated and privileged to include the working class and minority groups. Considering au the other health threats to black Americans, there is a most urgent need to sou rid the alarm about the compound ill effects of smoking (and the pernicious and pervasive influence of tobacco companies), especially by thooe who occupy positions of respect in the black commun ity. Finally, there is amp le evidence that doctors can change smok.ing habits of pa­tients. Approximately 25% of patients will stop perma­nently at the urging of the ir physician, making this ap­proach perhaps the single moot potent means of inOuenc­ing individual behavior. 18 \Vithin the medical community, grea ter awareness of the problem of CHD and lung cancer among blacks is needed, and this must be transla ted into increased anti-smoking efforts.

The black-white healt h different ia l remains because lit­tle is done about it. The gains that followed on the heels of the civil righ ts movement and the urba n rebellions or the 1960s and 1970s could be measured in improved health .19 Despite a temporary reduction of rac ial inequal ity, the op­posite trend has returned. Income among blacks was half t hat of whites unti l 1950; although the ratio rose to 0.61 in 1970, it has fallen back once again .20 The widening gap in black-white infant mortality suggests a paralle l outcome for health .11 Institutiona l racism is an indispensiblc pillar of American society; without it current profit levels could not be maintained and capi tal would suffer enormous dis­location. At the same time, to take a serious view of this problem requires acceptance of the conclusion that in• equality must no longer persist. Just as the ongoing power of the tobacco industry makes a mockery of any cla im that the business community and governme nt put the hea lth of the nation above all other interests, IO so the excess price in healt h demanded or the black popula tion belies any c laim that racism does not lie at the core of American society.

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IS. Community(.),rd iovueubr Sun'Cilla110e Progrnm: Fii,.al report to lhc Na• 1t0flal Ht.1r1. Lung, alkl Blood lnSlltutc. &.ttlniorc-. MO. CCSPCootdinatlng Ctt1· tu , Dcp.utmcnt or l:!J,idemlolQ8y and Prcvent.ive Me:did11C1, Unh-crsity ol ~bry• latld. 1984.

16. Oold,oa A.1-fcmdlke U, Lc:ffall LO.Scbnkd" Il l: b 1he~/I gcnctleMsb for the differences in cmoc r incidcnoc bctw«n Afro-Amcrie:nns 11nd Euro-Ameri• cnns-? J Nol l Mtd A.rs« 1931: 7):?01 -7()6,

I?, lxvesn SS. Di11niond 6L: Sodoc:co"°mie alkl niclal difkren«.$ in lung CfUlC:tt tnddetl«:, Am J 6pldrr,1h,I 1983; 118:813 .. 3) I.

IS. Cooper R, Soltero I. Stamkt J : SmoldDa ocssa.lion in lbc Chk:a.go Coro­t11tty PrC'\-ention Evu.hut ion Prognun. J Natl Mt'd All« 1982: 74:3-49-:US,

19. Cooper R. StdnhauC.f M, SchaukiB A, Miller W: lmprOYcd ttlOrln.llty lllflOfll us bbtks , 1968- 197!: the tole or antlraclSI StNg&le. / ,tf J 1/tahh Sm1 1911: 11:.$11-521.

20. Cooper R: A aote on 1he blolotle: OOflOCpt or ~ nnd it, application it1 ¢9ldcmiolo8)C rcscarc.h. Ai. 1 ll rart J 1984: 108:715-723.

21. ·111~ Wldt11f11t Cop: The lfft'ldtllU and /)lstrlb-MtiOII o-f ln/o.,a Mt>,talily alNI /,,ow Birth ll'tiglrt l,r 1hr Unltrd Stotts. 1978- 1981, W11,.slling1on. OC. Food Resc.lrdl and Action Ccri1er. 1934.

CIGARETI' E COMPA NIES GO TO COLLEGE On July 2S, 1984 the Forlielh A1tniverso.ry Gala of 1he Unilcd Negro College fu nd (UNCF), reprc ...

scnting 43 private•, predominantly black colleges, was held in New York City at the world hc.1dquarters of Philip Morris. mnkerso f Marlboro and Olher cigaretles, Miller beer, and 7•Up soda. Hu,gh Cullman. chairman and chief executive officer of Philip Morris. is a member or the UNCF Board or Directors and served asco-c.hair mnn of the 1984 corporate campaign for the UNC F along wi1h lhe president and chief executive officer of Time, Inc.

On the afternoon of the reoeption, Christopher Edley, executive direclor of lhc UNCF, was asked by the editor of the Journal , Ala n Blum. MD, if the organi1.ation had ever questioned the morality of the aoccptanec of money from n cigarette producer in light of the dispropotlionately high rate of lung cancer among blacks.

"This is the first time J'vc heard of il (the moral issue). Philip Morris gave to black colleges long before tl1ere was a cancer scare. In 1hecasco f RJ Reynolds• and Philip Morris, they arc located right in the heart of {regions with) black colleges. Philip Morris was originally a Richmond, Virginia company. The Cullman family is largely identified with black colleg~. Let's face it. They have p.r. problems they did not have many years ago. Sure. they know there's a double purJ>O$C to be painted as good guys. But take RJ Reynolds. They've diversified. l 'm not eve11 sure a majority of their profits arc from tobac-co ....

" I don't make thooe strong moral j udgments . . . We have been more troubled by (funding from) alcohol [oompa11ies) because some of our schools arc sponsored by religious denominalions."

Asked if he were aware tha t Philip Morris holds nearly half of the South African cigarette maker , Rolhmans, Edley responded. '' I'm nol surprised. f ord, I OM, and lots of companic.~ lhat give to us have investments in South Africa. Ou ring the civil rights struggle and the rigid segregation 4gainsl blacks in the South. you never heard anyooc in lhe North sayiog doo' t buy from ocna in companiC$ ICha t acqui­esced in discriminatory policies]. So now we reach 6000 miles across the ocean and speak with impuni• ty .. ..

'' We get se,•cral hundred thousand dollars a year from cigareue companies. I am not about to lead a cru.sadc lO get thnt money removed . .. .

"h may be 50 years from now. or even 2.5 years from now when we will look closer lO our contribulors and quesiion some of chem. bul for now we won't turn down a reception or a donation."

-E ditor

• J\('()C)tdingto TheChnrlou.- Of,sm ,'tr, Nov 12. 1984, RJ Reyoold:sm11rkcd the40th a.n..nivcuaryofth,c UNCfbydQnn ting a S250,000 ruby•and,din1nond ncckh1<:t fro,n Tiffany & Co Nthc:,r tMn money, n.s JXl.rl of the tra.dilion of giving rubles on 40th o.nnh-er,o.ries. Acttess Ruby Dec nuide the prcscntntiQfl in Chicngo on Novcrnbcr 10, 1984 duting the intermiss ion ot the P..bony Fashion Fair. In 1983 Reyoold,p ledgcd $ I mm ion to tbc: UNCP <ivcr four )'CIIU, a.nd the noc;k.lace: repre.sc:ntcd 1he second inst:illmcnt. ()\·er;1II in 198-4 UNCF sough1 $18 million, ineluc,ling $10 million fr<1m corp011uioni.

J ULY 198$/NEW YORK STATE JOURNA L OF MEDICINE 349