Document 3N3YOZbdEqvadq7zmOZdmxJwn

Mortality among Individuals 'OccupationallyExposed to Benzene - M.GERALDOTT,MS. JEAN C. TOWNSEND, MS. WILLIAM A. FISHBECK, M.D. RALPH A. LANCNER, Ph.D. DOWolemica4 Company wdhnd, Michigm The mortality experienceof 594 individualsoccupationallyexpared to benzene ms investigated using a retrospectivecohort d a i p . Ihre+hundred thirty-fiveof the employeesbegan working in benzene areas prior to 1950, which provided a sound data b w from which to examine latency. Data derived from work historiesand industrial hygiene records permitted estimation of exposure intehcitia md cumulativedosages for each empioya. No mortnlitiesdirecdy tttributableto benzene expome werc obscmd. S e ~ d of 1eulcemLm d other blood disorderswere noted and discussed. REPORTS of human deaths associated with benzene toxicity date back to the late nineteenth century.' At that time, in chronically exposed individuals aplastic ashneipmbieatwwaesena pchroromniincebnetnc7o.nmditeixopno. sTuhree panodssliebulekeremlaiatiohansbeen the subject of a number of studies, primarily using ( the casehistory approach. Erf and Rhoads,' and de ;Owin: reported cases of myelocytic leukemia, follow- ing anemia which had been associated with earlier benzene exposure-At the University of forty-seven patients with benzene hemopathy were studied from 1942 to 1963.4 Siof the patients were leukemic, one of whom exhibiterdepapolratesdticoannaemCioarpboefraotrieonleSuukrevmeyiaO.fIneig1h9t7E4,uropean affiliates that handled benzene.' Although eighteen cases ofleukemia were identified in the period 1962 through 1971, the observed number of leukemia deaths was less than expected from mortality rates Of the general poPda- - tion. As in Inany Of the previous studies, minimal environmental measurements and exposure histories were available forTchoerrperlaestieonnt wstiutdhymeexdaimcailnfeisndthineglso.ng-term mortality experience of a cohort of 594 workmen exposed to benzene at the Michigan Division Of DOW Chemical. Availability of employee work histones and exposure data enabled cor- of mortality With Cumulative dosage and latency. Envkonmental Considerations Three production areas which use benzene on a continuh g basis were selected for inclusion in the present study: I. Chlorobenzol, date of operation-1920 to present, 11. Alkyl benzene (propylbenzene, ethylbenzene. styrene), date of operation-1935 to present, 111. Ethyl cellulose, date of operation-1936 to present. In the first two production areas, benzene is a raw material consumed in the process whereas, in Production 1x1 b e m n e is employed sa ooinnt. -ne concentrations in the work areas were estimated from industrial hygiene surveys and discussions with plant-operating personnel. Other compounds were present in the occupatied environment throughout & manufacturing complex, therefore, none of the employeesin the study experienced exposure to benzene alone. Many long-term workers may have been exposed to a wide range of chemicals as a result of transfers to and from non-benzene prod e o n areas. A description of the environment in ea& be-e in the paragraph that follow. Z4oduction Area I. In this area benzene is chlorinated to produce monochlorobenzene and dichlorobenzene. Benzene is a starting matend in the process, and is a potential hazard during the initial chlorination step. Further d o h a t i o n and separationj,,to component parts are also carried out within the production area. The unreacted benzene is separated for recycling purposes, and thus, exposure to benzene in these latter operations is mini- d."&le 1summarizes the measurementsof benzene levels in Produdion k e a I from 1944through 1973. few process changes had occuned between the opening and 1944,it was assumed that early exposures were similar to those found in 1944. The low time-weightedaverage concentrations (TWA) reflect the use of closed continuoussystems. The following categorization rules were adopted for jobs in Production Area I: Low Exposure (2 to 9 ppm W A ) : Mechanics and still operators in the primary chlorination area. Very Low Exposure (<2 ppm TWA): Jobs in Jauary/February 1978 3 i' \. . ..-I Table l.-Summuy of Mmsuxamona of Benzene Lm-b in Roduca* onA m I, 1944 to 1973 Job Categories Not spccifIed Jobs in early chlorination steps Other jobr in production arm Jobs m early chlorination steps Otherjobs in production area Yean of S-Y 19-a 1964 1964 1973 1973 Sam@= Number Ty96 (perjob clasdlUtlOn) 43 &ea samplcs 2- 5 Breathing zone 1- 7 Breathing zone 18-24 Breathing zone 3-39 Bruthins zone Ranp of samples ppm Benzene 0-259 33.9 0.2.1 J-62 .142 *Indicates an average of sample poinu rather than estimate of TWA. Estimated TWA ppm Bmzsnc 15' -.s 2 8 -.1 1.0 -4.6 6.2 .1 -4.6 the production area other than those in the low exposure group. Because of limited sampling performed prior to 1960, the categorizationmay be conservative for exposures occurring during that earlier period. In addition to monochlorobenzene and dichlorobenzene,tri- and tetnchlorobenzene were detected in those areas of very low benzene concentrations. Roduction Ana U.Ethylbenzene production began in 1935 as a semi-plant operation and expanded in 1937 when styrene production was initiated. The benzene is alkylated with ethylene to produce ethylbenzene and diethylbenzene, and with propylene to produce isopropyl benzene. Dehydrogenation leads to the end products styrene, divinylbenzene, and u-methyl styrene. The processes are closed continuous systems, with unreacted ben: m e being recovered by distillation and recycled. Highest exposures occur in the benzene unloading areas and dur- ing sampling of process lines. The levels of benzene found in the alkyl benzene units arc shown in Table 2. The fol- lowing categorization rules were adapted for jobsin Production Area I1 (shown in abridged form): High Exposure (25+ ppm TWA): Operating and maintenancejobs in the ethylbenzene process before 1943. Moderate Exposure (10 to 24 ppm TWA): Operating jobs, ethylbenzene, 1943 to 1960; maintenance mechanics, ethylbenzene unit. 1943 to 1971; operating and maintenancejobs,propyl benzene unit, 1943 to 1968. Low Exposure (2 to 9 ppm TWA): Operating and maintenancejobs, styrene unit, 1937 to present; miscellaneousjobs in propyl and ethylbenzene over varying periods since 1943. Very Low Exposure (<2 ppm TWA): CIerical and supervisory jobs in a l l areas, and several operating jobs in styrene, from beginning of the process. Other materials considered to be of toxicologic importance were known to be present on a routine basis in Production Area 11, including ethylbenzene, divinyl- benzene, toluene, xylene, isopropyl benzene, styrene, diisopropyl benzene, and a-methyl styrene. Production Area III. In the production and fabrication of ethyl cellulose resins, benzene is used as a solvent. The highest exposures occurred in the sheeting operation where operators entered closed ares to make adjustments on the w i n g equipment. High concentrations in the sheeting operators were found in 1953. As a result, engineering cfianges were adopted, indud- increased localized ventilation. In late 1963 and 1964, concentra- tions were found to be high due to process changes and the deterioratingcondition of the equipment. At that time, detailed m e d i d examinations were given to employees, a continuous monitor was installed, and improvements were made to lower exposure levels. A brief description of the medical fudings in ten workmen was reported by Stewart et al.' A current review of the medical records of the ten workmen has shown no subsequent hematopoietic abnormality. The sheeting process was shut down in 1967 for economic reasons. The resin-producingoperation, with the loading and unloading of batch reactors, frequent sampling of the process, and existing work practices also contributed to high benzene exposures. In recent years, concentrations have been reduced below 10 ppm TWA. Table 3 summarizes the measurements of benzene levels in Production Area 111. Categoation was developed for the ethyl cellulose units similar to those devised for Production Areas I and 11. Additional toxic materials in the environment were ethyl chioride, ethyl ether, and ethyl alcohol. In all production areas, 'WAs reflect average exposures for employees on a given job rather than exposures particular to an individual whose work practices may differ from the norm. t% i t t 't f ! i ! Method The population of interest was identified from annual departmental census lists for the years 1938 to 1970. Employees who were assigned to job classific3tionsinvolv- 4 Archives of Environmental Health 5-25 Bre8thiagtona 2-36 Bmthing~me -0 >loo 0-56 3- 4 Breathiagzone 6250 2-39 B m t h i ~ g u u r ~ 30.135 Bmthingzone 0-56 0-283 30-94 Breathing zone 0-283 13-195 Bttothingzone G74 -9.0 11.0 -1.0 7.3 -1.0 10.0 -1.0 5.3 -3 13.0 -1.3 14.7 --6 5.3 Jobs in manufacturing ptop Jobs in mrnufacnving ax88 1952 1965 Jobs in mpnufacnving 1973 ax88 T ~ m k b o r a t o r y 1961 Tadmidaninkbontoly 1974 F8briatbn area 1953 Fabdadonax88 1965 13-25 4-24 25-38 4 29 9 Breathing zone 0-x o o Breathing zone .2-575 Breathing zone .1-321 Bmthia~gzone 105-210 Breathing zone 3-184 Breathing zone 10937 -Continmu monitoring o >lo0 with infrs-md mdY=s ~- -17 35.5 5 * 17 -3.8 4.0 16 4.0 35 11 -32 in8 exposure to benzene m the 2 to 9 ppm range from Roduffion A n a I, and all employees from Production n m,and were indudad in the study. Job histories QItrrrctad from personnel reoords for each employee w d according to the categorizationoutlined above. h e tojob mobility within the units and changesin envi- 'oamsm, most employees were sxpotsd at mom than one AU job assignmentsfor one or mom months wen categorized. In the imalysis, cumulativedosage WPI calculatedby multiplying the mean T W A value for each ategory of intensity by the number of months spent exposed to each level. The mean TWA value of 1 ppm was used for the very low level, 5 ppm for low level, 17 ppm for moderate level, and 30 ppm for high level. The mortality data were analyzed by productionarea, 5 F aceording to cumulative dosage, and intermi since fint exposure. Expected deaths were calculated by the indirect msthod from US.white male mortality for the years 1942,1947,1952,1957,1962,1967, and 1971. Age and causc-rpedtlc stan- mrtaiity ratios(SMIL) were utilized in the comparisons. The analysiscovered the yean 1940 through 1973, and included employees working for the company on or after January 1,1940. Follow-up of employees who left the company was obtained from the Social Security Administration. Since Social Security identification of decedents may be less than 100%(approximately 94%for a sunpie of known company deaths), several could have been missed. A subsequentverification of vital status based on personal contacts of former employees, or someone directly howledgeable regarding their current v i t d status, revealed two additionaldeaths and 96 individualsdefinitely aiive. Thus, for 49 individuals vital status determi- nation was made from Social Security records alone. Copies of death certificates were not obtained for three decedents traced thmw Social !hcwity, all of whom were exposed to benzene dosages estimated to be less than 1OOO ppm X months of exposure(ppm months). In the present benzene cohort, there were 53 persons who were e x p o d to arsenicals, vinyl chloride, or asbestos at levcis associated with excess mrlignanaes.'These employeeswere excluded from analyses that deait with dose response in relation to benzene exposure. Raults The vital and occupational status of the total cohort (594 individuals)is presented in Tabla 4. Through company records we found 255 employeesstill working for the company, 87 retired,and 71 known deceased. Of the 181 former employees for whom Social Security checks were performed, 31 were identifid as dead. Sixty-four of the 181 individuals had worked for less than 1 year in benzene areas; 165 had worked for less than 10 years in benzene areas. Total population stillworking Retired 594 US 87 71 181 31 101 49 541 233 75 62 171 29 95 47 121 152 321 56 65 134 27 25 35 21 24 26 I7 38 126 2 14 15 IO 19 72 5 5 39 108 135 298 54 57 122 23 19 33 16 22 24 15 37 119 2 13 14 9 19 67 4 5 38 'Does not includeemployeesexposed to ammids, ybcstos,and high vinyl chiondo levcis. 6 Archives of EnvironmentalHealth .. pnldn,clionAre8 I Tod <lWO 1940.1949 1950.1959 19w p#&&OaM111 To& e1940 19404949 1950-1959 1%0+ Roductbf~Area III T<o1ta9l40 1940-1949 1950.1959 196W 108 36 20 2s 5 7 42 12 3 21 2 9 20 17 1 135 21 21 3 62 13 31 3 21 2 64 23 12 1 21 lo 17 7 14 5 298 96 139 39 37 1 13 13 147 55 65 13 64 21 30 13 50 19 31 0 Population with Ivsnis arbesfos,or high VcLurPoarn Total 53 3 29 6 e1940 20 0 93 1910.1w9 20 1 12 1 19So-1959 10 2 61 1- 30 21 43 13 22 -8- 27 5 18 -4- 24 10 14 -0- 15 8 6 1 Duration of exposure to benzene by year of initial exposure is given in Table 5 for each production area, and separately for the 53 employees who were a h exposed to arsenicilfs, asbestos, or vinyl chloride. Employment tended to be more stable in Production Areas I and 11, than in Area 111. Overall, 108 employees in the study worked for 20+ years in areas of benzene exposun; 175had been potentially exposed to benzene in excess of 25 ppm TWA for at least 1 month. The cauwpe&~c mortality trends shown in Table 6 rlree with results of a cohort study of over 8,000 employsft at the same location." Observed deaths were consider&lY 1sthan expected based on US.white male mortality. No strtisti4y s i ~ l c a nitnfxcaseswere found in any aw*fdeath category in the population excluding mMYeaSwith arsenicals, asbestos or high vinyl chloride eXpOSW. Cardiovarmiar,accidental, and residual causes o f d a t h wen much lower in the industrial cohort than expcaed. Five deaths due to suicide were observed versus 3.1 expected. No astociation with intensity of benzene exPmn or cumulative dosage was found with respect to thaa individuals. review of medical and occupational records Was W R a k e n for five decedents whose medical findings w e d to be of clinical interest with regard to ben- me toxicity. Two of the employees died from causes of death categorized under anemias. One death was due to aplastic anemia and the second was due to pernicious anemia; the second diagnosiswas confirmed by autopsy. This second employee tint worked for the company from 1916 to 1919.Details ofexposure for that period are unknown. In 1931 he returned as a laborerin chemical sewage disposal,and had potential exposum to a variety of chemicals. From 1936 to his ntinmcnt in 1951,he was exposed to benzene (ProductionArea IlX [184months of high exposwe; estimated dosage, 5520ppm months]) This person died in 1955 at the age of 68 yean. No Com- pany medical record was available for review. An autopsy was not performed on the individual who died of aplpstic anemia. "he decedent's work history at the company began in 1929 with exposwe to rrrenicals for 5 months. He held a variety of jobs until 1934.Be@ning in 1934,he was exposed to low levels of benzene for 98months (estimated dosage, 453 ppm months)in the chlorobenzol area. From 1942until his retirement in 1955,he worked in thm different locations and hb potmtial exposures included many other chtnaicrlj. He died in 1957 at the age of 67. No family history of cancer or blood diseaseswas noted in the medical record. The remaining three case historieswere of amployaws with leukemia.h e death was due to leukemia, another to acute myelogenous leukemia, and a third to myelo- 7 L. -c ._ lOU 1 2 8 3 30122.8 11.8 916.9 ion.2 111.4 U1.5 211.5 2h.O 312.6 213 46164.2 312.9 312.3 313.6 111.4 2II2.0 513.4 4115.4 31-- 80 1*32 130 125 a * 72 * * * a 147 * -- 911114.1 24120.3 11.7 916.1 716.3 011.3 111.3 211.3 11.9 312.4 11.1 43157.3 312.6 212.1 313.2 111.2 2110.8 513.1 4113.6 31- 80 108 131 111 * * * 75 * * * * 161 *Larrth.nfl=obra*sddaath& tIncMes one person for whom myeloblastic leukemia was listed under "other significant conditions" at death. blastic leukemia which was hted under "other sipEcant conditions." The fintdecedent's employment at the companybeganin 1946,and he spent two y w r in an area where potentidexposures mduded nitrobenzene and bmdne. From 1948 to Mar& 1950,he had several short work dgnmentswith varied exposures. From Much 1950 throughJuly 1960,he worked in a locationwhere he had 65 months of potential exposure to vinyl and VinylMew chloridethat could have been over 200 ppm. From August 1960 until Mueh 1971, he worked inan -1 benzene area whero his exposure was ategodzed as Iow (estimated dorage, 545 ppm months). No family history of cancer was noted for thisindividual, who died in 1971 at 45. The second decedent was employed for 30 monthsby the c o m p y ; 18 months (October 1950 to April 1952) involved potentipi exposure to very low concentrations of benzene (<2 ppm T W A dosage: 18 ppm months). This pnon died in 1965 at age 5 1. Other occupationalhistory included four yean in the milirvy and employment from 1948 to 1950in a saw mill which mnnufacturedveneer. Data on family medid history are lacking. 8 l'hethird death was categorized as bronchopneumonia ibilateral, with myeloblastic leukemialisted under "other signitlcant conditions." Thir decedent bcgan w o r e at Dow chemirrl in 1943. Industrialhygiene surveys taken inhisworklrbetwcen1943and 1955indicatedhehad 5 probable sxposuze topchlorophenoi,ethyl chloride, phenetidine,acetic anhydride, pad phenacstin dust. From 1955 untilhis retinment in 1962, the decedent was poten- tially exposed to low levelsof benzene (estimated dosage, 305 ppm months). Family bistory included mother's death due to cancer. He died in 1970at the age of 72. In Table 7, selected causes of death in the population (leuthe group exposed to arsenicals,asbestos, and vinyl chlocide) axe examined with mpcct to career do- and interval since initial exposure to benzene. Prior pnolysis by production area had d e d no statistidy s i g n i b n t Mennoes in mortality(Production Area I, S M R = 89; Production Area II, SMR =90;Radlrction Area III, SMR = 72).For any dosage therewere no sienificpat increasesin mortality relative to the US. population, by causeofdeathcategory (Table 7). In the intend of less that 15 yoan since Rnt exposure, the SMRs were considerably Archives of Environntental Health -. ,w AIIO- foul 911114.1 0.499 ppm months 41165.1 500.999 ppm months 18116.2 ioooC ppm months 31132.8 -dinasE 43157.3 ~ 9 9 p p m m o n t h r 15132.9 w p p m m ~ n t h r 917.7 ppm month, 19D6.7 -t neoplumr 24120.3 0-499 ppm months 11111.2 500.999 ppm months 512.9 1ooOC ppmmonths 816.2 Mother a- 22136.5 0-499 ppm months 14121.0 500.999 ppm months 415.6 1OOO+ppm months 519.9 80 63 111 98 75 46 117 114 118 98 172 129 60 6t7 51 17140.6 121275 215.9 3R.2 5117.6 3f12.0 1rU 113.1 616.3 414.3 110.9 111.1 6116.7 5111.2 012.5 113.0 42 44 t t 2t8 t t 9t5 t t 36 4t5 t 40141.9 18124.0 1115.9 11112.0 181226 6/13.4$ 512.9 $ 7/63 1017.5 5/4.2$ 3/1.1$ 212.2 10111.8 616.3 $ 212.0$ 2/35 95 75 186 92 80 45 172 111 133 119 t t 85 t95 t 34131.6 11113.6 514.4 18113.6 20117.1 6t7.5 312.3 iin.3 816.5 212.7 110.9 512.9 618.0 313.4 111.1 2/35 108 81 114 132 117 80 t 151 1t23 t 172 75 tt t lower thanexpected for cardiovascular disease and aIl ported increased myelocytic leukemia in similar work other causes, as might be anticipated in view of pre- situati~ns.'~Ward et al." have suggested that in cases of selection factors. leukemia associated with benzene exposure,genetically- - controlled sensitivity and other environmentalfacton- 3 Dimdon especially during childhood-should be investigated. These No statistidy signifcant increases in total mortality researchershave been unsuccessful in producing leukemia dative to the US.white d e population were observed in laboratory animals subcutaneously exposed to benzene. id =pact to production area or estimated career dorage ofbenzane. Exposure andhealth records-re reviewed on Aa assessment of tho case history of the individual with aplastic an- is similady difficdt. In a series of 1 n- iadividualbash for several employeeswith medical find- aSwciated in the literature with benzene poisoning. "hmcam histories of employees withleukemia wen over 2.000 deaths dating back to 1940known to the com- pany, this was the only death due to aplastic anemia. From an environmental standpoint, his potential exposure 3 Iwiswed.The three leukemias were myelocyticwith two to numerow chemical agents including aneLLical com- h g dttdfied as acute, Vi- reported in his investip pounds, and the latency with respect to benzene exposure, tht berwlle-rela&d leukmnhs wum m d y acute (uc factors to be considered. hmocytoblastic or mye~oblastic?~nour population the A review of multiphasic health inventories for 282 incidence of leukemia, exctudiag lymphocytic employees in the curnnt study has been undertaken and It ormoDocyti~an types, wu0.8 eaws[based on the Thiid h t i o n t l Cancer Survey, Incidence Data) compared with three obmved cases(Pe .047). bthare cases,varied workhistoria and the lack of win be reported when compiete. ********** Submitted for pubUation December 30.1975; revised. acaptad Aprfl28.1976. history matie a retrospectiveasmment of the M i d o copier M.vrilnble from: M.Gerald Ott. Coqmnte relationship to benzene exposure very judgmental. Medial Dept,The Dow ChemicalCompany,2030 Dow Cmter, b w o y - t with a veneer company further compti- Mdlmd. W 48640. ated *e assessment for one pem~as -has re- ********** 9 i. REFERENCES 1. Hunter, D. 1969. 7hc direas- of ocm~potfoonr4. th e&. pp. 506521. London: The English Universities Pres. 2. Erf. L F.. mi Rho- C. P. 1939. The hematobigi4 effects of benzene (benzol)poironiug. J Ind Hyg Taxieol21:421-35. 3. de Gowin, R L. 1963. Benzeneexposurs and aplasticanemia followed by leukemia NUan years inter. JAMA 185:748-51. 4. VleilipN. E. C.. and Saita. G. 1964. Benzene and leukemia. N h g i JMed 271:872-76. 5. Thorpe. J. J. 1974. Epidemiologic m y of leukemia in pmons potentiplly axposed to bsnzsns. J &cup Med 16:375-82 6. Stewart, R. D.; Dodd, H.C.; Bamtta, E. D.; Schlsffer, A. W.; and Mutdrler. J. E. 1967. Chronicoversxposurs to benzene f ttvapor. Toxic01 Appl Phmnac01 10:381. 7. Ott, M. C.; Lyypru. R R.; and Holder, B. 8. 1975. Vinyl chlo~. ida exposure in a controlled krdumipl anviro~lentA. rch Envimn Health 30333-39. 8. Ott. M. G.; Holder, B. B.; d Iaatpmr. R. R. 1976. 171-77. E m h H RU 11:122-27. 10. Milham. S. 1976. Neoplasia in tha wood and pulp industry. AnnNYAcadofSd271:294-300. i 11. w u d ~~..;wcirburgr,~.~.;~?momoto,~.s.;~snjomin,r[.; iBrown, C. A; and Weisburger, E.IC. 1975. Long-tm effect of benzene in CSfBL/6n mice.Arch Envimn H d t h 30:22-25. Residence under an Airport Landing Pattern as a Factor in Teratism F. NOWEU JONES, P U . Depsrtmentof Psychology JUDY TAUSCHER Scboolof PublicH a l a U~ofcamrnil LorAngalsqcJilorni. An anaiysk of aU Lor A@es County birth lcoolldl for ~JIO yepr 1970,191, and 1972 raved8a &&aindd4nco of raportibb birth defects in thos amur kacts lyhg wholly or p d y within the 90dbA budnasrcontom unda the b d b g PI- at Lor InternationalAirport than in the rest of theCounty. whiie not proving that noise isnrpoariblsfor the in- in taatian, them d t s point to a potenti8Uy important physicd envimnmentaleffect with sig&hnt public health impliationr RECENTLY,considerable attention has been given to the possible mental health effectsof aircraft noise on the residents of affected areas near airports. The original impetusappears to have stemmed from a report by AbeyWickma et 4.who found a higher incidence of psychiatric problems among persons living under the Heathrow flight patterns than among those who lived in comparable, but quieter areas.' McLean and Tarnopolsky' have reviewed this and other similar reports and have reached the conclusion that the evidena for psychiatric d t i e s from noise is not compelling, although there is room for further resaarch. Ando and Hatt0ri3 report that babies born to mothers livingnear the noisy Osaka airport are of rela- tively low weight, presumably because of skess to the mothen. It has aIso been reported that teratogenic effects occur in pregnant rats upon exposun to noise.' A British r e p o d remarks that the still-birthrate is higher in Hourislow (in part, a very noisy district under the Heathrow traffic pattern) than elsewhere in Greater London. The analyses which we report here tend to c o d m the above fmding, in that mom than expected abnonnal births were found to occur to mothers residing in the noisiest census tracts on the approaches to Los Angeles International Airport. The authors were able to obtain taped compilations of all births recorded in Los Angeles County for the years + 1970,1971, and 1972. The data available included, among : other things, observable birth defects, race, and census 3 tract of residence. Based on previous work by Meecham andT Smithuwe chose tracts iyiug wh~nyor in part within the 90dbA contour around the l a n a pattern. This pattern, which was altered for night landing in 1974, extends r5 roughly eastward over a populated area. "ke "noise area" 5was divided for all practical pu~posesinto a largely black, ; eastem region, and a largely white, western region (Spanish Surname births were too few for reasonable statistical treat- f ment). Approximately one-half of the birthsin the noise ; area were black. (It should be noted that the largely white area was the noisier.) Finding proper controltracts presented a difficult problem; since the n o h tracts were middlesf- 4 the-mad so far as the white population was concerned, and more afluent than average so far as the black population : was concerned, we chess to use the remainder of the entire county for our comparisons. This choice biases the results against finding noise effects because there are other airports (not so heavily used) and many fmways scattered through- out the county. Figure 1 shows the location of the target 10 Archives of Environmental Health