Jfournal of Epidemiology and Community Health 1994;48:237-247

Is living near a coking works harmful to health?A study of industrial air pollution

Rajinder S Bhopal, Peter Phillimore, Suzanne Moffatt, Christopher Foy

AbstractObjective - To determine whether therewas excess ill health in people living neara coking works, and if so whether it wasrelated to exposure to coking works'emissions.Design - Populations varying in proxi-mity to the coking works were comparedwith control populations. Health datawere correlated with available environ-mental data.Methods - Analysis of routinely collectedmortality, cancer registration, and birthstatistics; community survey using selfcompleted postal questionnaires; retros-pective analysis of general practice (GP)records; tests of respiratory function;and analysis of available environmentaldata.Main results - Study and control popula-tions were comparable in terms of re-sponse rates, gender, and most socioeco-nomic indicators. For adults, agestandardised mortality and cancer ratesof the population closest to the cokingworks were comparable with those forthe district as a whole. Gender ratios,birthweight, and stillbirth rates werecomparable in the study and controlpopulations. For several indicators ofrespiratory health including cough, sinustrouble, glue ear, and wheeze (but not forasthma and chronic bronchitis) therewas a gradient of self reported ill health,with the highest prevalence in areas clo-sest to the works. For example, sinustrouble was reported by 20% of adultsand 13% of children in the area closest tothe works compared with 13% and 6%respectively in the control area. GP con-sultations for respiratory disordersincreased when pollution (measured bySO2 levels) was high: annual consultationrates per 1000 varied from 752 in the topgroup of daily pollution levels to 424 inthe bottom group. Analysis of locally col-lected smoke and SO2 data indicated thatSO2 concentrations were highest closestto the works and, after closure of thecoking works, the number of days onwhich SO2 and smoke levels exceeded100,ug/mi and 90,ug/m3n, respectively, fellsteeply.Conclusion - Routinely available indic-ators failed to provide convincing evid-ence that the coking works had harmedhealth. Self report and GP consultationsindicated that respiratory ill health inthe people living close to the works wasworse than expected. Some of the excessprobably resulted from exposure to cok-

ing works emissions. The health effects ofrelatively low level but intermittentlyhigh air pollution from a point sourcemay be subtle, contributing to respira-tory morbidity, but not apparent in ana-lysis of routine health indicators.(J Epidemiol Community Health 1994;48:237-247)In producing coke from coal, coking worksrelease mixtures of air pollutants so complexthat they remain incompletely characterised.'Coke oven gases are extremely toxic and in-clude carcinogens. Coke production is alsoassociated with environmental disturbance inthe form of noise, smell, and dirt. People wholive close to coking works have shown under-standable concern about both the potentialdanger to their health of exposure to the airpollution, and the inconvenience of living closeto dirty industry.2

Studies of coke oven workers in severalcountries have consistently shown their higherthan expected risk of lung cancer,35 a riskwhich is generally acknowledged to be causallyrelated to exposure to coke oven gases andfumes. The few studies which have examinedthe health of people living close to cokingworks, however, have failed to answer thequestion, "Is living near a coke works a healthrisk?" Studies around the steel coke ovens inSydney, Nova Scotia, suggested that mortalityamong men in the area was higher than in theprovince.2 German studies on the fluorine,6arsenic,7 and phenol8 concentrations in popu-lations living near coking works have indicateda higher than expected phenol concentration inblood and urine, and by inference, benzeneexposure.The scientific evidence available to the local

and health authorities in 1988 was insufficientto resolve a long standing and increasinglyacrimonious dispute between residents livingnear Monkton Coking Works in the SouthTyneside health district in the north east ofEngland, the management of the coking works,and the local authority on the health hazards ofcoke works. Indeed, the controversy was suchthat the health concerns were central issues ina public inquiry, and received extensive mediacoverage. Our study was requested by the localauthority, to help resolve this controversy.SettingThe coking works was built with 33 ovens in1937 in a "green field" site. Between the late1940s and 1960s, housing estates (largely localauthority owned) were built north, east, andsouth east of the site. The capacity of theworks over the 53 years of production variedbetween 33 and 66 ovens. From 1980, 66 ovenswere in operation.

Department ofEpidemiology andPublic Health,Medical School,School of Health CareSciences, FramlingtonPlace, NewcastleNE2 4HHR S BhopalP PhillimoreS MoffattC FoyCorrespondence to:Professor R S Bhopal.Accepted for publicationOctober 1993.

237

Bhopal, Phillimore, Moffatt, Fox'

The coke ovens were in continuous opera-tion except from April 1984 to January 1986,when closure followed a national miners'strike. Production finally ceased at short noticein October 1990.

Local residents' complaints concerned dirt,noise, unpleasant odours, and fumes, and illhealth including chest diseases such as bron-chitis, cancer, and early death. The areas con-cerned have, for residents, been smokelesszones since 1968.

MethodsSTUDY DESIGN, HYPOTHESES, DATA SOURCES,AND ETHICAL APPROVALDetailed health data and limited environmen-tal data were collected on study and controlpopulations matched on 1981 census data. Thepopulation of greatest interest was that livingnear the coking works. For each data set wedefined an area close to the coking works, and asecond area surrounding that. The health ofthe populations in these areas was comparedwith that in an area some 6-10 km distant fromthe coke works (control area), and in addition,for routinely collected health statistics only,with the whole of the health district.The size, population, geographical relation

to the coking works, and the terminology forthe areas is given in table 1. The boundaries ofareas under study were defined either on thebasis of distance from and perceptions aboutexposure to coking works emissions, or using acomputer model of emissions of SO, from thecoking works.

Figures 1 and 2 show, for example, thelocation of the coking works, the two sets ofboundaries used for the analyses of the mor-tality and cancer data, the control area, andstandardised mortality ratios for "all causes"and for lung cancer by housing estate (seeresults).The four prior hypotheses which guided the

analysis and interpretation of the data werethat the health effects, if any, of emissions fromthe coking works would be:

(1) Greatest for respiratory conditions;(2) Most marked for people living closest to

the works;(3) For acute conditions, diminished when

the works was not in production or pollutionlevels were low;

(4) For acute conditions, most clearly seenin children.The source, validity, and analysis of these

data are described below. The South TynesideMedical Research Ethics Committee approvedthe research.

HEALTH DATAMortality, cancer registrationPostcoded mortality data for 1981-89, andpostcoded cancer registration data for 1986-89, were obtained. Counts of cases were aggre-gated by housing estate and then by the areasshown in table 1.The 1981 census and projections for 1987

from the organisation CACI gave populationsat enumeration district level. We estimated the1984 population by taking the mid-point of thefigures for 1981 and 1987.Age and sex standardised rates and ratios

were calculated with direct and indirectmethods of standardisation, respectively,using the populations for 1981, 1984, and1987. Because the results were influenced littleby the method or the denominator, we subse-quently used the indirect method yieldingstandardised mortality/morbidity ratios, withthe 1984 (for 1981-89 mortality data) and 1987denominators (for 1986-89 cancer morbiditydata). The probability (p value) of theobserved number of cases occurring in an areawas calculated using the Poisson distribution.The p value for each cause was adjusted formultiple comparisons using the formula:adjusted p = 1-(I-p)tm where m is the num-ber of areas compared. These analyses used acomputer program called GENRATE.'Birth dataPostcoded birth data for 1982-89 were ex-amined for the ratio of male to female births,birthweights, and stillbirths in the areas com-pared.Postal surveyA systematic sample of the population in theareas described in table 1, part B, was drawnfrom the family health services authority regis-ter. The sample size was calculated to allow adifference of 5% between two proportions,15% versus 20%, to be detected with 80%/,power, at the 5% level of statistical signific-

Table I Size, population, and distance from the coking worksNearest Furthest

No of 7otal distanice distaniceenunmeraticon population to coking from cokintg

Data source and study areas districts (1981 census) works works

(A) Mortality, cancer, and birth statistics:(i) Perceived exposure areas 78 39451 0 25 km 4 5 km

Perceived highert 42 23 092 0 25 km 30 kmPerceived lower 36 16 359 1-5 km 4-5 km

'ii) Modelled area 67 32 761 0-25 km 3 5 kmModelled higher 29 13 367 0 25 km 20 kmModelled lower 38 19 394 1 00km 3 5 km

(iii) Control area* 37 20 929 6 00 km 100 km(iv) Whole of South Tyneside* 349 158 972

(B) Community, GP, and lung function surveys: 28 21 364 0-25 km 2 5 kmInner area 12 10 581 0-25 km 1-75 kmOuter area 16 10 783 1 75 km 2 5 km

* Fixed for all comparisons.t "Perceived" refers to the judgement of the research team based on the views of the public, the local authority and health authoritystaff, and general knowledge about aerosol dispersion patterns and wind direction.

238

Is living near a coking works harmful to health?

w4)

C40

CUm(UCu

CO Cu0Cu

239

0CoC

VV

O) Cws Is

z-X C

iOi OVCBuca

I*XL ^D0^

z *-_

Cu

E

E0

K--o

:

.

.

-

,o

;=

CN

o

.

o

S

* ,lv

.

-

;5On

Bhopal, Phillimore, Moffatt, Foy

Modelled lower exposure

Modelled higher exposure

0 1 mileII

0 1 kilometre

Figure 2 The boundaries based on the dispersion model

ance. Of the 4601 questionnaires sent out, 258were returned as wrongly addressed, while69-4% of the remainder were returned (67-8%of questionnaires to adults, and 75 1% of ques-tionnaires to children) after two postalreminders to all the sample and use of tele-phone reminders. The response rates weresimilar for adults and children in all three areas- for example, for adults 69-6% in the inner,65-3% in the outer, and 69-0% in the controlarea.

The questions concerned demographic de-tails, health status, socioeconomic circum-stances, individual behaviour, and perceptionsof the factors that affect health.The Medical Research Council's respiratory

symptoms questionnaire was incorporated.'0Parents completed the questionnaire for chil-dren.

Comparisons between inner, outer, and con-trol areas used the x2 statistic for trend test.The survey took place between November

1990 and February 1991.

GENERAL PRACTICE MORBIDITY DATAFour general practices were selected, twolocated in the inner area which served bothinner and outer area residents, and two in thecontrol area. The case notes of all thosepatients registered with three practices and asystematic sample of one in four from the(largest) fourth practice, all of whom had alsobeen sampled for the community survey, wereexamined (231 individuals lived in the innerarea, 136 in the outer area, and 254 lived in thecontrol area). Data on consultations, chronicconditions, hospital admissions, and currentdrug treatment were extracted from the medi-

-__ Approximate higher exposure area boundarybased on pollution dispersion model-----Annual average ground level SO concentrations,

,ug/m3 all sources (x2 interval)Approximate lower exposure area boundarybased on pollution dispersion model

153 Standardised mortality ratio (lung cancer)(98) All-cause standardised mortality ratio(98)* Indicates statistical significance

240

Is living near a coking works harmful to health?

cal record and entered onto the AAH MedicalComputer System which assigned the Readcodes. Consultation data for the 56 monthswhen smoke and S02 levels were availablewere used. Details about the environmentaldata are given later. Analysis was by log-linearmodelling of the daily number of respiratoryand non-respiratory consultations in each ofthe areas. Day of the week, mean daily temper-ature, and S and smoke levels (mean of threesites) were used as explanatory variables. TheGLIM statistical package was used.LUNG FUNCTIONA sample of 142 children aged 8-14 years and354 adults was drawn from the local familyhealth services authority register. The samplewas drawn from the inner and outer areasdefined for the community postal survey.People were invited to a local health centreover a six day period (9am to 9pm) in the weekthat the coking works closed. In addition,children who had not attended were visited inschools. The response rate for adults was 44%,and that for children 78%. For this reason onlydata on children are reported.A brief questionnaire was used to collect

demographic details and past medical history.Vitalograph spirometers were used to measureforced expiratory volume (FEVI) and forcedvital capacity (FVC), and a Wright peak flowmeter for peak expiratory flow rate (PEFR).Height (using a Harpenden Stadiometer) andweight (using calibrated Avery Scales) weremeasured. The expected value for lung func-tion was derived from formulae provided byCotes."I

ENVIRONMENTAL DATAAt three local authority sites (1 km north east,1 5 km south east, and 0 75 km west of thecoking works) 24 hour mean daily measures ofSO2 and smoke had been made by the localauthority over 56 months (1987-91) specifi-cally to address concerns about the cokingworks. These data were used, in conjunctionwith meteorological data obtained from the

Table 2 Gender and age characteristics of the community surveyArea

Gender and age Inner Outer ControlAdults:Male (%) 46 44 44Mean (SD) age (y)Males 43 (17) 43 (18) 44 (17)Females 43 (17) 44 (18) 45 (16)

Age group (no (%))16-24 138 (19-1) 149 (18 4) 110 (13-9)25-34 112 (15 5) 126 (15-6) 149 (18-8)35-44 139 (19 2) 152 (18 8) 132 (16-7)45-54 106 (14-6) 130 (160) 121 (15-3)55-64 143 (19-8) 148 (18-3) 171 (21-6)65+ 86 (11-9) 105 (12-0) 109 (13 8)

Children:Male (%) 48 54 56Mean (SD) age (y)Male 8 (4) 8 (4) 8 (4)Female 9 (4) 8 (4) 8 (4)

Age group (no (7))0- 4 57 (24-9) 59 (25-9) 52 (25-0)5- 9 66 (28-8) 68 (29 4) 77 (35-0)10-15 106 (46 3) 103 (44-6) 88 (40-0)

There are no significant differences in the sex ratio or age distribution between areas, for eitheradults or children.

Newcastle Weather Centre, to distinguishdaily variations in atmospheric pollution andweather conditions. As the nearest housing is250 metres from the coking works these moni-toring sites did not provide an absolute level ofexposure of the population. No routine data onair pollution were available for the controlarea. The nearest monitoring station was sitedat a busy intersection near the town centre ofSouth Shields (about one mile from the nearestboundary of the control area), and we obtainedSO2 and smoke data from there, mainly tocompare the pattern of change over time inthese air pollutants.MODELLINGBased on information provided by Her Maj-esty's Inspectorate of Pollution on the emis-sions from stacks at the coking works in 1989(with the permission of Coal ProductsLimited), published data on low level emis-sions,'2 and weather data, a model of the dis-persion of emissions was prepared on ourbehalf by National Power using the IndustrialSource Complex model of the EnvironmentalProtection Agency (USA).

ResultsSOCIOECONOMIC FACTORSThe social and economic circumstances of thepopulations in the inner, outer, and controlareas, and in the whole of South Tynesidewere similar, as shown by data from the 1981census and by the postal survey (tables 2 and 3show some of the data).MORTALITY AND CANCER REGISTRATIONTables 4 and 5 show that the adult "all cause"and cause specific standardised ratios for mor-tality and cancer registration in the higherexposure areas (whether perceived ormodelled) closest to the coking works were notsignificantly different from those of SouthTyneside as a whole, and were generally lowerthan those in the surrounding, lower exposureareas. For men in the areas closest to thecoking works, SMRs were comparable withthe control area. Women in the control areahad lower ratios than their counterparts livingnear the coking works and in South Tynesideas a whole, an observation which remainsunexplained.Table 4 shows that children in the perceived

higher exposure area had a 43 3% excess inmortality, and that in the modelled higherexposure area the excess was 75-2% (a statist-ically significant difference). The causes ofdeath were, however, diverse and only onedeath was from cancer and one from respira-tory disease.

BIRTH DATAThe male:female birth ratios in the perceivedhigher (1969 births), perceived lower (2066births), and control (1713 births) areas wereclose to unity (1 04, 0-97, and 1 00 respect-ively). In addition, the proportions of babieswith birthweights less than 2500 g were com-parable in the three areas (8-0%, 6-3% and7-5% respectively).

241

Bhopal, Phillimore, Moffatt, Foy

Table 3 Some social characteristics of the populations under study from the 1981 census and community surveyPerceived Perceived Allhigher lower Southexposuire exposure Control I vneside

1981 population 23092 16359 20929 158972(A) Census data ('/.)

Unemployment 16 20 17 17Households with no car 51 64 55 60Owner occupied households 32 31 31 31Households social class 1 & 2 18 11 17 19Households social class 4 & 5 22 30 31 27People in over-crowded households 11 11 11 10

(B) Commnunity survey data (adults): Inner Outer Conttrol(n=725 (n =812) (n=793)

Mean years at current address 15 6 16 5 15 2Exposure at work to:

dust 16 7 17 6 20-1fumes chemicals 8-7 9 3 8 0

Occupation in shipyards, mines coke, gas, lead,iron steel and chemical works 28-7 30-0 29 6

Current smokers 32-8 28-8 37 0

Table 4 Standardised mortality ratios* (numbers of deaths) by area, selected causes, and population subgroup;indicating statistical significancet

Perceived Perceived Modelled ModelledControl higher lower higher lower

(A) All cause mortality:Both sexes, all ages 95 (2110) 100 (2269) 109 (1934) 100 (1407) 107t (2166)Males, all ages 102 (1201) 97 (1184) 1 10t (973) 98 (745) 105 (1091)Females, all ages 88t (909) 104 (1085) 108t (961) 103 (662) 110t (1075)0-14 years, both sexes 119 (28) 143 (41) 82 (19) 175t (24) 92 (24)15-64 years, both sexes 100 (622) 97 (612) 120t (500) 95 (371) 113t (577)65+ years, both sexes 93t (1460) 101 (1616) 106 (1415) 101 (1007) 106 (1565)

(B) Cause specific mortality (ICD code):Lung cancer, both sexes (162) 102 (213) 108 (225) 99 (152) 99 (130) 108 (193)Lung cancer, males (162) 102 (156) 103 (158) 95 (104) 91 (88) 105 (136)Lung cancer, females (162) 101 (57) 122 (67) 110 (48) 123 (42) 116 (57)All other neoplasms except lung

(141-161, 163-239) 88t (362) 100 (413) 118t (373) 107 (274) 110 (400)Respiratory system (450-519) 97 (247) 104 (274) 100 (212) 108 (177) 94 (222)Circulatory disease (390-459) 97 (1008) 99 (1040) 107 (893) 98 (639) 108 (1017)

* The SMR is based on the mortality rates for South Tyneside District Health Authorityt p < 0-05 after adjustment for multiple comparisons.

POSTAL QUESTIONNAIRE SURVEYThe gender and age distributions of thesamples in the three areas were matched, asshown in table 3. In answer to the open ques-tion, "Do you have any long-standing illness,disability, or infirmity?" there were no statist-ically significant differences: in adults, 28 6%in the inner area, 26 9% in the outer, and25-4% in the control answered "yes", and inchildren the figures were 16 4%, 16 2%, and13 9%.Eight respiratory and 15 non-respiratory

disorders were listed and adult respondentswere asked whether they had ever had any ofthem. For children the list was of eight respira-tory and five non-respiratory disorders. Theprevalence data for all respiratory disorders,and for non-respiratory disorders where dif-ferences were statistically significant, areshown in table 6(A). Notably, there was nodifference between areas in asthma and bron-chitis prevalences. Table 6(B) gives responsesto the questions from the Medical ResearchCouncil's respiratory health questionnaire.Table 6 shows that for some, but not all,respiratory problems there were substantialdifferences between the inner, outer, and con-trol areas, usually with a gradient with thehighest prevalence in the inner area and thelowest in the control.

GENERAL PRACTICE MORBIDITY DATAThe comparison populations were comparablein gender and age. Forty eight per cent of thesample were male in the inner area comparedwith 52% in the outer area and 50% in thecontrol area. The mean (SD) age of the sub-jects was 32 5 (23 7) years in the inner areacompared with 37 0 (24 8) in the outer and34-9 (21-9) in the control areas. Sex and age didnot differ significantly between areas.Table 7 shows that for each air pollution

level (measured by SO2) annual GP consulta-tion rates for respiratory disorders were higherin the inner and outer areas than in the controlarea, whereas non-respiratory disease consul-tation rates were lower. The table also showsan association between the daily consultationrate for respiratory conditions and SO2 levelson the same day in the inner and outer areas.The association was not seen in the controlarea and was independent of daily tempera-ture.This association between daily SO2 levels

and respiratory consultation rates was notobserved when data were aggregated overlonger periods - for example, comparing 1986-90 with 1984-86, when the coking works wasnot in production because of the nationalminers' strike.

242

243Is living near a coking works harmful to health?

Table 5 Standardised cancer registration ratios* 1986-89 (number of cases) by area, selected causes andpopulation subgroup; indicating statistical significancet

Perceived Perceived Modelled ModelledControl higher lower higher lower

(A) All malignant neoplasms (ICD 140-208):Both sexes 92 (302) 104 (360) 112 (276) 110 (233) 110 (324)Males 98 (167) 107 (195) 111 (138) 113 (128) 108 (162)Females 85 (135) 101 (165) 112 (138) 106 (105) 112 (162)0-14 years 0 (0) 173 (3) 73 (1) 97 (1) 196 (3)15-64 years 90 (124) 101 (146) 111 (108) 112 (100) 108 (129)65+ years 94 (178) 106 (211) 113 (167) 108 (132) 110 (192)

(B) Cause specific malignant neoplasms (ICD code):Lung cancer, both sexes (162) 81 (65) 108 (90) 126 (74) 89 (46) 130t (91)Lung cancer, male (162) 83 (47) 112 (67) 105 (43) 93 (35) 120 (59)Lung cancer, female (162) 76 (18) 98 (23) 174t (31) 76 (11) 154t (32)All other neoplasms except lung

(140-161, 163-208) 95 (237) 103 (270) 107 (202) 167 (187) 104 (233)Genito-urinary (179-189) 87 (47) 89 (51) 123 (50) 97 (34) 115 (56)Digestive (150-159) 100 (76) 108 (85) 108 (62) 119 (58) 110 (75)Lymphatic haematological (200-208) 114 (13) 107 (13) 58 (5) 95 (7) 106 (11)Lip, oral cavity, pharynx (140-149) 122 (7) 166 (10) 94 (4) 188 (7) 116 (6)Skin (172-173) 119 (37) 111 (36) 117 (28) 110 (22) 106 (30)Other and unspecified sites

(190-199) 69 (19) 108 (31) 130 (31) 145 (26) 105 (26)* The SMR is based on the cancer rates for South Tyneside District Health Authority.t p < 0-05 after adjustment for multiple comparisons.

Table 6 (A) Postal survey: Self reported past or present ill health in adults and children by area and (B) Medical Research CouncilRespiratory Symptoms Questionnaire

Adults ChildrenInner Outer Control Inner Outer Control(n= 725/ (n=812/ (n= 793) (n=231/ (n=233) (n=221

2(00/ (0/0/ (00/ y- trend (0J (00 (00 g trend

(A) Postal survey:Respiratory problems:Asthma 59 6-7 53 NS 113 10-3 11-3 NSBronchitis - - - 10.4 7 3 9-5 NSChronic bronchitis 8-1 8-0 7.4 NS - - -Glue Ear - - - 15-2 8-6 9-0 5-87 p

Bhopal, Phillimore, Moffatt, Foy

Table 7 Relation of air pollution level and annual general practice consultations per 1000 populationlInner n = 231 Outer tl 136 ) Control it = 259

(Co)nssultation CotnsultatotiuConsultationrate rate rate

Air pollution level No of No of Non- No of NVon- No o!f Non-measured by SO, days consultations Respiratory respiratorV Consultations Respirators' respirators consultations Respirators re.tpiratorvLevel* 1 (highest) 21 39 752 2182 27 1022 2428 49 547 2806

2 51 102 713 2448 60 789 2368 136 479 33533 253 478 625 2361 288 594 2461 621 585 29424 271 590 560 2880 326 505 2723 635 445 29225 (lowest) 328 586 424 2399 365 573 2414 723 442 2725

Residual dayst 452 788 489 2265 474 612 2203 1008 423 2782y- including residual days' 39 0.0 1 8 0-3 0 9 0(2y excluding residual days 7 4** 0.1 1-2 0.1 1.0 0(6* Actual air pollution levels are as follows: 1, SO2> 100 pg m3 at two or more monitoring sites; 2, SO,> 100 pg m3 at one monitoring site; 3, 62 pg m3 < SO, t 100 pgmi; 4,41 pOgm5

Is living near a coking works harmful to health?

hence assessing the specificity of the associ-ations. We also asked about respiratory healthin several ways in the community question-naire, and studied it at several levels of mor-bidity;

(iv) Differences in use of or access to prim-ary care services. We found that overall con-sultation rates were lower in the populationliving near the coking works;

(v) Confounding variables. We comparedour populations with regard to a wide range ofdemographic, social, economic, occupational,lifestyle, and environmental circumstances,adjusting for age and sex where appropriate;

(vi) Lack of power. We used all the mor-tality, cancer, and birth data available withpostcodes, and calculated sample sizes for thecommunity survey to detect prevalence dif-ferences of 5%.We believe that artefact does not fully

explain our observations.

IS THE HEALTH OF PEOPLE LIVING NEAR THECOKING WORKS DIFFERENT FROM THAT INCOMPARABLE POPULATIONS?The mortality and cancer experience of menand women living closest to the coking workswas similar to that of the South Tynesidepopulation, and for men, to that of the controlarea. The women in the control area hadsignificantly low rates compared with SouthTyneside women and, therefore, women inareas closest to the coking works. We cannotexplain this latter observation. Overall, foradults, there was no clear evidence that mor-tality and cancer rates were greater thanexpected in the populations most exposed tocoking works' emissions.

Mortality in children in the area closest tothe works was higher than in South Tynesideand the control area. The excess of mortalitywas distributed across a range of causes. Onbalance, we consider it unlikely that this excesswas attributable to exposure to works' emis-sions but we are re-examining the questionwith new data. Children in the areas close tothe coking works had birthweights, stillbirthrates, and gender ratios comparable with con-trol and South Tyneside populations. Thelung function of children in the inner andouter areas was as predicted on the basis ofphysiological norms." Lung function wastested as the coking works closed, and shortlyafterwards, so chronic effects only could havebeen detected.The community survey, and analysis of

general practice consultations, showed that inmany respects the populations closest to thecoking works had a similar health experienceto that in the control area. However, for anumber of problems, mainly of the upperrespiratory tract, there were large differences.Hay fever, glue ear, cough, and wheeze stoodout as problems with a high prevalence on selfreport. Notably, both asthma and bronchitisprevalence was not higher on self report. Ifprevalence differences had been caused byreporting bias resulting from Awareness of thehypotheses, then a self reported excess of thesetwo conditions would have been seen, for these

were problems identified by the community asbeing associated with the works. The preval-ence of chronic bronchitis on self report was nohigher in the inner area, but when it wasderived indirectly, based on a series of ques-tions in the Medical Research Council Respir-atory Questionnaire, there was a significantdifference. The community survey and GPstudy corroborated each other in demonstrat-ing differences in respiratory morbidity. Thefact that most of the differences in childrenconcerned the upper respiratory tract is com-patible with the findings on the lung functionof children.

HAVE COKING WORKS EMISSIONS BEENRESPONSIBLE FOR THE POORER HEALTH?Ideally, new, standardised environmentalmeasures of air pollution should have beenmade in the study and control areas. Unfortu-nately, the sudden and unexpected closure ofthe coking works forced us to rely on availabledata.The SO2 and smoke data from three sites

around the coking works do not reflect theactual levels to which the study populationswere exposed; these would have been highernearer the coking works. The data from thetown centre, South Shields, are used solely tocompare time trends in S02 and smoke levelswith data from around the coking works.

Study and control areas were chosen on thebasis of their similar housing, street layout,and traffic levels. No other major industrialsources of air pollution existed close to thecoking works or in the control area. On thebasis of the data on stack and fugitive emis-sions from the coking works, the changingmean levels of S02 in the air and the decline inthe frequency of SO2 readings exceeding100lg in relation to declining activity at theworks, field observations, and published ob-servations on the polluting nature of cokingplants,' we can assume that the plant was thelargest single contributor to local air pollution.Two computer models and an analysis of S02levels in relation to weather conditions indi-cated that pollution levels would be highestclosest to the works and diminish rapidly withdistance. In this context we infer that healthdifferences between the study and controlareas were not caused by another externalsource of air pollution.Three of our four prior hypotheses were

upheld and the fourth partly upheld. Thedemonstrable health differences were, with theexception of childhood mortality, specific andmainly for selected respiratory problems; thegradients in prevalence of problems we pre-dicted (inner > outer > control) were observedfor most of the respiratory problems; and thegreatest differentials in prevalence rates werein children. The hypothesis that respiratoryhealth would improve during the periods ofclosure of the coking works, tested by compar-isons of GP consultation rates over periods ofseveral months' duration, was not upheld;however, we found that there was a clearrelation between daily patterns of consultationfor respiratory disorders and periods when

245

Bhopal, Phillimore, Moffatt, Foy

daily air pollution was highest, as indicated byS02, a pollutant specifically associated withactivity at the coking works. The epidemiolo-gical criteria for causality were fulfilled asfollows:

TimingThe exposure preceded the effect. Thestability of the populations makes it implau-sible that populations susceptible to some, butnot all, respiratory problems selectivelymigrated into the neighbourhood of the cokingworks.

Strength of the association and dose-responseThe associations were moderate in strength,and an exposure-effect gradient was seen bothin the community survey data and the airpollution (SO2) and GP consultations data.

SpecificityThe effects agreed with prior predictions, andwere most marked for upper respiratory prob-lems. The fact that the excess was not seen inall respiratory problems, especially selfreported chronic bronchitis and asthma, isparticularly noteworthy as an argumentagainst the possibility that the differences aresimply a result of reporting bias. The mainexception to the observation that differenceswere fairly specific was childhood mortality,which we are studying further.

ConsistencyThe methodological problems of measuringexposure to air pollution in a community set-ting make the collection of convincing evid-ence of cause and effect extremely difficult, andthe evidence on the effect of industrial airpollution from point sources on human healthis conflicting. The studies of Lloyd et al"4 areunusual in demonstrating effects on mortality,cancer, and gender ratios of industrial air pol-lution from steel and foundry plants. Elliot etal found no excess laryngeal cancer aroundincinerators,'5 and Symington et al no excess ofrespiratory symptoms near a foundry.'6 Daleset al showed an association between livingdownwind of a gas refinery and self reportedrespiratory health but not with lung function,but were unable to exclude reporting bias as anexplanation.'7 The Harvard six cities study'8'9examined children's health at contemporarylevels of air pollution and found a link betweenair pollution and several aspects of reportedrespiratory health, including earache'9, but notlung function.'8'9 The asthma prevalence wasnot in excess in the most polluted cities.'9 Viegiet al compared the self reported health ofgeneral populations, both exposed and unex-posed to industrial air pollution, and showed astrong link between exposure and both upperand lower respiratory tract ill health.20 Kar-daun et al linked SO2 levels to GP consultationrates for respiratory disease in Amsterdam.2'Pope et al showed a link between fine particu-

late pollution from a steel mill and hospitaladmissions for several respiratory diseases.22The link between high levels of air pollution

and mortality is clear, but the effect of lowlevel air pollution is not. MacKenbach et alhave shown that an apparent link between lowlevels of S02 and mortality in The Nether-lands was lost when the data were adjusted forthe lagged effects of temperature.23S02 levels of the order measured here have

not been shown to produce respiratory prob-lems in experimental studies on humanbeings.24 These studies, however, concern highlevels of S02 over brief periods of time. Wemake no claim that S02, alone, was the cause ofrespiratory ill health but that it resulted fromthe combination of pollutants from the cokingworks (for the changing levels of which SO2levels provide an indirect measure). Other re-cent work, both published'7-22 (reviewedrecently24) and unpublished (Walters et al,paper presented to National Public HealthConference, West Midlands 1991; andMeduna S et al, "An epidemiological surveil-lance system for the management of air pollu-tion episodes: the ERPUS project," paperpresented to the Faculty of Public HealthMedicine, 1992 Annual Scientific Meeting,Eastbourne) supports our finding that air pol-lution levels of the order reported here, whichmay be measured using S02 and/or smoke asmarkers, are associated with morbidity.Our data, linking relatively low levels of

industrial air pollution to respiratory ill health(both self reported and as assessed by GPrecords) but not lung function tests or mor-tality, are consistent with contemporary epide-miological findings and add to the growingevidence that safe thresholds for air pollutionhave yet to be defined.'>2'

PlausibilityIt is plausible, as discussed in a recent review24(chapter 5), that long term, low level (butintermittently high) exposure to a complexmixture of pollutants including S02 wouldaffect upper and lower respiratory tract health.This research emphasises that the upper res-piratory tract may be affected by air pollution,an under-researched field in epidemiology. Itis notable that in air pollution epidemiologythe emphasis has been on inhalable particles,and that most measurement methods for parti-culates have not been designed to measureparticles which are likely to impact on theupper respiratory tract (personal communica-tion: Mark D, Hall D, Latest developments inambient dust and aerosol monitoring. Unpub-lished paper, Warren Springs Laboratory).

CONCLUSIONThe local community's observations that emis-sions from the coking works affected theirhealth were probably correct. The excess ofrespiratory problems observed in those livingclose to the works can best be explained as aresult of their exposure to its emissions. The

246

Is living near a coking works harmful to health?

observed excess in childhood mortality cannot,on our evidence, be attributed to such expos-ure but requires more research. This and othercommunities living close to coking worksshould be reassured by the finding that therewas no major and discernible impact on adultmortality and cancer, birthweight and still-birth, and lung function in children was aspredicted.

This work provides support for the viewthat health effects of environmental pollutionmay be subtle and not always be discerniblefrom mortality data,25 provides a frameworkfor an investigation focussing on morbidity,and emphasises further the need for a closedialogue between policy makers, researchers,and communities concerned about environ-mental health issues.'32627We wish to thank South Tyneside Metropolitan BoroughCouncil for funding the study and the following people for theirhelp: Angus McNay, Simon Raybould, David Chinn, JohnCotes, Peter Blain, John Edwards, Dennis Wheeler, MalcolmNewson, Tim Butler, Helen Groom, Ann Rooke, David Hall,Alistair Hay, Carolyn McGregor, Denise Howel, Fred Nimmo,Hebburn Residents Action Group, South Tyneside GPs,FHSA, DHA and schools, HMIP, AAH Meditel and NationalPower.

1 Lave L, Leonard B. Regulating coke oven emissions. In:Paustenbach D, ed. The risk assessment of environmentaland human health hazards. New York: John Wiley, 1989.

2 Donham P. No smoke, no baloney. Canadian Centre forOccupational Health and Safety. At the Centre. 1986;9:2-4.

3 Lloyd JW. Long term mortality study of steelworkers V.Respiratory cancer in coke plant workers. J Occup Med1971;13:53-68.

4 Redmond CK, Ciocco A, Lloyd WL, Rush HW. Long-term mortality study of steeelworkers VI. Mortality frommalignant neoplasms among coke oven workers. Jf OccupMed;1972;14:621-9.

5 Hurley JF, Archibald RMcL, Collings PL, Fanning DM,Jacobson M, Steele RC. The mortality of coke ovenworkers in Britain. Am J Ind Med 1983;4:691-704.

6 Einbrodt HJ, Prajsner D, Kuhne HJ, Frank K. Flourineexposure of persons at coking plants and their vicinity.Wissenschaft und Umwelt 1978;3:172-4.

7 Eikmann T, Michels S, Walliser L, Krauth W, EinbrodtHJ. The environmental burden of man by arsenic part I.Epidemiology of adult residents near to a coke works.Staub-Reinhalt Luft 1984;44:144-8.

8 Eikmann T, Muller W, Prajjner D. Phenol excretion and

haematological values as parameters for a benzene bur-den. A comparative study of the adult population of twoprovincial towns. Wissenschaft und Umwelt 1980;4:183-9.

9 Nimmo AW. Review of computer mapping of health data.Health Bull (EdinJ 1989;47:40-54.

10 Committee on the aetiology of chronic bronchitis. Defini-tion and classification of chronic bronchitis for clinicaland epidemiological purposes. Lancet 1965;i:775-9.

11 Cotes J. Lungfunction assessment and application in medicine.4th ed. Oxford: Blackwell, 1979.

12 Gemmil RJ, Moodie J, Thomas BS, Smith FB. The envir-onmental impact of coke-oven discharge. Experimental andtheoretical approaches. 1st international Coke-makingCongress, Essen, Sept 13-18, 1987, Paper H4.

13 Bhopal RS. The impact of industry on the health ofsurrounding communities: an analysis of epidemiologicaland public health challenges. In: Hedley AJ, et al. Pro-ceedings. The role of the ASAIHL in combating healthhazards of environmental pollution. Hong Kong: Univer-sity of Hong Kong, 1992;65-73.

14 Lloyd DW, Barclay R, Lloyd MM. Lung cancer and otherhealth problems in a Scottish industrial town. Ambio1985;14:322-8.

15 Elliot P, Hills M, Beresford J, et al. Incidence of cancers ofthe larynx and lung near incinerators of waste solventsand oils in Great Britain. Lancet 1992;339:854-8.

16 Symington P, Coggon D, Holgate S. Respiratory symptomsin children at schools near a foundry. Br 7 Indust Med1992;48:588-9 1.

17 Dales R, Spitzer W, Suissa S, et al. Respiratory health of apopulation living downwind from natural gas refineries.Am Rev Respir Dis 1989;139:595-600.

18 Ware JH, Ferris G, Dockery DW, Spengler JD, Stram DO,Speiger FE. Effects of ambient sulfur oxides and sus-pended particles on respiratory health of preadolescentchildren. Am Rev Respir Dis 1986;133:834-42.

19 Dockery DW, Speizer FE, Stram DO, et al. Effects ofinhalable particulates on respiratory health of children.Am Rev Respir Dis 1989;139:587-94.

20 Viegi G, Pasletti P, Carrojji L, et al. Prevalence rates ofrespiratory symptoms in Italian general populationsamples exposed to different levels of air pollution.Environ Health Perspect 1991;94:95-9.

21 Kardaun JWPF, Van der Maas PJ, Habbema JDF, Leent-vaar-Kuijpers A, Rijcken B. Incidence of diseases of thelower respiratory tract in family practice and low level airpollution. Fam Pract 1989;6:86-91.

22 Pope AC, Schwartz J, Ransom HR. Daily mortality andPM'0 pollution in Utah Valley. Arch Environ Health1992;47:21 1-17.

23 Mackenbach JP, Looman CWN, Kurst AE. Air pollution,lagged effects of temperature, and mortality. The Nether-lands 1979-1987. .7 Epidemiol Community Health1993;47: 121-126.

24 Advisory Group on Medical Aspects of Air Pollution Epi-sodes. S02 acid aerosols and particulates. London:HMSO, 1992.

25 Anonymous. Environmental pollution: it kills trees, butdoes it kill people? Lancet 1992;340:821-2.

26 Brown P. Popular epidemiology and toxic waste contamina-tion: lay and professional ways of knowing. 7 Health SocBehav 1992;33:267-81.

27 Paigen B. Controversy at Love Canal. Hastings Cent Rep1982;12:29-37.

247