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UNDOOR AIR QUALITY Il~T ASTA Proceedings of the International Conference He1d at the Central Plaza Hotel', Bangkok, Thailand on 28'-29th November, 1991. Edited by B. R. Reverente Jun Philippine Refining Co Inc 1351 United~ Nations Avenue Mani1ia PO BOx 1176 PliilipPpines D. F. Weetman School of Health, Sciences University of Sunderland Sunderlan& England~ and' AS. Wongphanich Occupational: Health Department Faculty of Public Health Mahidol University 420/1 Rajvidhi Road Banokok 10400 Thailand Published by Indoor Air International The InternationalU Associataon for Indoor 4irQualitv, Postfach 2 CH-4467 Rothenfluh Switzerland ISB.N 3-906470=001S April 1993 1

, Indoor Air Qualin,, Ventilation and Enerp7 Saving Qigao Chen , Refrigeration Using Waste Heat To Improve Working Condiuons. Jiajie Liu, Xianying Liu and Chunw-u Sun~ Reliability of Quesuonnaire Data. Jun b:aSa,wai A Survey of' the Quality of Indoor Aii in Manila Office Buildings. Benito R. Revererite„Jr. Sources of Polltition The Effect of Outdoor Air Pollution on The Mortality of Indoor Residents. l:in-hua Chen and Qih-uan Deng Industrial Pollution in Vietr,am: An Important Ea-ternal' Source of Ind'oor Air Polllrtion. Le Van Trung, The Environmental Impacr of Carcinogens from Motor-Car Exhausts. Manfred Buck Identification of the Sources of Airborne Particulate Matter in Urban, Suburban„ and Industrial Areas of Korea. Sung-Ok Baek and Myuns Ho Hahn~ Non-occupational Exposure to Lead in an~ Occupational Setung; Eiji Yano Sources And Indicators Of Indoor Air Pollution In The Occupauonal! Setting. D. Soedirman Airborne Asbestos Concentrations in, Rooms 'with Sprayed-On :A-sbestos Materials. Iziiyoshi Sakai,. Naomi Hisanaga:, I:azunori Mitani„ Hironobu Tsuchiva, Itian Huang, Eiji Shibata, Yuichiro Ono, Akinori Kojima and Yasuhiro Takeuchi' The Contamination of Indoor Air with Asbestos and Man-made Mineral Fibres. John A. Hoskins and Robert C. Bro'wn. V1 83 97 107 117 121 127 133 141 155 161 171 ~ ~ 185 w ~ F"a 0 Ph ~

Concentration And Exposure Dose Of Radon And Its Progeny In Public Bath Houses at Two Hot Springs. Qing-Xiang Zeng, Yan Li, Zhao-Hui Huang, Hui Su, Hong-LiniWang, and~hiu-Ian Hui 95 Level and Dose of Radon and Its Progeny in linderground Buildings in Wuhan City. Qing-Xiang Zeng, Yan Li, Zhao-Hui Huang and Hong-Lin Wang. 199 RadoniConcentration in Drinkino Water and the Dose Received by the Exposed' Population: Yibin Chen 205 Control of Welding Fumes in the Metal Fabrication Industry: R.C. Panjwani ?13. Control of Dusts for Small Cement Factories with Shaft Kilns. Guangquan Liu, Jiang Liu, Chen Zhou andi Gushua Hu 2?9' Asbestos Concentration In Indoor Air And Management, Of Asbestos-Removal Works In Japan. Susumu Tod'a and Mikiharu Aoyagi 237 Standardization, of the Measurement of Asbestos Fibres in Indoor, Air. Norbert Hoefert 243 Continuous Measurement' of Indoor, Air Quality in Office Buildings in Japan. Akiyoshi Ito 251 PIXE Application to Indoor Air Quality Measurement. Toshitami Ro, Takeshi IShiguro;,Mitsuru Fujimura and Yoshikazu Hashimoto 261 Health Effects A critique of the methods used to assess the toxic effects on maniof combustion products, Di F. aJeetman 275

Health Problerns in a Thermoelectric Plant in Vietnam, Nguyen Do Nguyen~ Nguyen The Dung and Pham Nboc Len ?S7 Concentrauons of Pyrethroids in the Air of Dividins and Packing Workshops. P Yao, J Sun; Y W.u, S Wang, L Liu and F He 293 Prevalence of Welders' Pneumoconiosis in Workers Exposed to Welding Fumes. Changqi Zou,. Kangji Xng„ Yanhua Yuan, Qingchens Du„ Yuxi~ Hbu and! Zonsshu Mao 299 Key T infect Neurotoaic Effects Of Carbon Disulfide On Ravon Workers: Fengsheng He, Zhemin Zhang; Shi Yang, and' Shoulin Zhang 305 Further Anallhses of the Role of' Confounding Variables in Epidemiolobic Studies of Environmental Tobacco Smoke and the Respirator}'System in School'-age Chiidren. Raphael J, W'itorsch, JosephiM. Wu, Ronald Di Hood and Philip Witorsch 313 n envirc partict. Factor Th( t}ie pu kind c inapp-n

E 0 in order to seek a. j within buiidings ,f air conditiotdng ronment„ and willl :hanism Of indoor A CRTTIQUE OF THE METHODS USED TO ASSESS 'I'HE TOMC EFFECTS ON MAN OF COMBUSTION PRODUCTS. D, F. R'TEETMAN'N spaces". n ' n. R _, DOE-ER.6()493-7-vol ,~ 1 Analysis. John W-del events in Japan duriq sources of indoor a:id -336. as detennined by PDcE Nucll lns4r, h'larhPho School of Health Sciences, University of SunderJand , Sunderland, Tyne and Wear, England Key Words: combustion~producrs, epidemiology, risk assessment, environmental tobacco smoke, cardiovascular diseases. ABSTRACT Combustion of organic material results inahe release ofpaniclds, gases,,and~pyrolyuc products. all of which can accumulate in the indoor environment, and could damage health. The methods of assessing risR to mamare reviewed, and it is conduded that epidemiology provides the bestsingle approach. The problems in unerpretatiorrof epiderniological studies are reviewed; with, particular, eemphasis on the specific problem of environmental tobacco smoke (ETS) and cardiovascular disease. tt is cond'uded that too many important potentially confounding factors have been overlooked to decide if there is an, association between exposure to ETS and cardiovascular diseases. NATURE AND SOURCE OF CO."vfBUSTION' PRODUCTS Iti is difficult to imagine life v,ri•,hout~ combustion. In addition to domestic heating, combustion of some form of fuel occurs in cooking, many forms of transportation, most industrial processes and most of the generation of electrical power. The common factor is that some form of fuel is burnt, and the fuel is derived from organic matter, a•ith the inevitable release of pollutants. Not all combustion, contributes pollutants to the indoor environment, but in those situations where this effect appears to be minimal„it should be remembered that the indoor air is derived from, that outdoors, so the dirtier the air outside a building; the more polluted it will be inside.. When organic matter is burnt, three classes of pollutant, are formed. Firsr.there are gases. As the pred'orninant chemical process is oxidation, which usually occurs without sufficient oxygen to allow complete oaidation, there is the release of 2: complex mixture of'~ oxides. Thus amongst the gases generated bvy combustion, there are oaides of carbon, nitrogen and sulphur. 275 3SM

Assessmenr of the Toxic Effects of ComBusrion Products Organic molecules can undergo complex re-arrangements without, the consumption ofoaygen in a!process called pyrolysis; which is largel', deterrriir,ed by the temperature of' combustion. Finally, there is the generatjon of pardcles which are the small globules of organic matter that give rise to the visibility. of smoke. Particles vary in size, and undergo complex changes in shape andli surface area when they cool down to the ambient temperature. Large panicle5 do not stav suspended in the air for long. Particles up to 10}en are readily i.nhaled, and may not be rapidly cleared by from the lung;, large particles (1oj,, aerodynamic diameter) are deposited in the upper respiratory tract„ whereas small ones (O1yn) are exhaled Ill. The important aerodynamic diameter with respeet to potenval pulinonarytoxiciry is probably about O.S;an [1]. Much the same tnucture of gases, pyrolyuc products and particles are generated from the combustion of any organic matter. For example, there is more similarity than difference in the products released from burning woo& and tobacco. With combustion of organic matter that has undergone some degree of inetamorpho- sis; as with coal, oil and natural gas, there is variation in the proportions o; components generated from eachs,but again there is a mixture of gases, pvrol±,tic products and particles. METHODS OF RISK DETERNII.hA.TIOh investigations. Any reliable findings about risks to the health from combustion products can be used i.n attempts to regulate levels of'the offending substances, and~ thus protect man., justifi-the funds they consume„so there need to be an acceptable purpose oflthe ' The purpose of determining the risk to rnanftom combustion products arises from~ the ubiquitous distributioni of these substances. Scientific knowledge is sought because of man~s insatiable curiosity;, but increasingly scientists have to Iaboratory Studies Laboratorv animalscan be exposed to smoke and then assessed for anv effect. However, this type of eaperimentation is fraught with difficulty. There is always some carbon monoxide generated by combustion, which prev.ents high~doses of smoke being administered. The anatomy of'the respiratory system of, say.,,rats, is quite different from that of man, so it is difficult to~predict the outcome in this latter species from effects seen in the former. Any experience of pharmaceutical research teaches that there is no completely reliable way of translating effects seen in laboratory animals to man. To determine what happens in man, ii is necessaryto investigate in man. Direct eaperimentation in man can be achieved'in exposure chambers. The problems here are that exposure must be shon-teran, and there is still an upper ?76 ltmit to the dosc course,,it is pos to volunteers ir but then it is b:, components. administering in vitro svster inadequate for Epidemiolog, It is possil combustion p population of outcome in th study designs with a conditi to the suspea, The second'a; determine wi method does causes of d'ea summarises t: Table 1 Prc The bes: gation is to regulators 2 exposure to ate exampl( disease. so the investii products fr

Assessment of the Toxic Effects of'Combustton Products without the ~ determine& of particles, e visibility of' nishape and irge particles 3dilv inhaled, -icles (10Fan -act, whereas iiameter with _1 . Much the ated from the irnilarity dian bacco With : netamorpho- roportions of ises, pyrolytic ~1 )ts arises knv.wledge is 2ntists have to ourpose of the rn combustion ag substances, i for any effect- here is always nts high doses :em of, say, rats )utcome in this :)harmaceutical aslating effects zs in man; it i5 -hambers. 'rne :s sull an uppef limit to the dose that can be tested due to the presence of carbon monoxide. Of course, it is possible to separate the various chemicals in smoke, and apply them to volunteers in exposure chambers, either individually, or in defined mixtures, but then it is barely possible to measure any interactions between the differenrt components. Anv reduction in the scale of the test system, for example by administering smoke to tissue cultures, still involves an extrapolation from the in vitro svstem to intact man. The experimental methods available are inadequate for this purpose. Epidemiology It is possible to measure the effects of long-term exposure of man~ to combusnon products by epidemiological techniques. With this approach; a population of exposed individhals is identified and the rate of any medical outcome in this group is compared with that in a suitable controligroup. Two study designs are possible. First, one can either start by identifying individualss with a condition (i.e: cases) and attempt to show a greater exposure in; the past to the suspected cause thanloccurs in a demographically matched control group.. The second approach is to assemble a population (i.e. cohort) of individuals and determine what happens to them medically over several' years. The cohort method does not provide rapid answers, especially with the most frequent causes of death„which frequently have a slowly developed pathology. Table 1 summarises the problems associated with such studies. Table 1 Problems in Epidemiology 4. 5:. Selection of exposure and control groups Multifactorial nature of disease Difficulty imcontroV?ing,confounding variables Only associations detected Intervention studies are difficult. The best way to understand the difficulties of such epidemiological investi- gation is to examine the quality of the evidence in a specific case. As the regulators are currently considering the health effects that may result from exposure to environmental tobacco smoke (ETS), this will serve as an appropri- ate example. The latesn claims are that ETS is causally relatedto ischaemic heartt disease, so the quality of this evidence will be considered in detail. However, the investigator is confronted by comparable difficulties with, combustion products from any fuel source. 277 E M 0 0 ®

Assessment of the ToxicEffects ofCombusrion Products Study Design The study design is shown in figure 1. The exposed group are obtainedby selecting non-smokers who are married to smokers,, whereas non-smokers married to non-smokers provide the unexposed group: The rarlonale of tlis design is that the non-smokers (usually wives) would be exposed to ETS in the home from the smoking of their spouses. With these two populations, it is possible to compare the rates for ischaemic heart disease, either in ~ case-control 1 or cohort studies, The problems of interpretation arise from the imprecise distinction between the two exposure groups, and because there is no allowance made for exposure to ETS outside the home. A second difficultyy is the determination of' the smoking, status of the spouse, whichi is usually achieved from the response of individuals to questionnaires. Any wTongl~ classified partners tends to reduce the precision, of the study. Exposed rate - events/population J' [ adjusted I t RR EXPOSED RATE UNEXPOSED RATE I [ adjusted J 1 Unexposed'rate - eventsLpopulation 1 NON-SMOKER married to a NON-SMOKER . A qu ~-holha that the [2). As eaampl I [3]), the patient If t}i scienris~ second to card cardiov risk fac: scicntis sugges not to c or behh cardio% studies to be r,Mucc by Gla: respon studies suppos Glantz connec study, [I Tat cardio, contair follow: arteriostrokel inform

0 Dbtained by:)n-smokers nale of this .) ETS in the .ations„ it is :ase-controt : imprecise :) allowance =ulry is the 'y achieved v classified M Assessment of tbe ToxicEJJects ofCombustion Products A quite differenuset of'problpms relate to the definition of an effect. i.e. those who have the disease. If one relies on deatli certificate information, then the fact that the individual has died is reliable, but the cause of death is prone to error 12). As few autopsies are now performed in most countries of the world (for er.ample, currently, less than 1'3°/p of bodies nthe USA are subjected to autopsy [3l), the cause of death lias to be deduced' from ~ the signs and ~ symptoms of the patient alone: If the possible causes of' ischaemic heart disease are considered, medicall scientists do not have an unequivocal answer. This has resulted in a sort of' second level approach, where risk factors apparently predisposing individuals to cardiovascular disease are identified. In other words, the aetiology of' cardiovascular disease is considered to be multifactorial. To date„over 200 such risk factors have been proposed by various research groups [4) (not allimedical scientists agree with, this approach: McCormick and Skrabanek [5) have suggested that we should refer to risk markers, as opposed to risk factors, so as not to confuse association with causatdon): However, if there are constitutional or behavioral characteristics of individllals that could predispose them to cardiovascular disease, each one should be controlled! for in epidemiological studies, otherwise they may acuas confounders, allowinganiincorrecrconclusion to be reached. Much of the interest in ETS and cardiovascular disease arises from a: review by Glanz and Parmley 161, in which, the authors presented! a case that' ETS was responsible for a proportion of the cases of the disease. Nine epidemiotogical studies were identified in the literature (5 with a statisticallv significant effect, supposedly from spousal exposure (7-11)), and'4 without (12-151, which allowed Glantz and Parmley to conclude "These epidemiological studies demonstrate a connection between ETS exposure and' death from heart disease." One other study [16] has been added to the ones covered by Glanz and Parmley: Table 2 contains a summary of ohe epidemiological i studies linking ETS with cardiovascular disease. The medical endpoint varies from study to study, and contains both "death from" and "possession of" the specified condition;, the following conditions were taken as the endpoint: ischaemic heart disease, arteriosclerotic heart disease, coronary heart disease, myocardial infarction, stroke, and all cardiovascular diseases. The reliance on~ death certificate information as the medical endpoint is also indicated in table 2. 279 M ~ ® ® FS © 0

Assessment of tbe Tozic EJfects of Combustion Products Table 2 The Epidemiological studies of ETS and cardiovascular diseases. STUDY REFERENCE DISEASE END POIN'T TOTAL EVELTS 7ESTS sig/tota] BUTLER [121 CHD D.C ~ 0/1 HIRAYAb1A 1101 IHD D:C. 494 1/3, GAR1A.h'D 113]1 I.HD D:C 19 0/1,0 LEE (a51' IHD * STROKE DIAGNOSIS 121 0,130 SVENDSEN 1111 CHD PA','EL 13 ?j17 HE 181! CHD DIAGNOSIS 34 24Y47. HELSING 171 AHD D.C. 2014 10/22 HOLE I 191 ' IHD D:C + PA'.'EL 84 1/5 HUMBLE (14] All CVD D.C. 76 0/24 DOBSON [aG hiI D.C - PAN'EL 382 2!1~ Under EYELTS ;,the numbers refer, to those in the CONTROL * E7TOSED groups for the cohor, studies. and'thenumber of'cases in the case-control studies, and give an indicauon of'the ability of the tests to detect aneffect. The values are for males and itmalts combinedi,and both home and work place exposure to ETS. IHD - ischaermc heart diseasc CHD = coronary, heart disease AHD - anenosclerouc heart disease Ml - myocardial' infarction CVD - cardiovascutar disease D.C. - death ceruficate PANEL - evidence reviewed by a panel of' experu DIAGNOSIS - disease deternuned by standard diagnostic techniques The large number of comparisons made in the papers is indicated in Table 2. When multiple comparisons are made on one set of data, the comparisons are not,truly independent(some values will be used andthen re-used indifferent tests); so anv study containing a stausucally significant outcome willl be considered furuher. The positive studies are re-considered in Table 3. It has already been stated' that cardiovascular diseases are thought to, be multifactorial in their aeuology, so anv putauve causes other than exposure to ETS that are not controlled for will be capable of confounding.the epidemiologi- cal studies. For this reason, some of the best established risk factors for cardiovas cular diseases have been identified from the literature (Table 4), and the ex[ent of the control over these potential confounders has been detemlined (Table 3). -i Table 3 Missing epidem S7L'D1.. HIRA1'A'`!A 110) SvEI\'DSEI\ I1'1]1 HE [8] HELStN'G [ 71 HOLE 19) DOBSON' 1]61 in no study was the : Fami]y history of ca: [81- The Svenden behaviou:. Table 4 The be: RISK FACTOR Family history, of' d. H,vpenension Cigarette smoking Dietrv fat loa& Diabetes Lack of exercise h9enopausal' status. Alcohol l consumpuc Obesu}• From table 3 i same standard. Svendsen et a] (`. exposure to ET` concentration). dietan~ fat intakc population selecti the U.S. populati The cardiovascui were high blood and those most a anvy effect of ETS