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I I I I I l I I I I I i ! I ! I I I i LAW OFFICES SHOOK, HARDY& BACON ENVIRONMENTAL TOBACCO SMOKE & INDOOR AIR QUALITY COMPILATION 4 JANUARY-MARCH 1993 * ISSUES 38-43 SHB

TABLE OF CONTENTS LUNG CANCER ........................................................................................ 1 CARDIOVASCULAR ISSUES .......................................................................... 2 RESPIRATORY DIsEasEs AND CONDITIONS - ADULTS ................................... 4 R_~SPIKaTORY DIS~.aSES AND CONDrrIONS - CHI~.DP,~N ............................... 6 OTHER HFoU.TH ISSUES .......................................................................... 11 ETS ExposuP,£ AND MONITOPdNG ......................................................... 16 INDOOR AIR QU,~LITY ............................................................................ 20 SMOKING POLICIES AND RELATED ISSUES ................................................. 24 STATISTICS AND PvISK ASSESSMENT ........................................................... 28 INDEX ................................................................................................... 3 1 Please note: This document is nor intended to be an encyclopedic summary, of scientific literature relating to ETS. Rather, it contains exclusively those studies included in Reports on Recent ETS and IA Q Develo2ments. This document has been prepared for use by Shook, Hardy & Bacon attorneys and analysts. Please, do not distribute this document to persons outside the firm.

I JANUARY-MARCH 1993 ETS/IAQ ARTICLE SUMMAPdES ENVIRONMENTAL TOBACCO SMOKE & INDOOR MR QUALITY I I I I I I I I I I I I I I I I I I LUNG CANCER [1] Adlkofer, F.X., "Lung Cancer Through P~sive Smoking at the Workplace -- A More Theoretical Issue," Zentralblatt fur Arbeitsrnedizin, Arbeitsschu~z Prophylaxe und Ergonomie 42 ( 10): 400-424, 1992 [Issue 42, Item 43] The author of this article reviews ETS composition, ETS exposure data, and the epidemiologic literature on ETS exposure and lung cancer. He concludes that lung cancer risk purportedly due to ETS exposure "can neither be entirely ruled out or proved, let alone quantified." [The article is written in German; however, an English abstract is provided. The article was first discussed here in Issue 38, JanuaW 7, 1992.] "Environmental tobacco smoke (ETS) differs in composition and biological activity, from mainstream smoke inhaled by, the smoker to such an extent, that the amount of toxic substances taken up by exposure to ETS cannot be expressed in terms of cigarette equivalents. In contrast to smoking, the uptake of gaseous phase con- stituents is of major importance during exposure to ETS whereas the uptake of particle phase constituents, to which the development of lung cancer has been attrib- uted, is very low. Moreover, ETS is inevitably mixed with substances from other sources." "Under experimental conditions, involving exposure to ten to thirty times higher concentrations of tobacco smoke than found under normal conditions, non-smokers show slightly elevated levels of COHb in blood and of nicotine and cotinine in body fluids as well as an elevated excretion of benzene in exhalate and of thioethers in urine. The two last-mentioned provide evidence for the uptake ofelectrophilic, i.e. potentially carcinogenic, substances from the gaseous phase. In contrast to smok- ers, neither an increase in DNA-adducts in monocytes nor an elevation in urinary mutageniciry could be found in non-smokers despite extreme exposure to ETS. In non- smokers exposed to ETS at the workplace, only nicotine or its metabolite cotinine are likely to be found in body fluids. All other parameters, particularly those indicating genotoxic effects, are indistinguishable from the back- ground levels." "The results from thirty epidemiological studies on exposure to ETS axe currently available. Most of these studies show a relative risk of>l (mean value: 1.35), but a significant increase in risk is found only in few cases, and it has rarely been possible to demonstrate a dose- response relationship. Any elevated risk is most probably due to methodological errors of which misclassifying smokers as non-smokers and disregarding confounding factors are the most significant. The present analysis leads us to conclude that a lung cancer risk due to ETS can neither be entirely ruled out nor proved, let alone quantified. If the risk really exists, it must be extremely, low. Therefore, ifETS does not constitute a major lung cancer risk, the working population would not benefit from confining the reduction of toxic substances to tobacco smoke by bans on smoking as toxic substances form other sources present at the workpIace might be ignored by this procedure." [2] Letters to the Editor Regarding Bums, D.M., "Environmental Tobacco Smoke: The Price of Scientific Cerrainvy," Journal of the National Cancer Institute 84: 1387-1388, 1992 [Issue 40, Item 18] The Journal of the National Cancer Institute recently published two letters concerning this editorial, published at the same time as the Stock-well, et al., case-control study on ETS exposure and lung cancer in nonsmoking women. As discussed in Issue 31 of this Report, Septem- ber 25, 1992, the author, David M. Burns, called for the development of public policies based on his belief that a causal relationship between ETS exposure and lung cancer has been "clearly established." Dr. Burns is an antismoking activist and a member of the EPA's Science Advisory Board committee that reviewed the Draft Risk Assessments on ETS. The first letter in the current correspondence is from Gio B. Gori, and is followed by' a reply from Burns. The letters appear in Journal of the National Cancer Institute 85(1): 66-67, 1993. Gori comments that Burns' original article suggests that "either the editorialist [Burns] did not read the report carefully or his perception of certainty is a curious one." Gori writes that Stocle~vell, et al., referred to suggestion, rather than certainty, in their article. He also points out "incongruities" of ETS epidemiologic studies. In particu- SHB

ET$/IAQ ARTJCLE 5U.MMAR/E5 ISSUES 38-43 lar, Gori states that the odds ratios reported by StockwelI, et al., "vary from apparent protection to apparent risk," and that the reported results on adenocarcinoma "conflict with the much quoted and larger study ofFontham et al." Gori continues with a reference to potential confounding variables, biases, uncertainties in exposure estimates, and other problems, which he chzracterizes as "weaknesses of epidemiologic data." Gori suggests that epidemiology should not be "interpreted in an equivocal dialectic context," calling the certainty referred to by Burns "an assertive policy proposition." In his response, Burns describes Gori's letter as "a fine example of the 'reasoning' used by the tobacco industry to delay and confuse the development of scientific cer- tainty." Burns writes that neither the Stockwell, et al., study nor his own editorial implied that the Stoclcwell, et ad., stud)' provided sufficient data to reach scientific certainty. He calls for using "multiple lines of evidence and all of the data available" in judging causality. Burns also accuses Gori of an "ad hominem attack suggesting that, because I [Burns] agree with the conclusion of every comprehensive scientific review of these data that has been conducted in the last 7 years, my position must be based on advocacy and cannot be scientific." [3] Heath, C.W., "Commentar~ Ens4ronmental Tobacco Smoke and Lung Cancer," The Lancet 341: 526, 1993 [Issue 43, Item 36] This brief article focuses on the recently-released EPA Pdsk Assessment on ETS. The author contrasts it with the other reviews on the topic that appeared in 1986, saying that EPA "strongly reaffirmed" their conclusions, and provided a "firm regulatory basis for increased societal action to eliminate ETS." "Since 1986, exposure to environmental tobacco smoke (ETS) (passive smoking) has been widely regarded in scientific circles as a cause of human lung cancer. In that year, the US National Research Council, the Surgeon General of the US Public Health Service, and the Interna- tional Agency for Research on Cancer issued expert reviews of the topic. Each concluded that lung cancer resulted from ETS exposure." "The same conclusions have now been strongly reaf- firmed in an updated review issued in December, 1992, by the US Environmental Protection Agency (EPA). Significantly, however, what the three earlier reports lacked, the EPA pronouncement now provides -- a firm regulatory basis for increased societal action to eliminate ETS from public buildings and places of business. Although the EPA itself has no direct regulator)" authority over indoor air conditions, its action classifying ETS as a class A carcinogen (i.e., a "known" human carcinogen) is widely expected to spur the US Occupational Safety and Health Administration to review and revise its rules governing smoking in workplaces. The EPA report is also expected to encourage businesses and governments to move voluntarily toward community-wide smoke-free conditions, in view of the greater vulnerability to litiga- tion arising from ETS exposures." "The evidence that ETS causes lung cancer rests solidly on a combination of epidemiologicai and toxicological data, all to be viewed against a background of longstanding knowledge about cancer occurrence in active cigarette smokers. The EPA report reviews this total fabric of evidence in considerable detail but gives special emphasis to the epidemiological findings .... Thirty epidemiological studies from eight countries are reviewed. • .. All thirty examined lung cancer risk in non-smoking spouses of smokers. Although some also attempted to measure risk in terms of ETS exposure in children and in workers, judging such exposure is less certain than between spouses and hence findings are more difficult to interpret." "The EPA report weights these various kinds of evidence in relation to the recommendations of Bradford Hill regarding the nature of information upon which causal associations can be identified .... In each instance, the collective findings here strongly support a cause-effect association. How quickly and completely will the report's findings be translated in effective community action?" CARDI OVASC~ ISSF~ [1] Leone, A., ~The Heart: A Target Organ for Cigarette Smoking," Journal of Smoking-Related Disorders3(3): 197-201, 1992 [Issue 41, Item 54] The author of this article reports briefly on several studies on "the role of smoking on the cardiovascular system." He includes a study of cardiac performance during exercise, in which men were exposed to a "smok- ing environment." The author claims that the study subjects "showed impaired cardiac performance" when exposed to smoke. "The purpose of this report is to discuss briefly our previous studies and to prove that cigarette smoking damages the heart." -2- I I I

JANUARY-MARCH 1993 ETS/IAQ ARTICLE SUMMARIES i i I I I I i I I I I I I I I I I I "We studied 19 non-smoking male volunteers. These consisted of nine healthy subjects and 10 patients with previous myocardial infarction. The volunteers under- went exercise stress testing ~vice; once in a smoke-free environment and once in a smoking environment (carbon monoxide concentration 30-35 ppm)." "In each studied subject we measured the peak of exercise (Watts), time for recovery to pre-exercise heart rate (rain) and plasma (%) and expired carbon monoxide concentrations (ppm) .... Each subject acted as his own control. No healthy volunteer developed chest pain during stress testing, but we stopped the exercise stress testing of four volunteers with a previous myocardial infarction in the smoking environment because of warning ventricular arrhythmias." "In summary, we reached the following conclusion. Acute exposure to passive smoking impaired cardiac performance of both survivors of infarction and healthy volunteers. Survivors showed a significant reduction of the peak of exercise, prolonged time to recovery to pre- exercise plasma carbon monoxide concentration and ventricular arrhythmias in a smoking environment. Healthy people showed prolonged time to recovery to pre-exercise heart rate in the same environment. There- fore, both groups showed impaired cardiac performance in a smoking environment, although with different results." "Cigarette smoking has to be considered a potential hazard of daily life. Smoke inhalation, either active (such as smoking a cigarette) or passive (such as breathing indoor smoke), can cause a severe impairment of cardiac function. The results we discuss in the present overview justify such a statement." [2] Tribble, D.L., and For,mann, S.P., "Reduced Plasma Ascorbic Acid Concentrations in Women Regularly Exposed to Environmental Tobacco Smoke (ETS)," Circulation 86(4): Supplement, 1992 [Issue 40, Item 19] The authors of this abstract propose that a reduction in levels of the vitamin ascorbic acid may be related to the pathogenesis of heart disease. Based on measurements of plasma ascorbic acid concentrations and dietary ascorbic acid intake in nonsmoking women, the authors report that "passive smokers" had lower plasma ascorbic acid levels, which they suggest "may contribute to increased heart disease risk associated with ETS exposure." "Oxidative processes have been implicated in the pathogenesis of heart disease, offering a potential explana- tion for the high risk attributable to smoking. Cigarette smoke contains numerous oxidants, and smokers exhibit reduced circulating concentrations of the antioxidant vitamin ascorbic acid (AA)... We measured plasma AA concentrations and dietary AA intake in nonsmoking women exposed to >_20 hr/wk ETS, i.e., passive smokers (PS), as compared with nonsmokers with >_2 hrs ETS exposure/wk (NS) and active smokers (AS), to assess whether PS also may exhibit suboptimal AA nutriture... • Both PS and AS exhibited reduced plasma AA relative to NS. Reduced plasma AA in PS may be partially due to reduced dietary AA. These results suggest that suboptimal AA nutriture may contribute to increased heart disease risk associated with ETS exposure." [3] Whig, J., Singh, C.B., Soni, G.L., and Bansal, A.K., "Serum Lipids & Lipoprotein Profiles of Cigarette Smokers & Passive Smokers," Indian Journal of Medical Research 96(B): 282-287, 1992 [Issue 39, Item 27] This study,, conducted in an Indian population, reports nonsignificant elevations in cholesterol and triglycerides in men reporting ETS exposure. The authors claim that the high density lipoprotein cholesterol/low density lipoprotein ratio was lowered in "passive smokers," and further claim that this suggests an increased risk of coronary heart disease in exposed persons. EXCERPTS: "Very little attention has been paid to the effect of passive smoking on serum lipids and lipoproteins. In view of the fact that [a] large population in India is exposed to passive smoking, the present study has been undertaken to know the effect of passive smoking on serum lipids and lipoproteins compared to that in chronic smokers and control subjects." "Serum lipids and lipoproteins of 50 active and passive smokers were compared with levels in 25 control subjects. Active smoking resulted in an increase in total cholesterol (To and triglycerides (Tr) as compared to control group. The passive smokers also showed relatively higher levels but the effect was not significant. Active smoking raised the low density lipoprotein cholesterol (LDL~) and very, low density lipoprotein cholesterol (V-LDL~) levels whereas high density lipoprotein cholesterol (HDL~) content was lowered, thus resulting in decreased ratios of HDL¢/T¢ and HDL/LDLc. The passive smokers also showed slightly higher levels ofLDLc and VLDLc but lower levels of HDL~ and a lower HDL¢/LDL¢ ratio." "Since the ratio of HLDc/LDL is also significantly' lower amongst passive smokers, ~t indicates that not only active smokers but also subjects who are in contact with -3-

ETS/IAQ ARTICLE SUMMARIES ISSUES 38-43 active smokers are at a relatively higher risk of developing atherosclerosis. The lower degree of risk amongst passive smokers compared ro that amongst active smokers could be due to the filterarion [sic] of smoke in the lungs of the smokers. Some of the components like nicotine and tar are deposited in the lungs of active smokers and therefore the passive smokers are exposed to a lower density of harmful components .... IT]he levels of serum lipids and lipoproteins were altered in passive smokers in such a manner that it may have a deleterious effect on [the] cardiovascular system." "The passive smokers also show relatively less altered lipid and lipoproteins, in a trend similar to that of smokers. The alteration in the individual value oflipids and lipoproreins is not significant in [the] case of passive smokers but the results are significant only in case of ratios ofHDLc/Tc and HDL~/LDLc As decrease in this ratio is responsible for the development of atherosclerosis, the results indicate that even the passive smokers are at a relatively higher risk of developing corona.D' heart disease." [4] Zhu, B.-Q., Sun, Y.-P., Sievers, R.E., Isenberg, W.M., Glantz, S.A., and Parmley, W.~L, "Passive Smoking Increases Experimental Atherosclerosis in Cholesterol-fed Rabbits," Journal of the American College of Cardiology 21(1): 225-232, 1993 [ Issue 39, Item 12] A paper based on this study, which was presented at the American Heart Association Meeting in November 1992, has now been published. It is essentially unchanged from the manuscript previously excerpted. See Compilation 3, p. 10. RESPIRATORY D~s~sss aND CONDITIONS ADULTS [1] Danuser, B., Weber, A., Hartmann, A.L., and Krueger, H., "Effects of Bronchoprovocation Challenge Test With Cigarette Sidestream Smoke on Sensitive and Healthy Adults," Chest 103: 353- 358, 1993 [Issue 42, Item 44] Swiss researchers report in this paper on a "cigarette bronchoprovocation challenge test," in which sidestream smoke (as a surrogate for ETS) was administered to 20 persons via mouthpiece. Lung function parameters reportedly did not change after smoke exposure in ten healthy subjects. However, the authors report statistically significant decreases in lung function parameters for ten subjects classified as hyperreactive. "The cardinal feature of asthma is a greater than normal variability in airway caliber occurring in responses to a variety of endogenous and exogenous stimuli. Even if results of lung function tests are normal, bronchial hyperreactivity can be detected by bronchoprovocation challenge testing with inhaled agents such as histamine or methacholine." "For the present study, persons with airways hyperreac- rive to methacholine were selected as sensitive. The cigarette bronchoprovocation challenge test with sidestream smoke is meant to allow comparison of the possible response to sidestream smoke with the response to methacholine in normal active and hyperreactive subjects." "Two groups of individuals were tested: ten persons with hyperreactive airways and ten healthy individuals, matched for age and sex .... All participants were nonsmokers verified by carbox-yhemoglobin measure- ments." "The challenge test was conducted by delivering increasing concentrations ofsidesrream smoke character- ized by the smoke-induced CO concentration. Subjects were told that they would breathe either smoke-polluted or normal air; no information about the increase of dose was given." "The short-time inhalation, even of high concentrations ofsidestream smoke, was well tolerated by both groups. Symptoms were in the mean weak even at the highest concentrations. Three of the ten hyperreactive persons and four of the ten healthy persons never indicated any symptoms." "The increase in symptoms score with increasing sidestream smoke concentrations was due to a combina- tion of progressively larger numbers of subjects experienc- ing symptoms with increasing exposure, and from the same subjects experiencing progressively more severe symptoms. With the exception of the symptom 'sore/dr), throat,' the hyperreactive group indicated more com- plaints than the healthy group." "Our subjects inhaled the sidestream smoke with a noseclip and the test room never got polluted, so that eyes and nose as primary detectors of smoke did not come into contact with the polluted air. Subjective airway symptoms were weak. No distinction between the different concen- trations of the sidestream smoke was possible and suggestibility can therefore be considered as minimal. Furthermore, contraw to room exposure, where especially the concentration of the particles fluctuates, the applied I I I i °1

JANUARY-MARCH 1993 ETS!IAQ ARTICLE SUMMAKIES I I I I l I I I I I I I I I I I I I dose was well defined. On the other hand, the exposure of 2 rain via mouthpiece does not copy ETS exposure in real-life situation [sic]." "With healthy persons, the inhalation ofsidestream smoke had no effect on FEV~, FVC, and MEF50." "Our data demonstrate that even a 2-rain exposure to the lowest concentration ofsidestream smoke induced a significant decrease in the measured lung function parameters of hyperreactive persons, which is greater than the expected variabiIiry during this length of time. The lowest sidestream smoke exposure of 2 ppm CO is a very realistic concentration." "The precise mechanism of ETS-induced impairment in lung function is unknown. On account of the short exposure of time of 2 rain, we propose a response of irritant receptors." "Nonspecific bronchial reactivity to methacholine and pretest lung function parameters do not sufficiently' predict and explain the reaction to sidestream smoke in all individuals, although methacholine does in most hyperreacrive people. The mechanisms underlying airflow obstruction caused by cigarette sidestream smoke need further research." [2] Lehrer, S.B., "Pulmonary Effects of Environmental Tobacco Smoke Exposure on Asthmatic Subjects," CZRR Cur'rents 2(2): 1, 4, 1992 [Issue 40, Item This article reports on a test chamber developed by a research team at Tulane University, in which asthmatics claiming smoke-sensitivity were exposed to sidestream smoke as a surrogate for ETS. The author reports that only 10 percent (17 out of 163 subjects) "reacted" to side- stream smoke at high smoke levels, corresponding to ETS concentrations that "would be extreme and rarely encountered" in actual environments. "Our studies have focused on the incidence and charac- terization of asthmatic responses to environmental tobacco smoke." "[A] dynamic test chamber was developed in which sidestream smoke (SS) test atmospheres, used as a surrogate for ETS, can be precisely controlled for any desired duration by varying the number of machine- smoked cigarettes and adjusting the air flow.... The exposure environment within the chamber is composed of the diluted SS from machine-smoked 1R4F research cigarettes and is characterized and monitored by concen- tration measurements of nicotine, respirable suspended particles, and carbon monoxide." "In our study, 163 asthmatics claiming smoke-sensitiv- ity were challenged with SS-ETS for up to 240 minutes. Total suspended particle (TSP) levels ranged 750-2000 ug/m~ and nicotine ranged 250-450 ug/m3. Twenty-eight (28)/163 asthmatics (17%) demonstrated a significant decline in lung function (decrease in FEV~ greater than or equal to 20%) after 90 to 240 minutes of exposure. While intermittent exposure to this ETS level is possible in an environment such as a very smoky bar, ETS particle concentrations greater than 300 ug/m3 would be extreme and rarely encountered. A typical indoor level is about I20 ug/m3 or less in smoking environments." "all reactors were sham (SS-ETS absent) challenged in the chamber. Eleven (11)/28 (39%) reactors had a positive sham challenge, were non-specific reactors, and were removed from the group. Thus 17/163 (10%) asthmatics reacted to SS-ETS." "Seven (7) of the 17 SS-ETS reactors were selected for dose-response challenge with decreasing levels of SS-ETS up to 360 minutes at 4 week intervals. No subjects reacted to any SS-ETS levels before 90 minutes, and 3/7 did not react to levels less than the highest .... No participants demonstrated a significant drop in peak flow rate when monitored overnight." "Our studies showed that about 10% of asthmatics claiming to be smoke sensitive actually demonstrated objective changes in their pulmonary function from high level SS-ETS exposure. These responses do not appear to be related to IgE antibody reactivity to tobacco allergens. Almost 40% of all reactors also exhibited a significant drop in their FEV~ in the absence of tobacco smoke which suggests that the nature of some forms of asthma are unstable and that controls are needed when evaluating cigarette smoke-induced responses. Future studies are directed at assessing the role of mediators in ETS-induced asthmatic and extrapulmonary responses, identification of the ETS components that might provoke asthmatic responses, and determining the effects of ETS on asth- matic responses to known environmental allergens." [3] Shephard, R.J., "Environmental Tobacco Smoke and Asthma," Chest 103(2): 330-331, 1993 [Issue 42, Item 45] This editorial comments on the Danuser, et al., stud),. The author praises their technique for smoke exposure, but calls for additional experiments to generate fuaxher data. ~'~ "There can be little argument that the accumulation of ".~ stale tobacco smoke is unpleasant and annoying to both the nonsmoker and the ex-smoker, and this will undoubt- -5-

ETS/IAQ ARTICLE SUMMARIES ISSUES 38-43 edIy remain the main reason why a smokefree environ- ment is guaranteed in public places." "There has been considerable discussion as to whether exposure to tobacco smoke provokes asthma .... One major source of difficulty in conducting more conclusive experiments is that the odor of tobacco smoke is well known, so that exposure can create psychological reac- tions... The technique adopted by Danuser and associates and described in this issue of Chest is attractive in this regard: the major eye and nasal symptoms that could precipitate psychological reactions are avoided, and nicely graded doses of smoke can be administered to the air~uys." "The choice of 'realistic' carbon monoxide readings is also very debatable, with complications from urban background levels of carbon monoxide. The subjects studied by Danuser et al had an average blood carboxyhemoglobin concentration of 1.5 percent, which suggests either that some of the subjects were unadmitted smokers or that there was a substantial carbon monoxide exposure in the center of Zurich .... [I]n crowded and poorly ventilated areas, such as bars, readings of 30 ppm have been observed. The range of 0 to 32 ppm of smoke- related carbon monoxide adopted in the experiments of Danuser and associates thus seems quite appropriate." "Unfortunately, the key question of the relative contri- butions of a biological and a psychological response is not completely answered by the experiments that they report, for while the symptoms show' a rather nice dose-response relationship, the physiologic reactions do not. Although they postulate a threshold, it is difficult to envisage a biological mechanism that would yield this type of response. Is the smoke so irritating that it provokes a secretion of fluid, which dilutes the initial stimulus? If so, why do the symptom scores remain dose-related? Plainly, more data are required: a larger sample of subjects, varying durations of exposure, and possibly measurements of small- airway function in addition to standard spirometry." t~ESPIRATORY Disuses AND CONDITIONS CHILDREN [1] C~ale, R., Natall, G., Colantonlo, D., and Pasqualerti, P., "Circadian Rhythm of Peak Expiratory Flow in Children Passively Exposed amd Not Exposed to Cigarette Smoke," Thorax 47: 801-803, 1992 [Issue 39, Item 30] This study measured circadian rhythm, i.e., an approxi- mately 24-hour cycle, in pulmonary function measure- ments in Italian school children. The authors claim that children exposed to cigarette smoke reportedly exhibited changes in the circadian rhythm, which they interpret as an early indication of airway obstruction. EXCERPTS: "This study aimed to investigate whether children exposed to passive smoking, assessed by questionnaire and urinary cotinine values, show" greater variation in the circadian rhythm of the peak expiratory flow (PEF) than children not exposed to cigarette smoke." "Questionnaires completed by 60 primaD' schoolchil- dren aged 10-11 years were analyzed and 20 children (12 boys and 8 girls) exposed to passive smoking were identified. These children were matched for sex and age with 20 respondents who had not been exposed to cigarette smoke." "The mean value of urinary cotinine concentration was 1.85 umoi/1 in unexposed children and 3.44 (0.52) umol/ 1 in exposed subjects." "Both groups showed diurnal fluctuations in PEF values with a peak in the afternoon. PEF showed a significant circadian rhythm for both the unexposed and the exposed children." "The circadian rhythm of PEF in the exposed children differed from that of unexposed children... Since any change in the normal circadian pat-tern of any variable can seen [sic] as abnormal and as a step towards clinically symptomatic disease, the increased PEF rhythm ampli- tude may be a measure of early airway obstruction in response to passive smoking." [2] Dagli, E., Cakan, N., and Ataman, A., "Urinary Cotinine Levels in Prima_,-y School Children: Evidence of Exposure to Environmental Tobacco Smoke," European Respiratory Journal 5: Supple- ment, 1992 [Issue 40, Item 37] These Turkish researchers use questionnaire data and urinary cotinine measurements to examine ETS exposure in school children. They conclude that "the dose of nicotine received by Istanbul school children from ETS was esti- mated to be equivalent to 1 to 5 cigarettes per day." "Smoking prevalence and passive exposure to environ- mental tobacco smoke (ETS) are estimated to be very" high in Turkey. Using a questionnaire, we found out that 75% of the 513 primary school children were exposed to ETS at their homes. We correlated this finding with . . . urinary cotinine measurements... Mean urinary cotinine concentration of 275 prima)' school children of non- -6-