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lL v% GZrtI t, -C.( . L YA-v, c`'o.-L iow Passive saokinq in 7emales and Coronary Seart Disease Dy Y. He, L.X.Li, C.C. Fong, Znatitute of Infectious Diseases, and L.S. Li, X.L. Chang, Q.L. Qua, Department of Cardioloqy and Internal M®dicina, Xian Medical College. ADBTRACT Thirty four cases of women with coronary heart disease (CHD) (22 cases diagnosed by coronary arterioqraphy, and 12 cases diagnosed as havinq myocardial infarction) were used in an investigation designed to assess the association between passive smokinq in women and the establishment of CxD. The odds ratio (OR) ot non-smoking women developing CHD as a result of exposure to passive smoke is 3.0-3.5 (p<0.05). A dose response relationship was detected between the number of'passive smoke exposure years and' the increase in OR for CHD. Multiple regression analysis shows that of the many risk factors for CHD, passive smoke exposure is significantly correlated with CHD. Women exposed to passive smoke also showed abnormal levels of serum LDL-C, HDL-C, apoAl and apoB, xey words Coronary heart disease, coronary arteriography, passive smoke Experimental investigations have demonstrated that the chemical constituents generated in the sidestream smoke often contain the same harmful chemicals as in mainstream smoke inhaled by smokers, and that there is considerable adverse otfects contributed by sidestream smoke to non-smokars who are passively exposad.'-= A number of reports have appeared showing a correlation between passive smoke and the damage to lunq l~unctions, increased incidence of lung cancer, and angina pectoris."6 A limited number of investigations have bean focused on the subject of passive smoke in the Paople's Republic of China, and have only concentrated on studyinq the influence of passive smokinq on lung functions.7 ' In this communication we report the relationship between passive smoke exposura and female patients who were hospitalized because of coronary heart disease.

t Yatsrials aaa xethods 6ubjects consisted of patients hospitalized betwesn 19flS-1987 and diagnosed as having coronary heart dlsease and myocardial infarction. They were matched employing the ls2 method as follows: those who were admitted because of possible coronary heart disease and were later confirmed by coronary arteriography to be normals; patients with endocrine dysfunctions but free of CHDs; and people randomly selected from the population. Thus three groups were included in the present investigation: Group 1, thoss hospitalized and diagnosed with Cf3IDs or myocardial infarction; Group 2, those hospitalized with endocrine problems but having no symptoms of CaDs, and Group 3, normals from the general population. Each of the subjects in the thres groups was interviewed using a standardized questionnaire. Some of the questions addressed included : subjects and the spouses smoking history, ths age at which smoking began, the average daily cigarette consumption. Active and passive smoking were dafined as follows : 1. Smoking at least one cigarette per day for a period of at least one year. The spouse is dofined as an ax-smoker if he has already stopped smoking at least 5 years at the time of interview. 2. Wife who is a non- smokar but has lived with a smoking husband for at least 5 years is classified as a passive smoker. 3. If husband is a smoker before marriage, the wife exposure begins at time of marriage. Alternatively, the wife can become exposed after marriage if the husband picks up the smoking habit after marriage. Total exposure time is determined by divorce, death of husband, or when the husband quits smoking and becomes an ex-smokQr. 4. Single female is considered to be equivalent to a female without a smoking spouse. To verify the accuracy of the data collected by the structured interview, tape recording was used and randomized re-interview was performed. Subject group consist of 34 casas (22 cases diagnosed with CHD, and 12 cases diagnosed with myocardial infarction). Control group consist of 34 hospitalized subjects (with 13 suspectsd of CHDa but later confirmed to be normals) and 34 randomly selected matched for race, occupation, residence and age (+/- 5 years). Multipla regressional analysis was performed and the data analyzed suing a 8un-68000 electronic calculator.9 Results i. Coaparison betrssa the *vDject and the Comtrol Qroups No significant differences exist between the two groups in regard to age, education, the marriaqe age. The mean ages of the diseased and control groups are 53.714.28 and 52.9315.24, respectively (t-2.282, ps0.05)

2. Effeats of tassive 4moxing Table 1 shows a comparison between disease and paired control groups. The OR of qetting CHD for nonsmoking women living with a smoking husband is 3.0:0, with a 95% CI of 1.256-7.168, i.e. the risk of women gsttinq C'HD is 3 times higher for those with husbands that smoke compared to those with nonsmokers husbands. Diseased + Group - Table 1. A comparison of Passive Smoking Status in Diseased and Control Groups Control Group + + + - - 4 12 9 3 4 3.00 1.256-7.168 6.117 (c 0.05) A. Dose Response Relationship Table 2 illustrates the association between husbandsr average daily cigarette consunption, passive smoke, exposure years, cumulative passive smoke amount index, and the ORe of getting CHD. There is a noticaabls mose response relationship, i.e. ac the amount of passive smoke exposure increasss, ths risk of getting CHD also becomes greater. Table 2. Dosa Response Relationship between Passive smoke Exposure and CHDs Subject Control OR X2 N O Kusbands daily N cigarette consumption G? Git 0 9 38 1.000 ..... }.i ~ .1~ 45

<20 12 22 2.303 1.8B0 >20 13 8 6.661 10.09B** Passive Smoke Exposure Years 0 9 36 1.000 ..... 510~ 4 9 1.877 0.266 $20 6 11 3.071 2.581 >20 13 10 5.489 8.230** Cumulative Passive Smoke index (Years) 0 9 38 1.000 ..... 1-199 4 11 1.535 0.066 200-399 6 11 2.303 1.009 400-599 6 5 5.067 4.054' 600' 9 3 12.667 11.35a~" p<o.05 p<a.01 B. Association with Clinical Diagnosis in the patients group, 21 cases were diagnosed with, angina poctoris and 13 cases with myocardial infarction. The number of passive smokars in both clinical settings is similar (X= - 1.298, p>0.5). Thsss results are illuctratnd in Table 3. The results show that angina poctoris is clearly and significantly correlated with passive smoking. Although myocardial infarction in the passive smoking group show an OR of greater than 1, it did not reach statistical significance, which may be related to the small sample size.

Table 3. Clinical Diagnosis in Passive Smoke Group Exposure to Passive Smoke Exposure to Passive Smoke Yes No Yes No Anq na Psctorxo Myocard,& -"n arct on Subject Group 17 ~ 8 5 Control Group 20 22 10 16 -OR 4.In 2. 550 X= 5.035 1.018 P c0.05 >0.05 C. n2ood cholesterol and Lipoprotein Level Changes in Passive Smokers By controlling for age, weight, and other risk factors, a decrease in serum HDL-C and apoAl isvel was found in passive smokers, whereas LDL-C, apoB and apo B/Al levels are higher than those not exposed to passive smoke. Tha level of HDL-C, apoAi and apoB/Al levels are significantly different between the subject and control groups (Table 4)

Table 4. 8lood Cholesterol and Serum Lipoprotain Levels in Female Passive Smokers Control Group CHD Group Non-txposed Eacposed Non-axposed Exposed Number 26 20 9 24 Total cholastarol (mmol/L) 4.42t0,6s 4.47±0.68 5.15t0.e6 5.80t0.73* LDL (mmol[L)2.34t0.68 2.5210.68 3.3510.86 3.85±0.71 HDL (mnol/L)1.41t0.18 1.Z9t0.18* 1.2610.21 1.12t0.17* LDL/HDL 1.74±0.51 1.98±0.60 2.75±0.79 3.42t0,.74rt apoAi (q/L) 1.27f0.24 1.1110.23* 0.95t0.18 0.81t0.13* apoB (q/L) 0.7110.17 0.7410.14 1.0320.17 1.1610.20 apoB/apoA1 0.61t0.19 0.67t0.22 1.2110.40 1.36t0.22* *Pc0.05, P values re er to compar-ison-,ba-tvQen non-exposed and exposed cases. 3. xultipis Loqistia ReqrOssion Analysis Srven risk factors believed to contribute to CHD were subjacted to logistic regression analysis. These factors include: history of hypertsnsion (xi}, lamily history of hypertension (x2), lamily history of CHD (x3), history of passive smoke exposure (x4), history of drinking (x5), exercise per.formanee test (x6) and history of hypercholsstersmia (x7). The results are shown Sn Table S. Table 5. Multipls Regression Analysis of CHD Risk Factors Hi Var(ni) 6(Bi) t2'D(si) OR G P ~ History or ~ Passive smoka 0.406 0.069 0.083 4.87 1.5004 16.93 <0~.01 ~ History of I-a Hypertension 0.714 0.052 0.227 3.147 2.0429 8.90 <0.01~A _j

DSSCIIassaN To avoid and minimize bias introduced in studies using hospitalized subjacts, the present investigations compared the subjects groups to two control groups, one group consisting of patients hospitalized for reasons other than CHDs, and a second group randomly selected from the general population. Thaze two control groups are compared to the CHD-diseasad group. Investigations on the effacts of passive smoking in females are more difficult to perform than comparable studies aimed at the effects of active smoking, because the effects of passive smoking may be dependent on such factors as humidity, ventilation and other indoor environmental considerations. Studies to date have not been ab2e to produce a widely accepted standardized protocol for this type of investigation. One of the methods which have been used to assess passive smoke exposure in females relies upon the smoking status of spousesfl`~~hich have been used in sevaral previous published reports. The method appears to provide a eartain degree of simplicity, feasibility, and relative objeetivity., lamale passive smokars have an OR of 3-3.5 in getting CHD, with 95% CI greater than 1. The exposure dose is associated with angina pectoris, in agreement with results of other investigators. The associations remain after adjusting for potential confounder6, suggesting that there is a direct correlation between passive smoking and CHD in females. Additionally, our invaFtigationa also showed alterations in blood cholesterol and lipoprotein levels, indicating that an alteration in the metabolism of cholesterol and/or lipoprotein could contribute to CHD in female passive smokers. According to Scott at al.1, 85= of indoor smoke is due to sidestream smoke, which is known to contain a higher concentration of many toxic chemicals than mainstream smoke, and presumably exhibit a more pronounced adverse health effect. Previous studies have shown that an increase in blood COHb levels capabl,e of producing an obviously untoward effect in people with heart and lung diseases.' Arrownow studied 10 subjecta with angina pectoris, and reported a doubling of blood COHb 2 hours after exposure to indoor tobacco smoke in a poorly ventilated environment. These subjects also showed a 334 reduction in time of exarcise before reachi'ng a perceived exertion. The mechanism, however, remains to be investigated. In peoplets Republic of China, 33.884 of population aqQ>15 years are smokers and 614 of yaales regular smokers. The indirect public health eoneequencas of smoxinq has not received enough attention. Despite the limited number of easeo used in the present investigation which obviously have sevare restrictions, it suggests that passive smoking is related to CKD in females. Thus, smoking in public should be restricted ~ 'CA ~