Passive smoking at work as a risk factor for coronary heart disease in Chinese women who have never smokedBMJ 1994; 308 doi: https://doi.org/10.1136/bmj.308.6925.380 (Published 05 February 1994) Cite this as: BMJ 1994;308:380
- Y He,
- T H Lam,
- L S Li,
- L S Li,
- R Y Du,
- G L Jia,
- J Y Huang,
- J S Zheng
- Department of Epidemiology, 4th Military Medical University, Xi'an, China Department of Community Medicine, University of Hong Kong, Hong Kong Department of Cardiology, 4th Military Medical University, Xi'an, China.
- Accepted 13 January 1994
Objective: To study whether passive smoking at work is a risk factor for coronary heart disease.
Design: Case-control study.
Setting: Xi'an, China.
Subjects: 59 patients with coronary heart disease and 126 controls, all Chinese women with full time jobs, who had never smoked cigarettes.
Results: The crude odds radio for passive smoking from husband was 2.12 (95% confidence interval 1.06 to 4.25) and at work was 2.45 (1.23 to 4.88). The final logistic regression model, with passive smoking from husband and at work as the base, included age, history of hypertension, type A personality, and total cholesterol and high density lipoprotein cholesterol concentrations; the adjusted odds ratios for passive smoking from husband and at work were 1.24 (0.56 to 2.72) and 1.85 (0.86 to 4.00) respectively. For passive smoking at work, statistically significant linear trends of increasing risks (for both crude and adjusted odds ratios) with increasing exposures (amount exposed daily, number of smokers, number of hours exposed daily, and cumulative exposure) were observed. When these exposure variables were analysed as continuous variables, the crude and adjusted odds ratios were also significant.
Conclusion: Passive smoking at work is a risk factor for coronary heart disease. Urgent public health measures are needed to reduce smoking and to protect non-smokers from passive smoking in China.
Whether passive smoking is a cause of coronary heart disease is still controversial
Previous studies have shown that coronary heart disease is associated with passive smoking at home but not with passive smoking at work
This study shows that for women's passive smoking at work there were significant linear trends of increased risks of coronary heart disease with increasing exposures, even after adjustment for major risk factors and passive smoking from husband
Urgent public health measures are needed to reduce smoking in China
Passive smoking has been confirmed as a cause of lung cancer in adults and respiratory ill health in children,1 but the role of passive smoking in causing coronary heart disease is still unsettled. Evidence that passive smoking is associated with coronary heart disease is increasing. Glantz and Parmley reviewed the results of 10 epidemiological studies, together with physiological and biochemical data, and concluded that passive smoking causes heart disease.2 The same conclusion was reached in a review by Taylor et al.3 There have since been two case-control studies, both associating passive smoking with increased risk of coronary heart disease.4, 5
As for the source of passive smoking, most previous studies reported associations with exposure from spouse exclusively. Of the 12 studies (eight prospective and four case-control studies) mentioned above, only two case-control studies presented data on passive smoking at work. In Britain Lee et al found no increase in risk for a combined index of passive smoking which included exposures at home, at work, during travel, and during leisure. This study had a small sample size, only 30 cases in men and 36 in women.6 In Australia Dobson et al found increased odds ratios for passive smoking at home for men and women, but the odds ratios for passive smoking at work did not suggest increased risk.4 This study had a larger sample, 174 cases in men but only 27 in women.
Steenland recently reviewed nine epidemiological studies, pointing out that the lack of data on exposures to environmental tobacco smoke outside the home was one of the major weaknesses in the epidemiological evidence.7 Glantz and Parmley also considered that the studies they reviewed understimated the risk because exposures at home are generally smaller than exposures at work.2
In China, our earlier study on non-smoking women in Xi'an included 34 cases and 68 controls.8 It found an adjusted odds ratio for passive smoking from husband of 1.50 (95% confidence interval 1.28 to 1.77). However, this study did not include details of exposure for passive smoking at work. The present study is a second case-control study which aims to study whether passive smoking at work is a risk factor for coronary heart disease in women who have never smoked. It takes into account passive smoking from the husband and other risk factors.
Subjects and methods
The cases were patients with coronary heart disease (non-fatal, incident cases) from the three large teaching hospitals of two medical universities in Xi'an between December 1989 and November 1992. The final diagnosis was myocardial infarction according to WHO criteria9 or coronary stenosis confirmed by coronary arteriography. Coronary arteriography was performed using Judkins's technique10 and analysed by two experienced cardioradiologists independently. The criterion of diagnosis of coronary heart disease was a finding of more than 50% occlusion in at least one of the major arteries. The agreement between the two radiologists was over 90%. Patients with occlusion of 50% or less were excluded.
The controls were from three sources: patients admitted because of suspected or diagnosed coronary heart disease but confirmed to be normal after coronary arteriography (no coronary stenosis at all); other medical outpatients attending cardiology departments (patients with psychosomatic symptoms, menopausal syndrome, dysrhythmia, or non-cardiac chest pain); and a random sample of healthy subjects from a community screening programme for coronary heart disease. The latter two groups were confirmed to be free of coronary heart disease by WHO criteria9 and normal exercise electrocardiography.
A standardised questionnaire was designed to collect information on demographic characteristics (such as ethnic origin, age residential history, educational level, occupation, and marital status); history of hypertension, hyperlipidaemia and diabetes mellitus; family history of hypertension, stroke, and coronary heart disease; history of smoking and passive smoking from husband and at work; drinking history; exercise; and psychosocial factors (such as Type A personality, experience of mental trauma, and stressful life events). The interviews were carried out by three trained interviewers, before coronary arteriography for patients scheduled for coronary arteriography or during recovery for those with myocardial infarction. The non-response rate was 8%.
Physical examinations followed standard methods and included height, weight, body mass index, systolic and diastolic blood pressure, chest radiography, and electrocardiography. Laboratory investigations included serum concentrations of total cholesterol, triglycerides, low density lipoprotein cholesterol, high density lipoprotein cholesterol, and apolipoprotein A-1 and B and tests of liver and renal function.
Only ethnic Chinese women who had never smoked (lifelong non-smokers) and who had a full time job were included (full time housewives, peasants, and those who were retired for five years or more were excluded).
Passive smoking from husband was defined as living with a smoking husband for over five years. Single women would have been considered as not exposed, but all subjects were found to be married. Passive smoking at work was defined as working with smoking coworkers in the same office or factory unit for over five years. Periods away from the work environment were considered as no exposure in the workplace. All subjects were found to be either not exposed or exposed for over five years.
Quality controls for interviewing included taperecording of the interviews (for 10% of hospital subjects), interviewing the husband to validate the data from the wife (for one third of hospital subjects), and single blind reinterview by a second interviewer who was not aware of the case-control status of the subjects (for 30% of hospital subjects). Furthermore, 26 patients had initially been diagnosed as having coronary heart disease and were interviewed before coronary arteriography but were subsequently confirmed by coronary arteriography to be normal. This group of “misdiagnosed” patients was accepted as controls and their exposure to passive smoking was compared with that of controls and cases who had not had coronary arteriography to check for subjective bias due to interviewers.
For the calculation of sample size required, it should be noted that the crude odds ratio for passive smoking from husband found in our previous study was 3.0.8 Assuming the proportion of exposure to passive smoking at work in the controls was 35%, for a significance of 5% and a power of 80%, 58 cases and 116 controls (one case to two controls) were required to detect a crude odds ratio of 2.5.
The data were managed and analysed by using the computer packages of Epi-Info (5.0) and SPSS-PC (3.1). The statistical procedures used included K, t test, X(sup2) test, X(sup2) test for trend, and standard multivariate techniques for unmatched case-control studies (stratified analysis and multiple logistic regression analysis).11
The present study included 59 cases of coronary heart disease (34 were confirmed by coronary arteriography and 25 with myocardial infarction) and 126 controls (61 confirmed as negative on coronary arteriography, 28 outpatients in cardiology departments, and 37 from community screening). Ages of cases ranged from 37 to 67 years and of controls from 42 to 66 years. About 70% of all eligible cases of coronary heart disease treated in the three hospitals were included.
The characteristics of the controls from the three sources were compared and no significant differences were found. The controls were therefore combined in subsequent analyses. Table I shows that the cases and controls were similar in marital status, occupation, and education but there were more older subjects among the cases. The mean (SD) age of the cases (58.0 (5.39) years) was greater than that of the controls (55.0, (5.05) years; t = 3.69, P = 0.002). All the subjects had lived in Xi'an for more than 20 years.
Results on single blind test-retest by two interviewers on 35 hospital subjects (16 cases and 19 controls) showed good agreement, ranging from 75% to 95% for the 10 risk factors tested, with K values ranging from 0.4 to 0.8 (nine K values with P < 0.01 and one with P < 0.05; data not shown).
Table II shows that the exposure to passive smoking in the misdiagnosed controls was similar to that of the controls shown not to have coronary heart disease but different from that of the cases. There was no history of excess exposure in the misdiagnosed groups, suggesting that there was no subjective bias in the interviews.
For passive smoking from husband, the crude odds ratio was 2.12 (1.06 to 4.25) (table III). The sizes of the living quarters of cases and controls who were exposed to passive smoking from husband were not significantly different. Table III also shows that the crude odds ratio for passive smoking at work was 2.45 (1.23 to 4.88). The statistical power, calculated from table III with a significance level of 5%, was 79%.
Table IV shows the results of stratified analysis for the two sources of passive smoking. The odds ratio for combined exposure to both sources, 4.18, was slightly higher than expected from the additive model (2.07 + 2.53 −1 = 3.60) but much less than expected from the multiplicative model (2.07 × 2.53 = 5.24). The crude odds ratio for any exposure (from husband or at work, or both) was 2.87 (1.28 to 6.55).
Table V shows the final model of logistic regression analysis which included passive smoking from husband and at work as the base (these two variables were included in the model before other variables were entered and tested) and age, history of hypertension, type A personality, and high density lipoprotein cholesterol concentration. Other risk factors had also been tested by forward and backward stepwise procedures but none affected the model significantly. The interaction term of the two passive smoking risk factors (passive smoking from husband multiplied by passive smoking at work) was also tested but was not significant. The adjusted odds ratio for passive smoking from husband was 1.24 (0.56 to 2.72) and at work was 1.85 (0.86 to 4.00). Both adjusted odds ratios were smaller than the respective crude odds ratios and became non-significant after the other five risk factors were included in the final model. When passive smoking was removed from the logistic model the adjusted odds ratio for passive smoking at work was slightly higher (1.92) but was still not significant. However, the adjusted odds ratio for any exposure (from husband or at work, or both) was significant (2.36; 1.01 to 5.55).
The relation between odds ratios and amount of exposure to passive smoking from husband and at work were examined. For passive smoking from husband, the crude odds ratios showed significant linear trends with amount smoked daily by husband, duration of exposure, and cumulative exposure (amount daily multiplied by duration), but the trends became non-significant after passive smoking at work and the other five risk factors were adjusted for in the final model (data not shown). However, for passive smoking at work, table VI shows that significant linear trends were found for the crude odds ratios in amount smoked daily, duration of exposure, number of smokers, exposure time daily, and cumulative exposure. For adjusted odds ratios, the linear trends were significant for all the variables except duration of exposure. When passive smoking from husband was removed from the logistic model, the odds ratios for passive smoking at work were only slightly higher, suggesting that the effects of multicolinearity of the two exposure variables were small. Table VII shows similar results when these variables were analysed as continuous variables, and table VIII shows that there were significant trends for the two indices of combined exposure from husband and at work.
The outcome or end point of this study is non-fatal incident cases of coronary heart disease. This is similar to those in the previous four case-control studies on passive smoking and coronary heart disease.*RF“MDSD” “MDNM” 4-6,8* Most previous prospective studies used mortality as the outcome measure. Despite the difference in end point, the relative risks for passive smoking were quite similar.2 Although there may be prevalence-incidence bias in using non-fatal cases, the obvious advantage is that the patients can provide more and better information on exposure and other confounding factors.
Questionnaires or interviews are the key instruments in studies on passive smoking. Cummings et al showed that subjects were able to report an accurate history of exposure to passive smoking: the level of agreement between subjects and surrogates on exposure to tobacco smoke at work was 78% (K = 0.5); the level of agreement for exposure to spouse smoking was 86% (K = 0.7).*RF 12“MDSD”*“MDNM” We used the test-retest method with two interviewers: the agreement for passive smoking at work was 74.3% (K = 0.5, P <0.001), and for passive smoking from husband the agreement was 91.4% (K = 0.8, P < 0.01). We did not interview subjects again on quantity of exposure, but for this aspect the agreement should be lower.
Validation by cotinine testing was not possible for past exposures in case-control studies. The analysis for trend should yield better evidence for causal inference of whether or not there is increased risk due to exposure but would not be precise enough for risk assessment for unit dose of exposure.
Because different sources of subjects might be a potential source of bias in the present study, exposures to passive smoking in each of the two series of cases (those confirmed by coronary arteriography and by myocardial infarction) were compared with exposures in each of the three sources of controls (cases confirmed negative on coronary arteriography, outpatients, and community controls). The crude odds ratios for passive smoking from husband ranged from 2.0 to 2.3 for cases confirmed by coronary arteriography and from 2.0 to 2.2 for those confirmed by myocardial infarction; for passive smoking at work, the crude odds ratios ranged from 1.8 to 3.6 and from 1.9 to 3.6 respectively. As the results of separate analysis were consistent, pooled analysis was justified.
Results of various quality control measures on selected subjects suggested that the data should be reasonably reliable and free from bias. Moreover, people in Xi'an were unaware of the issue of passive smoking, and bias due to overreporting of exposure in coronary heart disease patients was unlikely. The bias due to misclassification of current and ex-smokers as lifelong non-smokers should be small because the prevalence of female smokers in China was very low as compared with Western countries. The prevalence of regular smokers in females aged 40-65 was 8.6% in the province of Shaanxi, of which Xi'an is the capital.13
Both this and our previous studies showed that passive smoking from husband was associated with coronary heart disease. The crude odds ratio of 2.12 (1.06 to 4.25) in the present study was smaller but consistent with the value of 3.00 (1.26 to 7.17) in the previous study.8 Although the adjusted odds ratio of 1.24 (0.56 to 2.72) was not statistically significant, it was consistent with the previous adjusted odds ratio of 1.50 (1.28 to 1.77). The variables adjusted were not the same in the two studies, and passive smoking at work was adjusted in the present study but not in the previous one. Thus the results of these two studies, together with the evidence from other countries, are strong evidence suggesting that passive smoking from the husband is likely to be a causal factor for coronary heart disease in women in Xi'an who have never smoked.
To the best of our knowledge, this is the first study showing an increased risk of coronary heart disease with increasing exposure to passive smoking at work (crude and adjusted odds ratios were 2.45 (1.23 to 4.88) and 1.85 (0.86 to 4.00) respectively). With the exception of number of years of exposure, the linear trends for amount exposed daily, number of smokers, number of hours exposed daily, and cumulative exposure were all statistically significant. These results strongly suggest that passive smoking at work is a risk factor for coronary heart disease, even after passive smoking from husband is taken into account. When passive smoking from husband was not included, the adjusted odds ratios were slightly higher.
Comparing the odds ratios for the two sources of environmental tobacco smoke, the crude and adjusted odds ratios for passive smoking at work were slightly greater than those for passive smoking from husband (although the 95% confidence intervals overlaped). If these were not due to chance, the higher risk for passive smoking at work may be explained by the fact that exposures to tobacco smoke at work are higher than exposures at home because the density of smokers is higher at work, and the length of stay at work for a working woman is longer than the time she is exposed to her husband's smoking at home. Stratified analysis in the present study suggests that the effects of the two are additive and that there is no significant interaction. Because the prevalence of smoking among men is high in China and most men smoke freely at home and at work, women are heavily exposed to environmental tobacco smoke and the magnitude of the risks could be quite high.
To conclude, the present study provides further evidence that environmental tobacco smoke, including smoke at work, is likely to be a cause of coronary heart disease. The weaknesses of the present study are recognised and further studies are required to investigate the role of passive smoking at work and its interaction with passive smoking at home and from other sources. However, China is the largest producer and consumer of tobacco in the world—30% of the world's cigarettes are consumed by China's 300 million smokers. In 1984, the prevalence of smoking in the population aged 15 and above was 61% in men and 7% in women. Forty per cent of non-smokers were exposed to environmental tobacco smoke for over 15 minutes a day: 67% of the passive smokers were exposed at home, 14% at work or in public places, and 19% both at home and at work.13 Smoking among young people has increased in recent years.14 Despite the efforts to control smoking, most women are still exposed to tobacco smoke at home and at work. They are also unaware of the hazards of passive smoking and are in a disadvantaged position to protect themselves from environmental tobacco smoke. Urgent public health measures are required to reduce smoking in China so as not only to protect women from environmental tobacco smoke but also men from the hazards of active smoking.
We thank the 3rd International Conference on Preventive Cardiology for its Young Investigators Award, the Sun Yat Sen Foundation Fund, and the China Medical Board Fellowship of the Faculty of Medicine, University of Hong Kong, for supporting Dr Y He's research in Hong Kong; Mr C M Wong for statistical advice; Miss S F Chung for research assistance; and Miss M Chi for clerical assistance.