2023 Volume 30 Issue 8 Pages 863-870
Aims: We examined whether secondhand smoke exposure in childhood affects the risk of coronary heart disease (CHD) in adulthood.
Methods: In the Japan Collaborative Cohort Study, we analyzed data on 71,459 participants aged 40–79 years, with no history of CHD, stroke, or cancer at baseline (1988–1990) and who completed a lifestyle questionnaire including the number of smoking family members in childhood (0, 1, 2, and 3+ members) and followed them up until the end of 2009. The Cox proportional hazards model was used to calculate the multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) of CHD mortality according to the number of smoking family members in childhood.
Results: During the median 18.9 years’ follow-up, 955 CHD deaths were reported. There was a dose–response relationship between the number of smoking family members at home and CHD mortality among middle-aged individuals (40–59 years); the multivariable HRs (95% CIs) were 1.08 (0.76–1.54) for 1, 1.35 (0.87–2.08) for 2, and 2.49 (1.24–5.00) for 3+ smoking family members compared with 0 members (p for trend=0.03). The association for 3+ smoking family members among the middle-aged group was more evident in men than in women (the multivariable HRs [95% CIs] were 2.97 [1.34–6.58] and 1.65 [0.36–7.52], respectively) and more evident in non-current smokers than in current smokers (the multivariable HRs [95% CIs] were 4.24 [1.57–11.45] and 1.93 [0.72–5.15], respectively).
Conclusions: Secondhand smoke exposure in childhood was associated with an increased risk of CHD mortality in adulthood, primarily in middle-aged men and non-current smokers.
See editorial vol. 30: 851-852
Although secondhand smoke exposure in childhood was recognized as harmful, approximately 40% of children were exposed to secondhand smoke worldwide1). Considering its harmful health effects, the reduction in children’s exposure to secondhand smoke has been identified as a global public health priority by the World Health Organization2).
Living in households with smokers poses the biggest risk for exposure to secondhand smoke in children3). Parental smoking, low socioeconomic status, low educational level, and less negative attitudes toward secondhand smoke have been associated with children’s secondhand smoke exposure at home4). In this respect, it is important to build scientific evidence on the adverse effect of familial smoking at home in childhood on the future risk of cardiovascular disease in adulthood.
Recent studies have shown that parental smoking in childhood is associated with higher high-sensitivity C-reactive protein level5), decreased brachial flow-mediated dilatation6), and carotid atherosclerosis in adulthood, such as the presence of carotid plaque7) and increased intima-media thickness of the carotid arteries8). However, little is known about whether secondhand smoke exposure in childhood affects the risk of cardiovascular disease. Therefore, this study aimed to examine the association between secondhand smoke exposure at home in childhood and the risk of mortality from coronary heart disease (CHD) in adulthood using data from a large long-term cohort study on Japanese men and women.
The Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC study) is a nationwide community-based prospective study that started between 1988 and 1990, enrolling 110,585 participants (46,395 men and 64,190 women) aged 40–79 years and living in 45 communities across Japan. The methodology of the study has been described elsewhere9).
Briefly, 110,585 participants were asked to complete self-administered questionnaires, including demographic characteristics, medical histories, and lifestyle. Before completing the questionnaire, the participants or community representatives provided informed consent to be involved in this epidemiological study, according to the guidelines of the Council for International Organizations of Medical Sciences. Informed consent was obtained from each participant in 36 of 45 study areas (written consent in 35 areas and oral consent in 1 area). In the remaining 9 areas, group consent was obtained from each area leader9). The JACC study protocol conformed to the Declaration of Helsinki and was approved by the ethics committees of Hokkaido University (reference number: 14-044), Nagoya University (reference numbers: 177 and 227), and Osaka University (reference number: 14285-8).
Secondhand Smoke Exposure in ChildhoodAt the baseline survey, we asked the participants “Did your family member smoke at home when you were an elementary or junior high school student?” with the following three possible responses: “yes,” “no,” or “cannot remember.” In Japan, an elementary or junior high school student is between 6 and 15 years of age. For those who responded yes, we further asked “Which of the family members smoked at home?” (“mother,” “father,” “brother or sister,” “grandfather or grandmother,” or “others”). According to their responses to these two questions, we calculated the number of smoking family members as 0, 1, 2, and 3+10).
Of 110,585 participants, we excluded 18,255 (8,248 men and 10,007 women) living in eight communities because the questions on secondhand smoke exposure during childhood were excluded in the questionnaire, and 17,003 participants (5,293 men and 11,710 women) because they answered “cannot remember” in the first question (1,140 men and 2,210 women) or they did not provide their history of secondhand smoke exposure in childhood or their own smoking status (4,153 men and 9,500 women). Furthermore, 3,868 participants (1,827 men and 2,041 women) were excluded because of a history of CHD, stroke, or cancer at the time of baseline inquiry. A total of 71,459 participants (31,027 men and 40,432 women) were included in the analysis.
Assessment of Confounding VariablesOther information on demographic and lifestyle factors was derived from a self-administered questionnaire at baseline as follows: age, sex, height, weight, past medical history (such as diabetes and hypertension), smoking and alcohol drinking status, exercise and walking habits, mental status, educational level, occupation, and eating habits. Body mass index (BMI) was calculated as body weight (kg) divided by the square of height (m2).
Mortality SurveillanceIn each community, a systematic review of death certificates, all of which were forwarded to the local public health center, was conducted. It is believed that all cohort deaths were recorded, except for those who died after moving from their original community, in which case the participants’ data were censored. The date of moving from the community was verified using population registration documents. Mortality data were sent centrally to the Ministry of Health and Welfare, and the underlying cause of death was coded for the National Vital Statistics System according to the International Classification of Diseases, 10th revision (ICD-10). The follow-up was terminated at the end of 1999 in four areas, at the end of 2003 in another four areas, at the end of 2008 in two areas, and at the end of 2009 in the remaining areas. The median follow-up period was 18.9 years. Cause-specific mortality was defined using ICD-10 codes. The endpoint of death in this study was CHD (I20–I25). If participants died after they had moved from their original community, they were treated as withdrawals from observation when they moved out.
Statistical AnalysisPerson-years of follow-up were calculated from the date of the baseline questionnaire to the date of death or emigration from the community or at the end of 2009 (or 1999, 2003, 2008), whichever occurred first. Sex-specific and age-adjusted mean values and prevalence of cardiovascular risk factors were presented among the categories of the number of smoking family members at home in childhood. Generalized linear models were used to perform trend tests across groups. The sex- and age-specific multivariable hazard ratios (HRs) with 95% confidence intervals (CIs) of CHD mortality according to the number of family members who smoked at home in childhood were calculated after adjustment for potential confounding factors using the Cox proportional hazards model. The potential confounding factors were age (continuous), sex (women or men), history of hypertension (yes or no), history of diabetes (yes or no), BMI (sex-specific quintile), smoking status (never, ex-smoker, or current smoker of 1–19 or current smoker of ≥ 20 cigarettes per day), secondhand smoke status in adulthood at home (never, sometimes, 1–4 days per week, or almost every day) and outside of the home (never, sometimes, 1–4 days per week, or almost every day), alcohol consumption (never drinker, ex-drinker, or current drinker of 0.1–45.9 or ≥ 46.0 g ethanol per day), hours of exercise (almost never, 1–4 h, or ≥ 5 h per week), hours of walking (almost never, 0.5 h, or ＞0.5 h per day), perceived mental stress (low, moderate, or high), educational level (≤ 18 or ≥ 19 years of age on completion of education), and employment status (unemployed or employed). SAS version 9.4 (SAS, Inc., Cary, NC, USA) was used in all statistical analyses.
Sex-specific and age-adjusted baseline characteristics of the participants according to the number of smoking family members in childhood are presented in Table 1. Compared with those who had no smoking family member in childhood, those who reported 3+ smoking family members had higher proportions of a history of hypertension, higher mental stress levels, and adult secondhand smoke exposure at home and outside of the home. They were also more likely to be current drinkers and smokers. The proportion of current smokers increased according to the number of smoking family members at home during childhood for both sexes. The proportions of current smokers in men were 49.8% for 0 members, 54.0% for 1 member, 56.5% for 2 members, and 60.1% for 3+ members. The proportions in women were 3.3%, 5.2%, 7.2%, and 11.2%, respectively.
| No. of smoking family members | |||||
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3+ | P for trend | |
| Men | |||||
| No. of participants | 7277 | 18244 | 4842 | 664 | |
| Age, y | 58.5 | 56.5 | 56.5 | 58.5 | 0.94 |
| Body mass index, kg/m2 | 22.7 | 22.6 | 22.6 | 22.6 | 0.33 |
| History of hypertension, % | 20.6 | 19.9 | 20.5 | 22.7 | 0.18 |
| History of diabetes mellitus, % | 6.4 | 6.5 | 6.9 | 6.0 | 0.74 |
| Current smoker, % | 49.8 | 54.0 | 56.5 | 60.1 | ＜0.001 |
| Secondhand smoke at home ≥ 1day/week, % | 35.6 | 47.1 | 52.1 | 62.1 | ＜0.001 |
| Secondhand smoke outside of home ≥ 1day/week, % | 39.7 | 42.8 | 45.1 | 55.0 | ＜0.001 |
| Current drinker, % | 71.8 | 73.4 | 73.7 | 75.6 | 0.04 |
| High mental stress, % | 22.2 | 22.8 | 26.0 | 25.1 | 0.03 |
| College or higher education, % | 17.8 | 17.9 | 17.8 | 16.5 | 0.44 |
| Unemployed, % | 15.8 | 16.2 | 17.3 | 12.9 | 0.08 |
| Walking ≥ 30min/day, % | 88.3 | 87.9 | 88.1 | 85.5 | 0.05 |
| Exercise ≥ 1h/week, % | 31.1 | 31.1 | 31.6 | 33.1 | 0.27 |
| Women | |||||
| No. of participants | 10628 | 22795 | 6113 | 896 | |
| Age, y | 57.7 | 56.4 | 56.3 | 57.9 | 0.50 |
| Body mass index, kg/m2 | 23.0 | 22.9 | 23.1 | 23.1 | 0.11 |
| History of hypertension, % | 20.9 | 21.5 | 22.7 | 23.6 | 0.03 |
| History of diabetes mellitus, % | 3.2 | 3.7 | 4.0 | 4.0 | 0.17 |
| Current smoker, % | 3.3 | 5.2 | 7.2 | 11.2 | ＜0.001 |
| Secondhand smoke at home ≥ 1day/week, % | 47.1 | 57.3 | 61.0 | 65.6 | ＜0.001 |
| Secondhand smoke outside of home ≥ 1day/week, % | 15.8 | 17.6 | 20.4 | 25.7 | ＜0.001 |
| Current drinker, % | 14.3 | 16.1 | 19.4 | 19.9 | ＜0.001 |
| High mental stress, % | 20.0 | 20.8 | 21.9 | 22.9 | 0.03 |
| College or higher education, % | 10.4 | 10.4 | 10.1 | 7.8 | 0.02 |
| Unemployed, % | 17.9 | 18.8 | 19.2 | 19.2 | 0.25 |
| Walking ≥ 30min/day, % | 89.2 | 88.6 | 90.2 | 87.2 | 0.23 |
| Exercise ≥ 1h/week, % | 23.5 | 23.4 | 23.6 | 20.4 | 0.05 |
Data are mean for continuous variables and percentages for categorical variables.
During the median follow-up of 18.9 years, a total of 955 (589 men and 366 women) deaths from CHD were documented. Table 2 shows the sex- and age-specific multivariable HRs of CHD mortality according to the number of smoking family members during childhood. The number of smoking family members at home was linearly and positively associated with the risk of CHD mortality in adulthood in middle-aged men but not in older men and women. Adjusting for age, sex, history of hypertension and diabetes, BMI, smoking status, secondhand smoke status in adulthood, alcohol consumption, hours of exercise and walking, perceived mental stress, educational level, and employment status, the multivariable HRs of CHD mortality were 1.08 (0.76–1.54) for 1 smoking family member in childhood, 1.35 (0.87–2.08) for 2 smoking family members, and 2.49 (1.24–5.00) for 3+ smoking family members compared with 0 smoking family members (p=0.03). Such an association was not observed among older individuals (60–79 years). The excess risk of mortality from CHD associated with 3+ smoking family members among the middle-aged group was more evident in men than in women; the multivariable HRs were 2.97 (1.34–6.58) and 1.65 (0.36–7.52), respectively.
| No. of smoking family members | P for trend | ||||
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3+ | ||
| Men | |||||
| Middle-aged (40-59 years) | |||||
| Person-years | 63895 | 190711 | 50841 | 5564 | |
| No. of cases | 29 | 94 | 36 | 8 | |
| Mortality rate (per 1000 person-years) | 0.5 | 0.5 | 0.7 | 1.4 | |
| Age-adjusted HR (95%CI) | Ref | 1.16 (0.76-1.76) | 1.63 (1.00-2.66) | 3.22 (1.47-7.04) | 0.004 |
| Multivariable HR (95%CI) | Ref | 1.14 (0.74-1.74) | 1.59 (0.96-2.62) | 2.97 (1.34-6.58) | 0.009 |
| Older persons (60-79 years) | |||||
| Person-years | 46914 | 100159 | 25905 | 4000 | |
| No. of cases | 113 | 249 | 49 | 11 | |
| Mortality rate (per 1000 person-years) | 2.4 | 2.5 | 1.9 | 2.8 | |
| Age-adjusted HR (95%CI) | Ref | 1.03 (0.82-1.28) | 0.76 (0.55-1.07) | 1.21 (0.65-2.25) | 0.38 |
| Multivariable HR (95%CI) | Ref | 1.03 (0.82-1.29) | 0.77 (0.54-1.08) | 1.12 (0.60-2.10) | 0.35 |
| Total (40-79 years) | |||||
| Person-years | 110809 | 290870 | 76746 | 9564 | |
| No. of cases | 142 | 343 | 85 | 19 | |
| Mortality rate (per 1000 person-years) | 1.3 | 1.2 | 1.1 | 2.0 | |
| Age-adjusted HR (95%CI) | Ref | 1.05 (0.86-1.28) | 0.97 (0.74-1.28) | 1.64 (1.01-2.64) | 0.46 |
| Multivariable HR (95%CI) | Ref | 1.05 (0.86-1.28) | 0.97 (0.74-1.28) | 1.50 (0.93-2.44) | 0.58 |
| Women | |||||
| Middle-aged (40-59 years) | |||||
| Person-years | 104066 | 245266 | 67244 | 8447 | |
| No. of cases | 14 | 33 | 7 | 2 | |
| Mortality rate (per 1000 person-years) | 0.1 | 0.1 | 0.1 | 0.2 | |
| Age-adjusted HR (95%CI) | Ref | 1.06 (0.57-1.98) | 0.80 (0.32-1.99) | 1.83 (0.42-8.07) | 1.00 |
| Multivariable HR (95%CI) | Ref | 1.03 (0.54-1.95) | 0.82 (0.33-2.07) | 1.65 (0.36-7.52) | 0.99 |
| Older persons (60-79 years) | |||||
| Person-years | 69271 | 132768 | 34082 | 5570 | |
| No. of cases | 94 | 162 | 44 | 10 | |
| Mortality rate (per 1000 person-years) | 1.4 | 1.2 | 1.3 | 1.8 | |
| Age-adjusted HR (95%CI) | Ref | 0.92 (0.71-1.18) | 0.92 (0.65-1.32) | 1.15 (0.60-2.21) | 0.81 |
| Multivariable HR (95%CI) | Ref | 0.86 (0.66-1.11) | 0.83 (0.58-1.20) | 1.04 (0.54-2.02) | 0.43 |
| Total (40-79 years) | |||||
| Person-years | 173337 | 378033 | 101325 | 14017 | |
| No. of cases | 108 | 195 | 51 | 12 | |
| Mortality rate (per 1000 person-years) | 0.6 | 0.5 | 0.5 | 0.9 | |
| Age-adjusted HR (95%CI) | Ref | 0.94 (0.74-1.19) | 0.91 (0.65-1.26) | 1.24 (0.68-2.25) | 0.85 |
| Multivariable HR (95%CI) | Ref | 0.88 (0.69-1.12) | 0.83 (0.59-1.16) | 1.14 (0.62-2.08) | 0.47 |
| Total | |||||
| Middle-aged (40-59 years) | |||||
| Person-years | 167961 | 435977 | 118085 | 14011 | |
| No. of cases | 43 | 127 | 43 | 10 | |
| Mortality rate (per 1000 person-years) | 0.3 | 0.3 | 0.4 | 0.7 | |
| Age-adjusted HR (95%CI) | Ref | 1.20 (0.85-1.70) | 1.48 (0.97-2.25) | 2.87 (1.44-5.70) | 0.007 |
| Multivariable HR (95%CI) | Ref | 1.08 (0.76-1.54) | 1.35 (0.87-2.08) | 2.49 (1.24-5.00) | 0.03 |
| Older persons (60-79 years) | |||||
| Person-years | 116185 | 232927 | 59987 | 9571 | |
| No. of cases | 207 | 411 | 93 | 21 | |
| Mortality rate (per 1000 person-years) | 1.8 | 1.8 | 1.6 | 2.2 | |
| Age-adjusted HR (95%CI) | Ref | 1.00 (0.85-1.18) | 0.85 (0.66-1.08) | 1.19 (0.76-1.86) | 0.51 |
| Multivariable HR (95%CI) | Ref | 0.95 (0.80-1.13) | 0.81 (0.63-1.04) | 1.13 (0.72-1.78) | 0.28 |
| Total (40-79 years) | |||||
| Person-years | 284146 | 668904 | 178072 | 23582 | |
| No. of cases | 250 | 538 | 136 | 31 | |
| Mortality rate (per 1000 person-years) | 0.9 | 0.8 | 0.8 | 1.3 | |
| Age-adjusted HR (95%CI) | Ref | 1.04 (0.89-1.20) | 0.98 (0.79-1.20) | 1.47 (1.01-2.14) | 0.47 |
| Multivariable HR (95%CI) | Ref | 0.98 (0.84-1.14) | 0.92 (0.74-1.14) | 1.38 (0.95-2.01) | 0.90 |
HR, hazard ratio; CI, confidence interval. Multivariable HR: adjusted for age, sex, history of hypertension, history of diabetes, body mass index, smoking status, secondhand smoke status in adulthood at home and outside of home, alcohol consumption, hours of exercise, hours of walking, perceived mental stress, educational level, and employment status.
Table 3 shows the multivariable HRs for mortality from CHD according to the number of smoking family members during childhood, stratified by current smoking status. The excess risk of CHD mortality associated with 3+ smoking family members among the middle-aged group was more evident in never smokers or ex-smokers than in current smokers; the multivariable HRs were 4.24 (1.57–11.45) and 1.93 (0.72–5.15), respectively. Such an association was not observed in older individuals.
| No. of smoking family members | P for trend | ||||
|---|---|---|---|---|---|
| 0 | 1 | 2 | 3+ | ||
| Middle-aged (40-59 years) | |||||
| Never or Ex-smoker (n = 30570) | |||||
| Person-years | 132340 | 314491 | 82357 | 9502 | |
| No. of cases | 21 | 53 | 11 | 5 | |
| Mortality rate (per 1000 person-years) | 0.2 | 0.2 | 0.1 | 0.5 | |
| Age-adjusted HR (95%CI) | Ref | 1.13 (0.68-1.88) | 0.88 (0.42-1.82) | 3.41 (1.29-9.05) | 0.37 |
| Multivariable HR (95%CI) | Ref | 1.12 (0.72-2.00) | 1.04 (0.50-2.17) | 4.24 (1.57-11.45) | 0.16 |
| Current smoker (n = 11519) | |||||
| Person-years | 35621 | 121486 | 35728 | 4509 | |
| No. of cases | 22 | 74 | 32 | 5 | |
| Mortality rate (per 1000 person-years) | 0.6 | 0.6 | 0.9 | 1.1 | |
| Age-adjusted HR (95%CI) | Ref | 1.03 (0.64-1.66) | 1.48 (0.86-2.55) | 1.82 (0.69-4.80) | 0.08 |
| Multivariable HR (95%CI) | Ref | 1.06 (0.65-1.72) | 1.56 (0.89-2.73) | 1.93 (0.72-5.15) | 0.06 |
| Older persons (60-79 years) | |||||
| Never or Ex-smoker (n = 22198) | |||||
| Person-years | 93423 | 177867 | 45129 | 6859 | |
| No. of cases | 150 | 259 | 63 | 14 | |
| Mortality rate (per 1000 person-years) | 1.6 | 1.5 | 1.4 | 2.0 | |
| Age-adjusted HR (95%CI) | Ref | 0.92 (0.75-1.13) | 0.85 (0.64-1.15) | 1.17 (0.68-2.02) | 0.46 |
| Multivariable HR (95%CI) | Ref | 0.90 (0.73-1.10) | 0.82 (0.61-1.11) | 1.29 (0.74-2.23) | 0.44 |
| Current smoker (n = 7172) | |||||
| Person-years | 22762 | 55060 | 14858 | 2712 | |
| No. of cases | 57 | 152 | 30 | 7 | |
| Mortality rate (per 1000 person-years) | 2.5 | 2.8 | 2.0 | 2.6 | |
| Age-adjusted HR (95%CI) | Ref | 1.05 (0.77-1.42) | 0.74 (0.47-1.15) | 1.02 (0.47-2.24) | 0.37 |
| Multivariable HR (95%CI) | Ref | 1.10 (0.81-1.52) | 0.79 (0.50-1.25) | 1.03 (0.46-2.29) | 0.52 |
HR, hazard ratio; CI, confidence interval. Multivariable HR: adjusted for age, sex, history of hypertension, history of diabetes, body mass index, smoking status, secondhand smoke status in adulthood at home and outside of home, alcohol consumption, hours of exercise, hours of walking, perceived mental stress, educational level, and employment status.
In this large prospective study of Japanese men and women aged 40–79 years with a median follow-up of 18.9 years, we found a dose–response relationship between the number of smoking family members in childhood and the risk of mortality from CHD in middle-aged individuals. Compared with 0 family members, 3+ smoking family members during childhood was associated with an approximately twofold increased risk of mortality from CHD in middle-aged individuals after adjustment for smoking status and other confounding factors. The excess CHD mortality in the middle-aged group was more evident in men and never smokers or ex-smokers.
To the best of our knowledge, this is the first study to report that secondhand smoke in childhood is positively associated with mortality from CHD in adulthood. Our findings are supported by previous epidemiological studies on coronary risk factors and atherosclerosis. The Cardiovascular Risk in the Young Finns Study showed that, after 25 years of follow-up from childhood, carotid intima-media thickness in adulthood was greater in those exposed to both parents smoking in childhood than in those whose parents did not smoke, independently of their own smoking status and other potential confounding factors7). Additionally, the study has shown that parental smoking in childhood is associated with higher high-sensitivity C-reactive protein level5), lower brachial flow-mediated dilatation6), and development of carotid plaque8) in ages of 30–40 years, all of which are well-established surrogate markers of atherosclerosis11-14).
The association between secondhand smoke exposure in childhood and the risk of CHD mortality was stronger in the middle-aged than in the older-aged groups (p for interaction =0.017). In general, the associations between established risk factors and the risk of cardiovascular disease (the relative risk) are stronger in younger than in older age groups, while the absolute risk of cardiovascular disease increases with age. The weaker association between risk factors and the risk of cardiovascular disease among older individuals may be attributable to its increased absolute risk in persons with low levels of exposure of interest because they have other risk factors associated with aging.
The potential mechanism can be impaired endothelial function caused by exposure to secondhand smoke during childhood, resulting in the development of atherosclerosis early in life. Although endothelial dysfunction related to secondhand smoke exposure can be resolved after cessation of exposure15), when exposure to secondhand smoke occurs repeatedly, endothelial dysfunction is unlikely to be resolved16) and chronic adverse effects may develop with aging. The underlying cellular mechanisms related to endothelial dysfunction can include oxidative stress from environmental tobacco smoke, including increased levels of glutathione peroxidase and catalase, which are known to reduce the production and activity of endothelial nitric oxide synthase17, 18). Moreover, secondhand smoke exposure in childhood can cause dyslipidemia and thrombosis and reduce insulin sensitivity, leading to cardiovascular consequences19).
The greatest strength of the present study is its prospective study design, which eliminates the possible recall bias in exposure assessment. However, it has several limitations. First, the recall for secondhand smoke exposure in childhood can be misclassified. However, in this study, the proportion of participants who reported one or more family members to have smoked at home in childhood was approximately 75%. This result was almost consistent with the Japanese smoking prevalence from the 1950s to the 1960s20). Additionally, a previous study examined the validity of offspring-reported parental smoking status during the offspring’s childhood21). The results showed that adults report their parent’s smoking status during their childhood quite accurately; the sensitivity for offspring’s correct report of parent’s smoking status during childhood (0–10 years) was 0.82 (95% CI, 0.81–0.84) and the specificity was 0.95 (95% CI, 0.95–0.96)21). Therefore, the effect of misclassification in the present study is likely to be limited. Second, we used the self-report of the number of smoking family members in childhood as a proxy of exposure to secondhand smoke in childhood; therefore, the duration and intensity of secondhand smoke in childhood were not measured. This could have resulted in nondifferential misclassification. Biomarkers such as plasma or urine cotinine concentrations would help assess the secondhand smoke exposure level more accurately22). Further study including information on such biomarkers is warranted to validate the association. Third, although our study was conducted nationwide and the smoking prevalence was relatively high during the participants’ childhood, the number of observed CHD cases was small among middle-aged women who had 3+ smoking family members during childhood. Caution should be taken when interpreting these results. Fourth, despite our efforts to adjust for potential confounding factors, we cannot rule out the effects of unmeasured factors or residual confounding, such as family member smoking toward intrauterine exposure, behavioral change over time, and quantity of individual and secondhand smoking. We also did not have baseline information on dyslipidemia or changes in lipid quality. Further studies adjusting for the change in lipid profiles over the life course are warranted.
Secondhand smoke exposure in childhood can be an independent risk factor for CHD regardless of adult smoking status and other conventional risk factors and lifestyle in adulthood. An intervention to achieve smoking cessation among parents for the sake of the children may be recommended, as previously reported23). The present study expands the evidence recommending that parents should quit smoking for not only their health but also their children’s lifelong benefit.
None.
This study was supported by the Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (MEXT) (MonbuKagaku-sho); Grants-in-Aid for Scientific Research on Priority Areas of Cancer; and Grants-in-Aid for Scientific Research on Priority Areas of Cancer Epidemiology from MEXT (Nos. 61010076, 62010074, 63010074, 1010068, 2151065, 3151064, 4151063, 5151069, 6279102, 11181101, 17015022, 18014011, 20014026, 20390156, 26293138) and JSPS KAKENHI No. 16H06277. This research was also supported by the Grant-in-Aid from the Ministry of Health, Labour and Welfare, Health and Labor Sciences research grants, Japan (Comprehensive Research on Cardiovascular Disease and Life-Style Related Diseases: H20–Junkankitou [Seishuu]–Ippan–013; H23–Junkankitou [Seishuu]–Ippan–005); an Intramural Research Fund (22-4-5) for Cardiovascular Diseases of National Cerebral and Cardiovascular Center; and Comprehensive Research on Cardiovascular Diseases and Life-Style Related Diseases (H26-Junkankitou [Seisaku]-Ippan-001) and H29–Junkankitou [Seishuu]–Ippan–003).
MT conceived the idea for the study. MT and HI analysed the data. MT wrote the first draft. HI, IM, KS and AT provided revisions to the first draft. All authors approved the final draft.
We thank all staff members involved in this study for their valuable help in conducting the baseline survey and follow-up.
