The exposure level of environmental harmful substances related to the secondhand smoke in Korean non-smoker adults: data from the second Korean National Environmental Health Survey (KoNEHS 2012–2014): a cross-sectional study

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Ann Occup Environ Med. 2019;31.e30

Publication date (electronic) : 2019 October 15

doi : https://doi.org/10.35371/aoem.2019.31.e30

Sang Woo Kim, Sung Won Jung, Jae-Gwang Lee, Jae Han Joo, June-Hee Lee, Kyung-Jae Lee

Department of Occupational and Environmental Medicine, Soonchunhyang University Hospital, Seoul, Korea.

Correspondence: Kyung-Jae Lee. Department of Occupational and Environmental Medicine, Soonchunhyang University Hospital, 59 Daesagwan-ro, Yongsan-gu, Seoul 04401, Korea. leekj@schmc.ac.kr

Received 2019 April 08; Accepted 2019 September 23.

Abstract

BACKGROUND

Worldwide, 33% of male non-smokers and 35% of female non-smokers are exposed to secondhand smoke (SHS). SHS is associated with death from ischemic heart disease, lower respiratory tract infection, asthma, and lung cancer [1]. Annually, about 600,000 deaths are related to SHS and 10.9 million disability-adjusted life-years (DALYs) are lost, which is about 1.0% of the worldwide mortality and 0.7% of the total worldwide burden of diseases in DALYs [1]. In Korea, about 36% of non-smokers and 50% of current smokers are exposed to SHS. Men tend to be exposed mainly in the workplace and women mainly in the home by family members [2].

Tobacco contains more than 4,000 chemical compounds, most of which are harmful to humans [3]. Tobacco smoke consists of mainstream and sidestream smoke. Mainstream smoke refers to the smoke that emerges from the mouth during puffing, while sidestream smoke is the smoke emerging from the end of the burning cigarette. About 85% of SHS is sidestream smoke [4]. Sidestream smoke occurs at a lower combustion temperature and its particulate size is smaller than that of mainstream smoke [5]. Thus, particles from sidestream smoke can reach deeper portions of the lung than those of mainstream smoke [5]. Sidestream smoke was about four times more toxic than the same amount of mainstream smoke when inhaled and about 2–6 times more carcinogenic in skin tests [4].

Since the 1920s, the health effects of SHS have been widely known and a number of studies have been performed. But, compared to health effects associated with SHS, with a great deal of accumulated research, a little research has been performed regarding the relationship between SHS and exposure to chemical substances. Also, most of the studies for SHS and harmful substances were about measurement of indoor air quality. The health effects of SHS closely related to harmful substances contained in tobacco; therefore, to precisely understand the health effects of SHS, it is necessary to identify the level of chemical substances in the bodies of individuals who are exposed to SHS. So, this study analyzed the relationship between SHS and biomonitoring results of harmful substances and assessed the relationship according to sex.

METHODS

RESULTS

Table 1 shows the demographic characteristics and prevalence of SHS of the study participants. There were significant differences in terms of age, education level, marital status, drinking status, and exercise between exposed and non-exposed groups. In the exposed group, the proportion of subjects in their 20s, 30s, and 40s were relatively high among all age groups; thus, the average age was lower in the exposed group. A greater percentage of people in the exposed group were college and high school graduates and more people in the exposed group were single. The exposed group tended to drink more alcohol and exercise more than the non-exposed group, indicating that lifestyles related to drinking and exercise were not good in the exposure group. There were no significant differences in residential area, BMI, and economic level between the 2 groups. The prevalence of SHS was higher in male (30.6%) than female (18.3%). In male, prevalence of SHS was high in 20s and 30s. In female, greater percentage of people in 40s and 50s was exposed to SHS. According to marital status, the proportion of people who were exposed to SHS was higher in single people than married. Also, SHS was associated with lifestyle such as drinking and exercise. The prevalence of SHS was higher in people who do not exercise and drink more alcohol.

Table 1

General characteristics of the study subjects associated with SHS and prevalence of SHS according to sex (n = 3,533)

Table 2 shows the proportion exceeding 95 percentile of the concentration of harmful substances according to SHS and sex. The proportion exposed to high levels of blood mercury was higher in total and female exposure groups than in the non-exposed groups. Among the VOC metabolites, proportion exposed to high levels of the methylhippuric acid was significantly higher in the total and female exposure group. The proportion exposed to high levels of cotinine, an environmental tobacco smoke (ETS) metabolite, was significantly higher in the exposure groups of both sexes. The proportion exposed to high levels of of 2-hydroxyfluorene, a metabolite of fluorene, was high in exposure group but bisphenol A and triclosan, which are environmental phenols showed not significantly differences by sex.

Table 2

Proportion of exceeding 95 percentile of environmental harmful substances according to SHS exposure

In Table 3, the adjusted ORs of exposure to high levels of hazardous substances were calculated according to SHS exposure in model 1 and 2. We used 95% reference value as a cutoff point for exposure to high level. In model 1, for the male exposure group, the adjusted OR of exposure to high blood mercury and cotinine levels was 2.35 (95% confidence interval [CI]: 1.00–5.52) and 2.17 (95% CI: 1.01–4.68). For the female exposure group, the ORs of exposure to high levels of blood mercury, methylhippuric acid and hydroxyfluorene were 2.12 (95% CI: 1.42–3.16), 1.56 (95% CI: 1.04–2.33) and 1.76 (95% CI: 1.18–2.61), respectively. In model 2, adjusting cotinine levels as covariate, the adjusted ORs of exposure to high blood mercury levels was 2.43 (95% CI: 1.03–5.75) for men. For women, the adjusted ORs of exposure to high levels of blood mercury, methylhippuric acid and hydroxyfluorene were 2.06 (95% CI: 1.37–3.09), 1.24 (95% CI: 0.81–1.91) and 1.24 (95% CI 0.79–1.96), respectively.

Table 3

Adjusted ORs exceeding 95 percentile of harmful substances were calculated for SHS exposure group compared to control group

DISCUSSION

This study compared the concentrations of harmful substances in the body according to exposure to SHS and sex. About 18.3% of female non-smokers and 30.6% of male smokers reported exposure to SHS.

The proportion that exposed to high levels of cotinine was higher in the exposed group than that in the non-exposed group. Cotinine is a metabolite of nicotine, a biomarker with high sensitivity and specificity for exposure to tobacco and SHS[11]. Cotinine concentration in body fluids was related to the frequency of self-reported exposure to SHS and cotinine concentration tended to increase with more smokers in the home [1213]. In this study, similar to previous studies, self-reported exposure to SHS was associated with the proportion exposed to high levels of cotinine. Cotinine concentration represents the quantitative exposure to SHS during a short period of time [14]; thus, this result means that self-reported questionnaire about SHS is significantly associated with actual exposure.

The proportion exposed to high levels of blood mercury was greater in both total and female exposed group, but adjusted ORs were consistently significantly in model 2. Since cotinine concentration is an objective indicator of SHS, it can be assumed that there might be other factor if the OR is consistently significant after adjusting. There are controversial studies on the relationship between tobacco smoke and mercury exposure. Mortada et al. [15] reported no significant differences in blood, urine, and hair mercury concentrations between smokers and non-smokers. Richter et al. [16] showed that urine mercury levels in smokers were statistically lower than those in non-smokers, suggesting that smoking is not a major cause of mercury exposure. In contrast, a study on the relationship between mercury concentration in hair and blood pressure in smokers showed that smokers have a significantly higher hair mercury concentration than non-smokers [17]. Ho et al. [18] also showed that smokers had significantly higher blood levels of mercury than non-smokers. One cigarette contains 2.95–10.2 ng of mercury and most of the mercury contained in tobacco is released in smoke [19]. While it is clear that SHS exposure can result in exposure to the vapor form of mercury, few studies have assessed this relationship. In this study, the proportion exposed to high levels of mercury was higher in the total and female exposed group, but adjusted ORs in Table 3 showed similarly significant results in model 2. It means that although major factors like fish consumption was adjusted in our study, there can be still other covariate factors that affect the concentrations of mercury like occupational and environmental exposure, etc.

Muconic acid is a metabolite of benzene and trans-trans muconic acid in the urine is used as a biomarker for benzene exposure [20]. Benzene is a leukemogen, and tobacco smoke is one of the major exposure sources of benzene [212223]. The body burden of benzene in smokers is 6–10 times greater than that of nonsmokers and about 50% of benzene exposure in the United States is due to tobacco smoke [24]. The relationship between benzene and SHS has also been evaluated by a number of studies, most of which used indoor air measurements. Wallace et al. [21] reported that the concentration of benzene in homes with smokers was high, especially in autumn and winter months, and that the concentration of benzene in the breath increased when subjects were exposed to SHS during more than 50% of their office time [22]. In this study, the proportion exposed to high levels of muconic acid and adjusted OR did not show statistically significant results. Few studies have been conducted about the relationship between benzene and SHS, especially for biomonitoring results. Since the effects of SHS is much weaker than active smoke and the exposure assessment in this study was done by self-reported questionnaire, further study should be conducted for the people who exposed to SHS heavily and frequently.

The proportion that exposed to high levels of methylhippuric acid, a metabolite of xylene, showed significant differences between exposure and control groups in Table 2. Table 3 showed high OR in female exposure group in model 1, and after adjusting cotinine level, adjusted OR did not show statistically significant result. Xylene is also known to be associated with tobacco in previous studies [8]. In our study, both model 1 and model 2 showed similar tendency, xylene is likely to be associated with SHS exposure.

The metabolites of PAHs were measured for 1-hydroxypyrene, 2-hydroxyfluorene, 1-hydroxyphenanthrene, and 2-naphthol. Fluorene is relatively selective material in tobacco smoke compared to other PAHs [25]. Urine 2-hydroxyfluorene is a metabolite of fluorene, which is associated with exposure to the vapor form of cigarette smoke [26]. The concentrations of 2-hydroxyfluorene tend to be high in smokers [27]. In this study, the proportion exposed to high levels of the urinary fluorene was high in the total and female exposure group. Table 3 showed high ORs in model 1, but not in model 2. Hydroxyfluorene is known to be highly correlated with nicotine intake [25]; therefore, this could be associated with the higher ORs in our study's result.

On the other hand, the metabolites of PAHs, naphthol and hydroxyphenanthrene and urinary cadmium showed lower ORs in exposure group for male subjects, which did not show statistically significant result for total and female subjects. Compared to female, SHS in males is closely related to occupational factors [2]. Especially, since the PAHs are substance that occurs in the process of incomplete combustion, it is possible that this result comes from occupational differences between the exposure and control groups. Further studies are suggested to consider these occupational factors to obtain more accurate results in the male subjects.

The limitations of this study are as follows. First, it is difficult to objectively evaluate the amount of exposure based on responses to a questionnaire. SHS can be influenced by many factors, including the time and frequency of exposure, ventilation status, etc. Therefore, a more detailed questionnaire is needed, including the exposure time, route, and smoking history of family members, for accurate assessment. In addition, indicators or biomarkers need to be developed to objectively evaluate the exposure level to SHS. Finally, the second KoNEHS used in this research is a cross-sectional study; thus, it is difficult to determine time-based causality.

Despite these limitations, the strengths of this study are as follows: the KoNEHS is a national survey of large-scaled populations and provides useful data to assess the level of human exposure to various environmental harmful factors related to personal lifestyle. There are few Korean studies on the relationship between SHS and environmental harmful substances; thus, one strength is our comparison of exposure to environmental harmful substances in a large-scale population according to SHS and sex.

The health effects caused by SHS are clearly related to internal exposure of these harmful substances. Biological monitoring is an important tool for assessing the level of internal exposure to harmful substances taken up from environmental exposures. Therefore, to understand the health effects of SHS precisely, it is necessary to analysis the relationship between SHS and biological monitoring results of harmful substances. Future studies are needed to more accurately analyze factors such as exposure frequency, time, and pathway of SHS.

CONCLUSIONS

This study compared the proportion that exposure high levels of 16 substances related to tobacco according to SHS. In women, SHS was associated with methylhippuric acid, fluorene, and cotinine, while in men, it was associated with cotinine. After adjusting covariant factors, ORs of blood mercury, methylhippuric acid and hydroxyfluorene was greater than that in the non-exposed group. Especially, methylhippuric acid and hydroxyfluorene showed consistent result in female subjects, which means that these materials are likely to be associated with SHS. These results indicate that some of the harmful substances related to tobacco smoke are also present in SHS. The health effects caused by SHS are clearly related to these harmful substances. Future studies are necessary to more accurately analyze factors such as exposure frequency, time, and pathway of SHS.

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