Early-life exposure to secondhand smoke and polycyclic aromatic hydrocarbons: associations with epigenetic aging among children

No study has reported the relationship between secondhand smoke (SHS) exposure and hypertension in self-reported never-smokers verified by nicotine metabolite. The aim of this study is to determine the relationship between SHS exposure and hypertension in self-reported and cotinine-verified never-smokers. A total of 106,268 self-reported never-smokers, verified as nonsmokers by urinary cotinine, who participated in Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016 were included. Cotinine-verified nonsmokers were defined as individuals having urinary cotinine <50 ng/mL. SHS exposure was defined as current exposure to passive smoke indoors at home or the workplace. The multivariate regression model revealed that SHS exposure was associated with hypertension (odds ratio (OR) (95% confidence interval (CI)), 1.16 (1.08, 1.24)). Current SHS exposure that has been exposed to home SHS (1.22 (1.11, 1.33)) as well as current SHS exposure only at the workplace (1.15 (1.02, 1.29)) significantly increased the ORs for hypertension compared to no SHS exposure. There was no significant gender interaction for the relationships between SHS exposure and hypertension. This study showed that SHS exposure was significantly associated with hypertension in self-reported never-smokers verified as nonsmokers by urinary cotinine, suggesting necessity of health program and stricter smoking regulation to reduce the risk of hypertension.

Background No study has reported the relationship between secondhand smoke (SHS) exposure and new-onset hypertension (NOHT) in self-reported never-smokers verified by cotinine. Purpose This longitudinal study was conducted to evaluate whether the change of SHS exposure status at baseline and at follow-up affects NOHT in self-reported and cotinine-verified never-smokers. Methods Out of individuals enrolled in the Kangbuk Samsung Cohort study (KSCS) between 2012 and 2016, 65,169 self-reported and cotinine-verified never-smokers without hypertension at baseline visit (20,046 men; age 36±5.7 years) were included. The mean follow-up period in this study was 32 months (6–58 months). SHS exposure was defined as having experienced passive smoking indoors at home or the workplace. Individuals were divided into 4 groups on the basis of their SHS exposure status at baseline and at follow-up: no SHS exposure group (Group I) as individuals without SHS exposure both at baseline and at follow-up; new SHS exposure group (Group II) as those without SHS exposure at baseline and with SHS exposure at follow-up; ex-SHS exposure group (Group III) as those with SHS exposure at baseline and without SHS exposure at follow-up; continuous SHS exposure group (Group IV) as those with SHS exposure both at baseline and at follow-up. New-onset hypertension was defined as systolic blood pressure ≥140 mmHg or diastolic blood pressure ≥90 mmHg, or current use of antihypertensive medication(s) at follow-up. Results The incidence of NOHT in the overall population was 2.5%; the incidence in group I, II, III, and IV was 2.3%, 3.2%, 2.9%, and 3.1%, respectively (p&amp;lt;0.001). The results in a multivariate Cox-hazard model adjusted for the baseline variables including age, sex, body mass index, waist circumference, vigorous exercise, alcohol consumption and presence of diabetes showed that Group II and IV increased relative risks (RRs) for NOHT compared to Group I (RR[95% CI], 1.44 [1.17, 1.77] for Group II and 1.21 [1.01, 1.45] for Group IV) However, Group III did not increase the risk of NOHT (0.95 [0.83, 1.08]). In another model adjusted for the variables in the above model and creatinine, uric acid, total cholesterol, HDL cholesterol, LDL cholesterol, triglycerides and high-sensitivity C reactive protein showed that only Group II increased the risk for NOHT (1.43 [1.16, 1.77] in Group II, 0.94 [0.82, 1.07] in Group III, 1.18 [0.98, 1.41] in Group IV). Conclusions This study showed that the new and continuous SHS exposure, but not ex-SHS exposure, increased the risk for NOHT in self-reported never-smokers verified as nonsmokers by urinary cotinine. In particular, the relationship to increased risk for NOHT was more obvious in individuals with new SHS exposure than in those with continuous SHS exposure. These findings suggest that it is important to continuously minimize SHS exposure and prohibit smoking at home and at workplace to reduce the risk of developing hypertension. Funding Acknowledgement Type of funding source: None

IntroductionThe workplace remains a significant source of secondhand smoke (SHS) exposure. This pollutant is known to be associated with respiratory and cardiovascular problems, but its effects on specific pulmonary function...

Background No study has reported the relationship between secondhand smoke (SHS) exposure and metabolic syndrome (MetS) in self-reported never-smokers verified by nicotine metabolite. Purpose The aim of this study is to determine the relationship between SHS exposure and MetS in self-reported and cotinine-verified never-smokers. Methods A total of 118,609 self-reported and cotinine-verified never-smokers (38,385 men; age 34.8±7.1 years) who participated in Kangbuk Samsung Health Study (KSHS) and Kangbuk Samsung Cohort study (KSCS) between 2011 and 2016 were included. Cotinine-verified never-smoker was defined as individuals having urinary cotinine &lt;50 ng/mL. SHS exposure was defined as having experienced passive smoking indoors at home or the workplace. Results The prevalence of SHS exposure in the overall population was 22.6%, with rates of 27.4% for males and 20.3% for females (p&lt;0.001). The overall prevalence of MetS was 6.8%; the prevalence in males was higher than that in females (10.7% versus 4.9%, p&lt;0.001). In both males and females, the prevalence of MetS in group with SHS exposure was higher than that in group without SHS exposure (11.3% versus 10.4%, p=0.010 for males; 5.8% versus 4.6%, p&lt;0.001 for females). However, there was significant gender interaction for the relationships between SHS exposure and MetS (p for interaction=0.010). A multivariate regression model was adjusted for the baseline variables including age, body mass index, frequency of alcohol drinking and vigorous exercise, blood urea nitrogen, creatinine, uric acid, total cholesterol, LDL cholesterol, and hsCRP. The results showed that SHS exposure only in females was associated with MetS (odds ratio [95% confidence interval], 1.17 [1.06, 1.29] for females; 1.02 [0.94, 1.11] for males). In particular, females with SHS exposure of ≥1 hours/day, ≥3 times/week, and ≥10 years increased the prevalence of MetS compared to those without SHS exposure (1.21 [1.02, 1.45], 1.30 [1.14, 1.49], and 1.12 [0.99, 1.28], respectively. Conclusions This study showed that the SHS exposure in females was significantly associated with MetS in self-reported never-smokers with low urinary cotinine levels (&lt;50 ng/mL), suggesting that more active anti-smoking programs in the home and public are needed to reduce the risk of MetS.

Introduction: Due to the high prevalence of smoking in China, exposure to second hand smoke (SHS) is a serious public health issue. However, school-aged children’s behavioral responses to SHS exposure and the associated factors are unclear. Aims: This study aims to (a) identify the sources and settings of SHS exposure among school-aged sick children and their mothers in Guangzhou, China; (b) describe the behavioral responses of those children and mothers when exposed to SHS; and (c) examine the personal and environmental factors associated with children’s responses to SHS exposure. Methods: Qualitative and quantitative methods were combined in this study. Forty-five in-depth individual interviews were conducted to investigate sick school-aged children and their mothers’ understanding of and responses to SHS. A pilot survey was used to assess the validity and reliability of the questionnaire and the feasibility of the study. A cross-sectional survey was conducted with the children and their mothers at three hospitals in Guangzhou in 2012. All sick children who were aged 6 to 12 years, able to communicate in Mandarin Chinese, and not acutely or severely ill, along with their nonsmoking mothers, were invited to join this study. Results: A total of 339 pairs of sick children and their mothers were included in the data analysis. Of these pairs, 169 (49.9%) lived with smokers. All sick children and their mothers experienced high-level SHS and third hand smoke (THS) exposure inside or outside the home. Those living with nonsmokers were also at risk of household SHS and THS exposure from guests. Most of the sick school-aged children were unaware of the dangers of SHS and THS, while the mothers had a better understanding of SHS and THS. The majority of children would adopt self-protective behaviors when exposed to SHS. The regression model for children’s behavioral responses to SHS exposure by family smokers found two significant factors: amount of social support and family smoke-free policy. Five factors were associated with children’s behavioral responses to SHS exposure by guest smokers, including boys, living with smokers, amount of social support, family members informed of the dangers of smoking, and fathers protecting children from SHS. The amount of social support, and fathers protecting children from SHS were also associated with children’s behavioral responses to SHS exposure by stranger smokers. Conclusions: To our knowledge, this is the first study to describe self-protective behavioral responses to SHS exposure among sick school-aged children in mainland China and the personal and environmental factors associated with these responses. Boys, living with smokers, and a partial smoke-free policy at home were negatively related to children’s responses to SHS exposure; however, more information about smoking, fathers’ protection from SHS, and information about the harms of smoking by family members were associated with greater self-protection among sick school-aged children. Therefore, multiple-direction interventions should be considered for children’s health promotion about smoking and SHS.

Polycyclic aromatic hydrocarbons (PAHs), byproducts of incomplete combustion of organic compounds, have been linked to various adverse health outcomes; however, evidence associating PAHs with liver damage remains inconsistent. This study aimed to investigate the relationship between PAH exposure and liver enzyme levels among firefighters, who have an increased risk of PAH exposure. A total of 961 firefighters were included in the study. Urinary concentrations of 4 PAH metabolites (2-naphthol, 2-hydroxyfluorene, 1-hydroxyphenanthrene, and 1-hydroxypyrene) were measured and categorized into quartiles. Serum levels of liver enzymes, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were evaluated. Age, smoking status, alcohol consumption, body mass index (BMI), job position, and self-reported disease history were adjusted as covariates. Multivariable linear regression analyses were conducted to assess the association between PAH metabolites and serum AST and ALT levels. Logistic regression analyses evaluated associations between PAH metabolites and abnormal AST and ALT levels, defined as 40 IU/L or higher. Participants in the highest quartile of urinary 2-naphthol had an increased risk of abnormal ALT levels compared to those in the lowest quartile (odds ratio, 2.00; 95% confidence interval, 1.09-3.65). No significant associations were observed for the other PAH metabolites. The association between urinary 2-naphthol and abnormal ALT levels did not differ significantly by smoking status, alcohol consumption, or BMI. Elevated urinary 2-naphthol levels were associated with abnormal liver enzyme levels among firefighters, suggesting that monitoring and managing PAH exposure may help protect liver health in this occupational group.

7633 Background: The presence of EGFR mutations in NSCLC has strongly associated with never-smoking history. SHS exposure is associated with higher risk of lung cancer. We have conducted this study to evaluate the association between SHS exposure and likelihood of mutations in EGFR gene in NSCLC patients who had never smoked. Methods: SHS exposure information from a total of 93 never smokers (&lt;100 lifetime cigarettes) with newly diagnosed primary NSCLC was obtained using a standardized questionnaire. Patients were asked whether they were regularly exposed to SHS at home or work places, respectively. Nucleotide sequencing of the kinase domain of EGFR (exons 18 to 21) was performed using nested PCR amplification of individual exons. Results: Patient characteristics (n=93) included median age 57 years; female (n= 81); adenocarcinoma ± bronchoalveolar carcinoma (n= 82); EGFR mutation (1 mutation in exon 18 G719, 31 in-frame deletions in exon 19, 10 mutations in codon 858 in exon 21). Fifty-two (55.9%) of the patients reported having been exposed to SHS, including 46 (49.5%) exposed at home and 13 (14.0%) exposed at work. The incidence of EGFR mutations was not associated with female gender and adenocarcinoma histology. Patients with SHS exposure showed a trend towards lower incidence of EGFR mutations (36.5% vs. 56.1%, P= 0.060) and a significantly lower incidence of deletion mutations in exon 19 (57.9% vs. 87.0%, P= 0.033). When the incidence of EGFR mutations was compared, no difference between SHS exposure at home and work places was found. No significant differences were found for other clinicopathological factors according to SHS exposure. Conclusions: Our results indicate weak evidence of relationship between likelihood of mutation in EGFR gene and SHS exposure. The deletion mutations in exon 19 were significantly less common in patients with SHS exposure. No significant financial relationships to disclose.

Background No study has reported the relationship between secondhand smoke (SHS) exposure and diabetes mellitus in self-reported never-smokers verified by nicotine metabolite. Purpose The aim of this study is to determine the relationship between SHS exposure and diabetes mellitus in self-reported and cotinine-verified never-smokers. Methods A total of 131,724 self-reported and cotinine-verified never-smokers (42,681 men; age 35.0±7.1 years) enrolled in Kangbuk Samsung Health Study (KSHS) and Kangbuk Samsung Cohort study (KSCS) between 2011 and 2016 were included. Cotinine-verified never-smoker was defined as individuals having urinary cotinine &lt;50 ng/mL. SHS exposure was defined as having experienced passive smoking indoors at home or the workplace. Diabetes mellitus was defined as having a fasting blood glucose level of ≥7.0mmol/L, hemoglobin A1C ≥6.5% or taking anti-diabetic medication(s). Results The frequency of diabetes mellitus in the overall population was 1.6%; the frequency in males was higher than that in females (2.2% versus 1.3%, p&lt;0.001). The overall frequency of SHS exposure was 22.9%, with rates of 27.6% for males and 20.7% for females (p&lt;0.001). The frequency of diabetes mellitus in group with SHS exposure was higher than that in group without SHS exposure only in females (1.8% versus 1.2%, p&lt;0.001 for females; 2.2% versus 2.2%, p=0.956 for males). There was significant gender interaction for the relationships between SHS exposure and diabetes mellitus (p for interaction &lt;0.001). A multivariate regression model was adjusted for the baseline variables including age, waist circumference, body mass index, frequency of alcohol drinking and vigorous exercise, systolic blood pressure, blood urea nitrogen, creatinine, uric acid, total cholesterol, HDL cholesterol, LDL cholesterol, triglyceride, and hsCRP. Only in females, SHS exposure was significantly associated with diabetes mellitus (odds ratio [95% confidence interval], 1.40 [1.20, 1.65] for females; 1.00 [0.85, 1.19] for males). Higher frequency and longer duration of SHS exposure were also significantly associated with diabetes mellitus (p&lt;0.001) for all trends). In particular, females with SHS exposure of ≥1 hours/day, ≥3 times/week, and ≥10 years increased the risk of diabetes mellitus 51–64% above that for those without SHS exposure (1.64 [1.25, 2.13], 1.51 [1.21, 1.87], and 1.59 [1.30, 1.95], respectively. Conclusions This study showed that the SHS exposure in females was significantly associated with diabetes mellitus in self-reported never-smokers verified by urinary cotinine and this association was proportional to the frequency and duration of SHS exposure. These findings suggest the importance of banning smoking in the home and public to reduce the risk of diabetes mellitus. Acknowledgement/Funding None

A history of second hand smoke exposure: are we asking the right questions?

Passive smoking exposure is a topic of great concern for public health because of its well-known adverse effects on human health (International Agency for Research on Cancer 2004). Two news articles on this topic were published in the February 2011 issue of Environmental Health Perspectives (Burton 2011; Lubick 2011). Lubick (2011) discussed the global health burden of secondhand smoke, and Burton (2011) emphasized a new and alarming consequence of smoking in indoor environments—“thirdhand smoke”—a term first coined in 2006 (Szabo 2006). Secondhand smoke is defined as “the combination of smoke emitted from the burning end of a cigarette or other tobacco products and smoke exhaled by the smoker” (World Health Organization 2007). Thus, secondhand smoke exposure consists of an unintentional inhalation of smoke that occurs close to people smoking and/or in indoor environments where tobacco was recently used. Thirdhand smoke is a complex phenomenon resulting from residual tobacco smoke pollutants that adhere to the clothing and hair of smokers and to surfaces, furnishings, and dust in indoor environments. These pollutants persist long after the clearing of secondhand smoke. They are reemitted into the gas phase or react with oxidants or other compounds present in the environment to form secondary contaminants, some of which are carcinogenic or otherwise toxic for human health (Matt et al. 2011). Thus, thirdhand smoke exposure consists of unintentional intake (mainly through inhalation but also via ingestion and dermal routes) of tobacco smoke and other related chemicals that occurs in the absence of concurrent smoking. Exposure can even take place long after smoking has ceased, through close contact with smokers and in indoor environments in which tobacco is regularly smoked. Lubick (2011) considers secondhand smoke synonymous with passive smoking, as do the majority of the authors publishing on this topic. However, in light of new evidence about thirdhand smoke (Matt et al. 2011), it is no longer appropriate to use the term “secondhand smoke” as a synonym for passive smoking or environmental tobacco smoke, because it represents a pars pro toto. In other words, using the term “secondhand smoke” mistakes one part of the problem for the whole. Instead, we propose that “passive smoking” or “environmental tobacco smoke” be used as a more inclusive term to describe any tobacco smoke exposure outside of active smoking. This question of terminology is of particular concern for researchers evaluating passive smoking exposure in indoor settings, especially in domestic environments. Since numerous countries have introduced smoking bans in enclosed public places, domestic environments have become the main sources of passive smoking exposure (World Health Organization 2007). We believe researchers should determine the independent contributions of secondhand and thirdhand smoke when they assess the magnitude of pollutant intake due to passive smoking exposure.

Environmental polycyclic aromatic hydrocarbon exposure in relation to metabolic syndrome in US adults

Background:Exposure to secondhand smoke (SHS) is a risk factor for developing sporadic forms of sporadic dementia. A human tau (htau) mouse model is available that exhibits age-dependent tau dysregulation, neurofibrillary tangles, neuronal loss, neuroinflammation, and oxidative stress starting at an early age (3–4 months) and in which tau dysregulation and neuronal loss correlate with synaptic dysfunction and cognitive decline.Objective:The goal of this study was to assess the effects of chronic SHS exposure (10 months’ exposure to ) on behavioral and cognitive function, metabolism, and neuropathology in mice.Methods:Wild-type (WT) and htau female and male mice were exposed to SHS (90% side stream, 10% main stream) using the SCIREQ® inExpose™ system or air control for 168 min per day, for 312 d, 7 d per week. The exposures continued during the days of behavioral and cognitive testing. In addition to behavioral and cognitive performance and neuropathology, the lungs of mice were examined for pathology and alterations in gene expression.Results:Mice exposed to chronic SHS exposure showed the following genotype-dependent responses: a) lower body weights in WT, but not htau, mice; b) less spontaneous alternation in WT, but not htau, mice in the Y maze; c) faster swim speeds of WT, but not htau, mice in the water maze; d) lower activity levels of WT and htau mice in the open field; e) lower expression of brain PHF1, TTCM1, , and HSP90 protein levels in WT male, but not female, mice; and f) more profound effects on hippocampal metabolic pathways in WT male than female mice and more profound effects in WT than htau mice.Discussion:The brain of WT mice, in particular WT male mice, might be especially susceptible to the effects of chronic SHS exposure. In WT males, independent pathways involving ascorbate, flavin adenine dinucleotide, or palmitoleic acid might contribute to the hippocampal injury following chronic SHS exposure. https://doi.org/10.1289/EHP8428

Background: Polycyclic aromatic hydrocarbons (PAHs) are a group of environmental chemicals with aromatic rings and are generated by the incomplete combustion of organic materials. A few animal and occupational studies suggested a possible association between PAHs exposure and increased risk of diabetes mellitus. Objectives: We aimed to investigate the associations of urine levels of PAHs with diabetes mellitus in Korean adults. Methods: We examined cross-sectional data from the Korean National Environmental Health Survey (KoNEHS) 2012-2014. The study population consisted of 6478 adult subjects (≥20 years of age) from 400 sampling districts in South Korea. The urinary levels of 1-hydroxypyrene, 2-naphthol, 1-hydroxyphenathrene, and 2-hydroxyfluorene were measured in the study subjects. Analyses were adjusted for gender, age, BMI, household income, alcohol consumption, physical activity, urinary creatinine, and urinary cotinine. Results: We observed a positive association between urinary PAHs and cotinine after adjusting for all covariates. A higher geometric mean value of urinary 2-naphthol was observed in subjects with diabetes mellitus compared with controls (2.67 vs. 2.24 μg/L). There was no significant difference in other urinary PAHs according to the presence of diabetes mellitus. According to the elevation of urinary 2-naphthol quartile, the multivariate-adjusted odds ratio (OR) of diabetes mellitus significantly increased in both male and female adults (P-for-trend &amp;lt;0.05). Compared with subjects with urinary 2-naphthol in the lowest quartile, the OR (95% confidence interval) of diabetes mellitus in those in the highest quartile was 1.8 (1.24-2.63). Conclusions: Urinary 2-naphthol levels were positively associated with diabetes mellitus in Korean general populations. Prospective studies are needed to determine a potential causal relationship between PAHs exposure and diabetes mellitus in human. Disclosure Y. Nam: None. S. Kim: None.

Using caregiver report and urinary cotinine measures, we defined the prevalence of secondhand smoke (SHS) exposure among young, hospitalized children and compared exposure among those hospitalized with pneumonia versus those with acute, nonrespiratory illnesses. Children aged <6 years hospitalized with pneumonia or acute, nonrespiratory illnesses were enrolled on admission, and urinary cotinine, a nicotine biomarker, was measured. Caregivers were also queried on home SHS exposure. We modeled associations between sociodemographic characteristics and exposure intensity on the basis of cotinine level (none, light, and heavy) using multivariable proportional odds regression. We also examined associations between SHS exposure intensity and diagnosis (pneumonia versus nonrespiratory illness). For this analysis, diagnosis was the outcome of interest, and urinary cotinine was the primary exposure variable. Overall, 36% of the 239 enrolled children had reported home SHS exposure, although 77% had detectable levels of urinary cotinine, including 59% with heavy exposure. The highest urinary cotinine level was among children exposed to indoor smoking (7.78 ng/mL, interquartile range 2.93-18.65; P < .001). Increased SHS exposure was associated with non-Hispanic ethnicity, lower household educational attainment, and public insurance. There were no differences in SHS exposure by diagnosis. Among hospitalized young children, reported home SHS exposure was common but substantially underestimated when compared with urinary cotinine levels. The highest urinary cotinine levels were among children exposed to indoor smoking. Future public health interventions, as well as more robust SHS exposure screenings on hospital admission, are needed to reduce the prevalence of SHS exposure among young children.

Factors associated with second-hand smoke exposure in non-smoking pregnant women in Spain: Self-reported exposure and urinary cotinine levels