Passive smoking and urinary oxidative biomarkers: A pilot study of healthy travelers from Los Angeles to Beijing

Active smoking caused 6.4 million deaths worldwide in 2015 with cardiovascular diseases as the primary cause (GBD 2015 Tobacco Collaborators, 2017). Passive smoking, which refers to involuntary exposures to tobacco smoke that were either exhaled by smokers (secondhand smoke, SHS) or adhered to the surfaces of clothing, hair, furnishings, and dust (thirdhand smoke, THS) (Sleiman et al., 2010), is thought to induce cardiovascular effects nearly as large as active smoking (Barnoya and Glantz, 2005), and likely to impact adversely a greater portion of the population beyond smokers. It has been estimated that in 2004, more than 1/3 of global population was exposed to SHS at home or workplaces, which caused 603,000 deaths; 379,000 of which were due to ischemic heart disease (Öberg et al., 2011). Remarkably, substantial heterogeneity in SHS exposures across countries has been documented, with higher exposures in developing countries (Centers for Disease Control and Prevention (CDC), 2007; Öberg et al., 2011; Warren et al., 2011), likely due to higher smoking prevalence and the lack of regulatory policies (King et al., 2013; Thomas et al., 2008). It is less understood, however, whether this heterogeneity could lead to increased exposures to SHS, and subsequent adverse health effects among international travelers who usually spend short time at their destinations.

Previous studies have shown that even brief (minutes to hours) passive smoking could markedly perturb the cardiovascular system with increased oxidative stress as one of the underlying mechanisms (Barnoya and Glantz, 2005), which is largely attributed to its content of a large number of toxic redox active components. To date, at least 90 toxic components have been identified in SHS with biological half-lives ranging from milliseconds (free radicals) to years (cadmium) (Brewer et al., 2017; Talhout et al., 2011), some of which could react with gaseous pollutants, leading to the formation of even more toxic products in THS (Sleiman et al., 2010). Of note, polycyclic aromatic hydrocarbons (PAHs), a group of toxic byproducts of incomplete combustions, are of high abundance in tobacco smoke and thought to exert significant effects on the health of passive smokers. However, concrete evidence is lacking to what extent the adverse health effects of passive smoking could be attributable to PAHs exposure.

The United States (U.S.) and China are among the world's most populous countries, with marked differences in the exposure to tobacco smoke. The number of residences traveling between both countries increased rapidly in recent years, reaching 1.31 and 2.59 million in the U.S and China in 2015, respectively (Yearbook of Tourism Statistics, 2018). In our previous studies, we have identified a marked increase in personal exposures to PAHs among healthy young adults who traveled from Los Angeles to Beijing (Lin et al., 2016, 2019, 2021), a city with higher smoking prevalence, population density, and air pollution levels (Los Angeles County Department of Public Health, 2010; Zhang et al., 2016). Furthermore, we observed significant increases in the circulating levels of a panel of oxidative biomarkers, after the participants spent 6–8 weeks in Beijing, which reversed almost completely 4–7 weeks after the participants returned to Los Angeles, and were positively associated with urinary levels of PAHs metabolites (Lin et al., 2019; Lu et al., 2021). Importantly, typical oxidative stress markers have been associated with all major cardiovascular diseases (Daiber et al., 2021). However, our panel of lipid oxidation products in the blood failed to associate with urinary cotinine levels, suggesting that the observed effects were likely due to other sources of PAHs such as air pollution (Lin et al., 2019; Lu et al., 2021) or that other biomarkers would be required to reflect pro-oxidative effects potentially induced by SHS. Therefore, the health effect of increased passive smoking exposures during the travel remained largely unknown.

In the current study, we studied this group of travelers and focused on urinary oxidative biomarkers such as 8-isoprostane, malondialdehyde (MDA) and uric acid, which were measured in 190 urine samples, repeatedly collected from 26 healthy nonsmoking participants. This study aims to determine (i) whether changes in passive smoking exposures during the travel were associated with urinary biomarkers of oxidative stress; and (ii) to what extent the oxidative effect of passive smoking exposure was mediated by PAHs exposure.

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