Abstract
Smoking is the leading preventable disease worldwide and passive smoking is estimated to be the cause of about 1.0% of worldwide mortality. The determination of tobacco smoke biomarkers in human biological matrices is key to assess the health effects related to the exposure to environmental tobacco smoke. The biomonitoring of cotinine, the main nicotine metabolite, in human biofluids—including urine, serum or saliva—has been extensively used to assess this exposure. However, the simultaneous determination of cotinine together with other tobacco biomarkers and the selection of alternative biological matrices, such as hair, skin or exhaled breath, would enable a better characterization of the kind and extent of tobacco exposure. This review aims to perform a critical analysis of the up-to-date literature focused on the simultaneous determination of multiple tobacco smoke biomarkers studied in different biological matrices, due to the exposure to secondhand smoke (SHS) and thirdhand smoke (THS). Target biomarkers included both tobacco-specific biomarkers—nicotine and tobacco specific nitrosamine biomarkers—and tobacco-related biomarkers, such as those from polycyclic aromatic hydrocarbons, volatile organic compounds, metals and carbon monoxide. To conclude, we discuss the suitability of determining multiple biomarkers through several relevant examples of SHS and THS exposure.
Highlights
Passive smoking is estimated to be the cause of about 1.0% of worldwide mortality, responsible for approximately 603,000 deaths each year among children and adults, a number which has been increasing over the years [1]
Matsumoto et al studied the total nicotine and cotinine urinary concentrations of 117 Japanese nonsmokers, concluding that 54% of these nonsmokers presented higher nicotine concentrations than those found for cotinine [45] and, the simultaneous determination of both biomarkers provided a better characterization of secondhand smoke (SHS) exposure for that population group
As tobacco-specific nitrosamines (TSNAs) are formed while SHS ages, urinary NNAL/cotinine ratio is 10 times higher in SHS exposure compared to active smoking, without gender, race/ethnicity or age differences [50], and it is estimated to be even higher in young children exposed to thirdhand smoke (THS)
Summary
Passive smoking is estimated to be the cause of about 1.0% of worldwide mortality, responsible for approximately 603,000 deaths each year among children and adults, a number which has been increasing over the years [1]. Environmental tobacco smoke (ETS), most commonly called secondhand smoke (SHS), is a complex and reactive mixture made up of the mainstream smoke exhaled by the smokers and sidestream smoke emitted from the burning tobacco diluted with ambient air. This mixture contains over 4700 chemicals including hazardous amines, carbonyls, hydrocarbons or metals among others [2–4]. SHS exposure can cause several illnesses in nonsmokers including ischaemic heart diseases in adults and lower respiratory infections and asthma in adults and children, among other adverse health effects [1]. Public Health 2018, 15, 2693; doi:10.3390/ijerph15122693 www.mdpi.com/journal/ijerph
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