Elsevier

Chemosphere

Volume 82, Issue 3, January 2011, Pages 477-482
Chemosphere

Polycyclic aromatic hydrocarbons in cigarette sidestream smoke particulates from a Taiwanese brand and their carcinogenic relevance

https://doi.org/10.1016/j.chemosphere.2010.09.045Get rights and content

Abstract

Polycyclic aromatic hydrocarbons (PAHs) adsorbed on cigarette sidestream smoke particulates (CSSPs) have been regarded as important contributors to lung carcinogenesis in never smokers. However, limited information is available on PAH levels in cigarette sidestream smoke. Here we determine the concentrations of 22 PAHs, including 16 US EPA priority PAHs, in CSSPs generated from a high market-share domestic brand in Taiwan. Five of the 22 PAHs are undetectable. The remaining 17 PAHs constitute about 0.022% of the total mass of CSSPs. Near one fifth of the PAH mass come from IARC group 1 and group 2 carcinogens. Carcinogenic potency is equivalent to 144 ng benzo[a]pyrene per cigarette converted according to potency equivalency factors (PEFs). The CSSP condensate could activate AhR activity and induce AhR target gene expression. High concentrations of CSSPs also exhibited AhR-independent cytotoxicity. However, mixing the 17 PAHs as the composition in the CSSP condensate could not reconstitute either capacity. Since AhR activation and cytotoxicity are important mechanisms underlying carcinogenic potency, the results suggest that other component compounds play a more active role in carcinogenesis. The approach of individual PAH profiling plus PEF conversion commonly used in risk assessment is likely to underestimate the risk caused by environmental cigarette smoke exposure.

Introduction

Exposure to environmental cigarette smoke poses significant risks for cancers and a variety of respiratory and cardiovascular diseases (OEHHA, 2005). Passive smoking has been recognized as a major cause for female lung cancer in Taiwan, where less than 5% of women are smokers. Studies showed that spousal smoking increased lung cancer risk 2.1 times to nonsmoking women in Taiwan, much higher than a 20% excess risk observed in the Western countries (Lee et al., 2001, IARC, 2004). A number of polycyclic aromatic hydrocarbons (PAHs) found in cigarette smoke of US and European brands, such as benz[a]anthracene and benoz[a]pyrene, have been classified as carcinogens by the International Agency for Research on Cancer (IARC) (IARC, 1987, IARC, 2010). The US Environmental Protection Agency (EPA) has also designated 16 PAHs as priority environmental pollutants due to their toxicity and carcinogenic potential (USEPA, 2010). Although there are many uncertainties about the toxicity of PAHs in a mixture, the actual form present in the environment, the sum of the potency equivalencies of individual PAHs is commonly used to evaluate the carcinogenic risk of exposure.

Environmental cigarette smoke comprises mostly sidestream smoke emitted from smoldering cigarettes between puffs (85%) and to a lesser extent mainstream smoke exhaled by smokers (IARC, 2004). Most PAHs, particularly carcinogenic PAHs, are present in the particulate phase of cigarette smoke, and sidestream smoke contains 10-fold higher amounts of PAHs than mainstream smoke (Grimmer et al., 1987, Lodovici et al., 2004, Kalaitzoglou and Samara, 2006). Although cigarette sidestream smoke is a main source of PAHs in indoor ambient air (Sheldon et al., 1993, Georgiadis et al., 2001), little information is available on PAH levels in sidestream smoke generated from Taiwan domestic cigarettes. Therefore in this study, we prepared a condensate of cigarette sidestream smoke particulates (CSSPs) from a high market-share Taiwanese brand and examined the concentrations of 16 US EPA priority PAHs and 6 common PAHs in the CSSP condensate.

The carcinogenic potency of PAHs largely depends on their ability to activate aryl hydrocarbon receptor (AhR) as a ligand. Benzo[a]pyrene, a prototypical PAH, and PAHs adsorbed to urban airborne particulates induce tumors only in AhR-positive mice. Both lose carcinogenicity in AhR-deficient mice (Shimizu et al., 2000, Matsumoto et al., 2007). Ligand-activated AhR induces expression of cytochrome P450 enzymes, for example, CYP1A1. These CYP enzymes catalyze PAHs to form diol exposides, o-quinones, and electrophilic radicals, which in turn interact with DNA, RNA and proteins directly or indirectly through production of reactive oxygen species to cause genotoxicity and cytotoxicity. Genotoxicity is associated with mutagenesis, an important event for tumor initiation. Cytotoxicity triggers inflammatory responses that promote tumor progression (RamaKrishna et al., 1992, Casale et al., 1997, Bolton et al., 2000, Nebert and Dalton, 2006). Different from other investigations on the PAH content in cigarette smoke, we also determined the AhR activation capacity and cytotoxic effect of CSSPs and component PAHs to learn their carcinogenic potentials.

Section snippets

Preparation of cigarette sidestream smoke particulates (CSSPs)

Cigarette smoke was generated from a Taiwanese brand named Long Life Cigarette (white package) using a home-made smoking machine resembling that used by Pieraccini et al. (1992). Smoking was performed following a standard procedure agreed internationally by organizations such as the International Standards Organization and USA Federal Trade Commission (Peeler, 1996). Sidestream smoke particulates were captured onto glass fiber filters (47 mm in diameter, 1 μm pore size, Paul Life Sciences, East

Content of PAHs in the CSSP condensate

PAHs had been thought to be the major constituents responsible for AhR activation and related carcinogenesis of CSSPs. Hence, we examined the concentrations of 22 priority PAHs in the CSSP condensate by GC-MS analysis. Five PAHs, benzo[b]fluoranthene, perylene, dibenz[a,h]anthracene, coronene, and dibenzo[a,e]pyrene, were below detection limit. The levels of the other 17 PAHs ranged from 13 ng (naphthalene) to 1628 ng (phenanthrene) per cigarette (Table 1). The sum of the 17 PAHs was 5277 ng per

Discussion

PAHs are well-known environmental carcinogens. CSSPs are the major indoor PAH source (Grimmer et al., 1987, Sheldon et al., 1993, Kalaitzoglou and Samara, 2006). However, there are only limited data published on cigarette sidestream PAH levels. Our data demonstrate that the tar content of a cigarette is not a proper index for high-molecular-weight PAHs, which frequently possess a carcinogenic Bay region (Jerina et al., 1991). The PAH levels in cigarette sidestream smoke vary with tobacco

Acknowledgements

This work is funded by National Health Research Institutes (EO097-PP-04) and Department of Health (DOH97-TD-G-111-033). We thank Dr. Pei-Ni Chen and Ms. Chun-Ru Lin of National Health Research Institutes for technical assistance.

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    Present address: Department of Chemistry, Fu Jen Catholic University, Taipei 24205, Taiwan, ROC.

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