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      Thirdhand Tobacco Smoke: Emerging Evidence and Arguments for a Multidisciplinary Research Agenda

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          Abstract

          Background: There is broad consensus regarding the health impact of tobacco use and secondhand smoke exposure, yet considerable ambiguity exists about the nature and consequences of thirdhand smoke (THS).

          Objectives: We introduce definitions of THS and THS exposure and review recent findings about constituents, indoor sorption–desorption dynamics, and transformations of THS; distribution and persistence of THS in residential settings; implications for pathways of exposure; potential clinical significance and health effects; and behavioral and policy issues that affect and are affected by THS.

          Discussion: Physical and chemical transformations of tobacco smoke pollutants take place over time scales ranging from seconds to months and include the creation of secondary pollutants that in some cases are more toxic (e.g., tobacco-specific nitrosamines). THS persists in real-world residential settings in the air, dust, and surfaces and is associated with elevated levels of nicotine on hands and cotinine in urine of nonsmokers residing in homes previously occupied by smokers. Much still needs to be learned about the chemistry, exposure, toxicology, health risks, and policy implications of THS.

          Conclusion: The existing evidence on THS provides strong support for pursuing a programmatic research agenda to close gaps in our current understanding of the chemistry, exposure, toxicology, and health effects of THS, as well as its behavioral, economic, and sociocultural considerations and consequences. Such a research agenda is necessary to illuminate the role of THS in existing and future tobacco control efforts to decrease smoking initiation and smoking levels, to increase cessation attempts and sustained cessation, and to reduce the cumulative effects of tobacco use on morbidity and mortality.

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          Most cited references75

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          Tobacco carcinogens, their biomarkers and tobacco-induced cancer.

          The devastating link between tobacco products and human cancers results from a powerful alliance of two factors - nicotine and carcinogens. Without either one of these, tobacco would be just another commodity, instead of being the single greatest cause of death due to preventable cancer. Nicotine is addictive and toxic, but it is not carcinogenic. This addiction, however, causes people to use tobacco products continually, and these products contain many carcinogens. What are the mechanisms by which this deadly combination leads to 30% of cancer-related deaths in developed countries, and how can carcinogen biomarkers help to reveal these mechanisms?
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            Tobacco smoke and involuntary smoking.

            (2004)
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              • Article: not found

              Ozone in indoor environments: concentration and chemistry.

              The concentration of indoor ozone depends on a number of factors, including the outdoor ozone concentration, air exchange rates, indoor emission rates, surface removal rates, and reactions between ozone and other chemicals in the air. Outdoor ozone concentrations often display strong diurnal variations, and this adds a dynamic excitation to the transport and chemical mechanisms at play. Hence, indoor ozone concentrations can vary significantly from hour-to-hour, day-to-day, and season-to-season, as well as from room-to-room and structure-to-structure. Under normal conditions, the half-life of ozone indoors is between 7 and 10 min and is determined primarily by surface removal and air exchange. Although reactions between ozone and most other indoor pollutants are thermodynamically favorable, in the majority of cases they are quite slow. Rate constants for reactions of ozone with the more commonly identified indoor pollutants are summarized in this article. They show that only a small fraction of the reactions occur at a rate fast enough to compete with air exchange, assuming typical indoor ozone concentrations. In the case of organic compounds, the "fast" reactions involve compounds with unsaturated carbon-carbon bonds. Although such compounds typically comprise less than 10% of indoor pollutants, their reactions with ozone have the potential to be quite significant as sources of indoor free radicals and multifunctional (-C=O, -COOH, -OH) stable compounds that are often quite odorous. The stable compounds are present as both gas phase and condensed phase species, with the latter contributing to the overall concentration of indoor submicron particles. Indeed, ozone/alkene reactions provide a link between outdoor ozone, outdoor particles and indoor particles. Indoor ozone and the products derived from reactions initiated by indoor ozone are potentially damaging to both human health and materials; more detailed explication of these impacts is an area of active investigation.
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                Author and article information

                Journal
                Environ Health Perspect
                EHP
                Environmental Health Perspectives
                National Institute of Environmental Health Sciences
                0091-6765
                1552-9924
                31 May 2011
                September 2011
                : 119
                : 9
                : 1218-1226
                Affiliations
                [1 ]Department of Psychology, and
                [2 ]Graduate School of Public Health, San Diego State University, San Diego, California, USA
                [3 ]Indoor Environment Department, Lawrence Berkeley National Laboratory, Berkeley, California USA
                [4 ]San Francisco General Hospital Medical Center, University of California San Francisco, San Francisco, California, USA
                [5 ]Center for Child and Adolescent Health Policy, Massachusetts General Hospital, Boston, Massachusetts, USA
                [6 ]David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA
                [7 ]Stem Cell Center, University of California Riverside, Riverside, California, USA
                [8 ]Keck School of Medicine, University of Southern California, Los Angeles, California, USA
                [9 ]Environmental Toxicology, University of California Riverside, Riverside, California, USA
                [10 ]Department of Cancer and DNA Damage Responses, Lawrence Berkeley National Laboratory, Berkeley, California, USA
                [11 ]University of California Riverside, Department of Cell Biology and Neuroscience, Riverside, California, USA
                [12 ]Portland State University, Civil and Environmental Engineering and Chemistry, Portland, Oregon, USA
                Author notes
                Address correspondence to G.E. Matt, Department of Psychology, San Diego State University, 5500 Campanile Dr., San Diego, CA 92182 USA. Telephone: (619) 594-6262. Fax: (619) 594-1332. E-mail: gmatt@ 123456sciences.sdsu.edu
                Article
                ehp.1103500
                10.1289/ehp.1103500
                3230406
                21628107
                57aa7f96-d493-44d8-a232-00886fd7a39c
                Copyright @ 2011

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 January 2011
                : 31 May 2011
                Categories
                Review

                Public health
                cumulative exposure,biomarkers,policy,tobacco smoke,secondhand smoke,exposure,housing,nicotine,aggregate exposures

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