ChiroACCESS Article

Thirdhand Smoke: Understanding a Serious “New” Health Risk

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ChiroACCESS Editorial Staff



Published on

March 19, 2013

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Recent studies link DNA damage to thirdhand smoke and note that it is a special threat to children.  Cigarette smoking (first hand smoke) has long been associated with multiple and devastating risks to human health.  Subsequent research confirmed the dangers of exposure to environments where smoke lingers from those who are actively smoking (second hand smoke).  The most recent studies now describe the risk of environmental pollutants that remain even after the second hand smoke has cleared.  These pollutants remain on the surfaces of buildings, furniture, floors, clothing and other items exposed to smokers and are being referred to as third hand (or thirdhand) smoke.
A research study published on March 5, 2013 confirms that “thirdhand smoke causes DNA damage in human cells”.  The concern is especially great for young children who crawl on exposed floors or put items in their mouths that are contaminated.  As another study concluded, “Another threat to health and environment of our children, is the nicotine coming from indirect exposure to tobacco smoke. Residual nicotine that persists in high concentrations on the interior surfaces, including clothing, is forming in the reaction of nitric acid carcinogenic compounds of specific nitrosamines. In addition, ozone and related atmospheric oxidants react with nicotine smoke or smoke coming from the second-hand smoke, giving the smallest particles with high risk of asthma.”
Below are links to other articles on ChiroACCESS related to smoking:

Adult and Youth Smoking Predicts Low Back Pain.
Second Hand Smoke and Coronary Disease.
Smoking Cessation Counseling and Health Care Providers Evidence Based Review
Manipulation for Chronic Obstructive Pulmonary Disease-COPD

Note:  These mini-reviews are designed as updates and direct the reader to the full text of current research.  The abstracts presented here are no substitute for reading and critically reviewing the full text of the original research.  Where permitted we will direct the reader to that full text.

Thirdhand smoke causes DNA damage in human cells.  [Link]

Mutagenesis. 2013 Mar 5. [Epub ahead of print]

Hang B, Sarker AH, Havel C, Saha S, Hazra TK, Schick S, Jacob P 3rd, Rehan VK, Chenna A, Sharan D, Sleiman M, Destaillats H, Gundel LA.
Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA.

Exposure to thirdhand smoke (THS) is a newly described health risk. Evidence supports its widespread presence in indoor environments. However, its genotoxic potential, a critical aspect in risk assessment, is virtually untested. An important characteristic of THS is its ability to undergo chemical transformations during aging periods, as demonstrated in a recent study showing that sorbed nicotine reacts with the indoor pollutant nitrous acid (HONO) to form tobacco-specific nitrosamines (TSNAs) such as 4-(methylnitrosamino)-4-(3-pyridyl)butanal (NNA) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The goal of this study was to assess the genotoxicity of THS in human cell lines using two in vitro assays. THS was generated in laboratory systems that simulated short (acute)- and long (chronic)-term exposures. Analysis by liquid chromatography-tandem mass spectrometry quantified TSNAs and common tobacco alkaloids in extracts of THS that had sorbed onto cellulose substrates. Exposure of human HepG2 cells to either acute or chronic THS for 24h resulted in significant increases in DNA strand breaks in the alkaline Comet assay. Cell cultures exposed to NNA alone showed significantly higher levels of DNA damage in the same assay. NNA is absent in freshly emitted secondhand smoke, but it is the main TSNA formed in THS when nicotine reacts with HONO long after smoking takes place. The long amplicon-quantitative PCR assay quantified significantly higher levels of oxidative DNA damage in hypoxanthine phosphoribosyltransferase 1 (HPRT) and polymerase ß (POLB) genes of cultured human cells exposed to chronic THS for 24h compared with untreated cells, suggesting that THS exposure is related to increased oxidative stress and could be an important contributing factor in THS-mediated toxicity. The findings of this study demonstrate for the first time that exposure to THS is genotoxic in human cell lines.

Pediatrician interventions and thirdhand smoke beliefs of parents.  [Link]

Am J Prev Med. 2012 Nov;43(5):533-6.

Drehmer JE, Ossip DJ, Rigotti NA, Nabi-Burza E, Woo H, Wasserman RC, Chang Y, Winickoff JP.
Pediatric Research in Office Settings, American Academy of Pediatrics, Elk Grove Village, Illinois, USA.

BACKGROUND: Thirdhand smoke is residual tobacco smoke contamination that remains after a cigarette is extinguished. A national study indicates that adults' belief that thirdhand smoke (THS) harms children is associated with strict household no-smoking policies. The question of whether pediatricians can influence THS beliefs has not been assessed.

PURPOSE: To identify prevalence of THS beliefs and associated factors among smoking parents, and the association of pediatrician intervention on parent belief that THS is harmful to their children.

METHODS: Exit interview data were collected from 1980 parents following a pediatric office visit. Parents' level of agreement or disagreement that THS can harm the health of babies and children was assessed. A multivariate logistic regression model was constructed to identify whether pediatricians' actions were independently associated with parental belief that THS can harm the health of babies and children. Data were collected from 2009 to 2011, and analyses were conducted in 2012.

RESULTS: Ninety-one percent of parents believed that THS can harm the health of babies and children. Fathers (AOR=0.59, 95% CI=0.42, 0.84) and parents who smoked more than ten cigarettes per day (AOR=0.63, 95% CI=0.45, 0.88) were less likely to agree with this statement. In contrast, parents who received advice (AOR=1.60, 95% CI=1.04, 2.45) to have a smokefree home or car or to quit smoking and parents who were referred (AOR=3.42, 95% CI=1.18, 9.94) to a "quitline" or other cessation program were more likely to agree that THS can be harmful.

CONCLUSIONS: Fathers and heavier smokers were less likely to believe that THS is harmful. However, pediatricians' actions to encourage smoking parents to quit or adopt smokefree home or car policies were associated with parental beliefs that THS harms children.

Wipe Sampling for Nicotine as a Marker of Thirdhand Tobacco Smoke Contamination on Surfaces in Homes, Cars, and Hotels.  [Link]

Nicotine Tob Res. 2013 Mar 4. [Epub ahead of print]

Quintana PJ, Matt GE, Chatfield D, Zakarian JM, Fortmann AL, Hoh E.
School of Public Health, San Diego State University, San Diego, CA

INTRODUCTION: Secondhand smoke contains a mixture of pollutants that can persist in air, dust, and on surfaces for months or longer. This persistent residue is known as thirdhand smoke (THS). Here, we detail a simple method of wipe sampling for nicotine as a marker of accumulated THS on surfaces.

METHODS: We analyzed findings from 5 real-world studies to investigate the performance of wipe sampling for nicotine on surfaces in homes, cars, and hotels in relation to smoking behavior and smoking restrictions.

RESULTS: The intraclass correlation coefficient for side-by-side samples was 0.91 (95% CI: 0.87-0.94). Wipe sampling for nicotine reliably distinguished between private homes, private cars, rental cars, and hotels with and without smoking bans and was significantly positively correlated with other measures of tobacco smoke contamination such as air and dust nicotine. The sensitivity and specificity of possible threshold values (0.1, 1, and 10 µg/m2) were evaluated for distinguishing between nonsmoking and smoking environments. Sensitivity was highest at a threshold of 0.1 µg/m2, with 74%-100% of smoker environments showing nicotine levels above threshold. Specificity was highest at a threshold of 10 µg/m2, with 81%-100% of nonsmoker environments showing nicotine levels below threshold. The optimal threshold will depend on the desired balance of sensitivity and specificity and on the types of smoking and nonsmoking environments.

CONCLUSIONS: Surface wipe sampling for nicotine is a reliable, valid, and relatively simple collection method to quantify THS contamination on surfaces across a wide range of field settings and to distinguish between nonsmoking and smoking environments.

Environmental tobacco smoke as a source of polycyclic aromatic hydrocarbons in settled household dust.  [Link]

Environ Sci Technol. 2012 Apr 3;46(7):4174-83.

Hoh E, Hunt RN, Quintana PJ, Zakarian JM, Chatfield DA, Wittry BC, Rodriguez E, Matt GE.
Graduate School of Public Health, San Diego State University, San Diego, CA, USA.

Environmental tobacco smoke is a major contributor to indoor air pollution. Dust and surfaces may remain contaminated long after active smoking has ceased (called 'thirdhand' smoke). Polycyclic aromatic hydrocarbons (PAHs) are known carcinogenic components of tobacco smoke found in settled house dust (SHD). We investigated whether tobacco smoke is a source of PAHs in SHD. House dust was collected from 132 homes in urban areas of Southern California. Total PAHs were significantly higher in smoker homes than nonsmoker homes (by concentration: 990 ng/g vs 756 ng/g, p = 0.025; by loading: 1650 ng/m(2) vs 796 ng/m(2), p = 0.012). We also found significant linear correlations between nicotine and total PAH levels in SHD (concentration, R(2) = 0.105; loading, R(2) = 0.385). Dust collected per square meter (g/m(2)) was significantly greater in smoker homes and might dilute PAH concentration in SHD inconsistently. Therefore, dust PAH loading (ng PAH/m(2)) is a better indicator of PAH content in SHD. House dust PAH loadings in the bedroom and living room in the same home were significantly correlated (R(2) = 0.468, p < 0.001) suggesting PAHs are distributed by tobacco smoke throughout a home. In conclusion, tobacco smoke is a source of PAHs in SHD, and tobacco smoke generated PAHs are a component of thirdhand smoke.

The impact of second-hand tobacco smoke exposure on pregnancy outcomes, infant health, and the threat of third-hand smoke exposure to our environment and to our children.  [Link]

Przegl Lek. 2012;69(10):717-20.

Merritt TA, Mazela J, Adamczak A, Merritt T.
Loma Linda University School of Medicine, Children's Hospital, Loma Linda, California 92354 USA.

Smoking during pregnancy is associated with various adverse effects on pregnancy and fetal development, carries a lot of serious complications such as spontaneous abortion, placental abruption, and reduced birth weight of the newborn. Children of smoking mothers have an increased risk of premature birth, low birth weight, sudden infant death syndrome and respiratory diseases during infancy. Smoking also causes long-term risk of maternal health problems such as: heart disease, cancer, emphysema, chronic obstructive pulmonary disease and higher mortality rate. Because women are more likely to quit smoking during pregnancy than at any other time, there are attempts to increase motivation and help them to stop smoking at the procreative phase of their life. The article describes interventions that are carried out in Loma Linda, where the educational program "When You Smoke Your Baby Smokes" reminds parents about the health effects of smoking during pregnancy and harmful impact on child's health caused by second-hand smoke. Another threat to health and environment of our children, is the nicotine coming from indirect exposure to tobacco smoke. Residual nicotine that persists in high concentrations on the interior surfaces, including clothing, is forming in the reaction of nitric acid carcinogenic compounds of specific nitrosamines. In addition, ozone and related atmospheric oxidants react with nicotine smoke or smoke coming from the second-hand smoke, giving the smallest particles with high risk of asthma. Efforts towards reducing exposure to tobacco smoke coming from the passive and indirect smoking should be placed at a high priority throughout the European Union.

Third-hand tobacco smoke: Significant vector for PAH exposure or non-issue?  [Link]

Integr Environ Assess Manag. 2012 Oct;8(4):763-4.

Fleming T, Anderson C, Amin S, Ashley J.
Philadelphia University, Philadelphia, Pennsylvania, USA.

Third-hand smoking: indoor measurements of concentration and sizes of cigarette smoke particles after resuspension.  [Link]

Tob Control. 2010 Aug;19(4):347-8.

Becquemin MH, Bertholon JF, Bentayeb M, Attoui M, Ledur D, Roy F, Roy M, Annesi-Maesano I, Dautzenberg B.

Do your patients know about third-hand smoke?  [Link]

Nurse Pract. 2009 Feb;34(2):5.

Newland J.

The mutagenic hazards of settled house dust: a review.  [Link]

Mutat Res. 2004 Nov;567(2-3):401-25.

Maertens RM, Bailey J, White PA.
Mutagenesis Section, Safe Environments Program, Health Canada, Tunney's Pasture 0803A, Ottawa, Ont., Canada K1A 0L2.

Given the large proportion of time people spend indoors, the potential health risks posed by chemical contaminants in the indoor environment are of concern. Research suggests that settled house dust (SHD) may be a significant source for indoor exposure to hazardous substances including polycyclic aromatic hydrocarbons (PAHs). Here, we summarize the literature on the mutagenic hazards of SHD and the presence of PAHs in dust. We assess the extent to which PAHs are estimated to contribute to the mutagenicity of SHD, and evaluate the carcinogenic risks associated with exposures to PAHs in SHD. Research demonstrates that SHD has a Salmonella TA98 mutagenic potency of 1000-7000 revertants/g, and contains between 0.5 and 500 microg/g of PAHs. Although they only account for a small proportion of the variability, analyses of pooled datasets suggest that cigarette smoking and an urban location contribute to higher levels of PAHs. Despite their presence, our calculations show that PAHs likely account for less than 25% of the overall mutagenic potency of dust. Nevertheless, carcinogenic PAHs in dust can pose potential health risks, particularly for children who play and crawl on dusty floors, and exhibit hand-to-mouth behaviour. Risk assessment calculations performed in this study reveal that the excess cancer risks from non-dietary ingestion of carcinogenic PAHs in SHD by preschool aged children is generally in the range of what is considered acceptable (1 x 10(-6) to 2 x 10(-6)). Substantially elevated risk estimates in the range 1.5 x 10(-4) to 2.5 x 10(-4) correspond only to situations where the PAH content is at or beyond the 95th percentile, and the risk estimates are adjusted for enhanced susceptibility at early life stages. Analyses of SHD and its contaminants provide an indication of indoor pollution and present important information for human exposure assessments.

The new danger of thirdhand smoke: why passive smoking does not stop at secondhand smoke.  [Link]

Environ Health Perspect. 2011 Oct;119(10):A422.

Protano C, Vitali M.

Thirdhand smoke in review: research needs and recommendations.  [Link]

Environ Health Perspect. 2011 Sep;119(9):a399.

Tillett T.

The role of environmental tobacco smoke in genetic susceptibility to asthma.  [Link]

Curr Opin Allergy Clin Immunol. 2004 Oct;4(5):335-9.

Kurz T, Ober C.
Department of Human Genetics, The University of Chicago, Chicago, Illinois, USA.

PURPOSE OF REVIEW: The increase in asthma prevalence over the past 50 years suggests that exposures to environmental risk factors have also increased during this time. Environmental tobacco smoke is one of the most common indoor air pollutants and has been associated in epidemiologic studies with airway and allergic phenotypes in exposed individuals. However, symptoms occur in only some individuals, suggesting that individual genotypes determine sensitivity to environmental tobacco smoke exposure. In this review, we summarize studies evaluating the relationship between genotype, environmental tobacco smoke exposure and risk for asthma and related phenotypes.

RECENT FINDINGS: Using either candidate gene or genome-wide approaches, a number of studies have examined interactions between genotypes at specific loci or genome regions and environmental tobacco smoke exposure and risk for asthma or asthma-associated phenotypes. These studies implicate variation in the genes encoding the alpha(2)-adrenergic receptor, interleukin-10, glutathione S-transferase M1, interleukin-1 beta and interleukin-1 receptor antagonist, matrix metalloproteinases 1 and 12, interleukin-4 receptor alpha-chain, alpha(1)-antitrypsin, and microsomal epoxide hydrolase, as well as unknown genes on chromosomes 1p, 5q and 17p as contributing toward susceptibility in smoking exposed individuals.

SUMMARY: Considering environmental tobacco smoke exposure in genetic studies may help to identify more homogeneous subsets of patients that share a common disease etiology. By stratifying samples by environmental tobacco smoke exposure, associations or linkages with specific polymorphisms or chromosomal region may be revealed, as illustrated in the studies discussed in this review.
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