Thirdhand Smoke Exposure Research Articles

Tobacco toxins deposited on surfaces (third hand smoke) impair wound healing.

Third hand smoke (THS) is the accumulation of second hand smoke (SHS) toxins on surfaces in homes, cars, clothing and hair of smokers. It is known that 88M US nonsmokers ≥3years old living in homes of smokers are exposed to THS toxicants and show blood cotinine levels of ≥0.05ng/ml, indicating that the toxins are circulating in their circulatory systems. The goal of the present study is to investigate the mechanisms by which THS causes impaired wound healing. We show that mice living under conditions that mimic THS exposure in humans display delayed wound closure, impaired collagen deposition, altered inflammatory response, decreased angiogenesis, microvessels with fibrin cuffs and a highly proteolytic wound environment. Moreover, THS-exposed mouse wounds have high levels of oxidative stress and significantly lower levels of antioxidant activity leading to molecular damage, including protein nitration, lipid peroxidation and DNA damage that contribute to tissue dysfunction. Furthermore, we show that elastase is elevated, suggesting that elastin is degraded and the plasticity of the wound tissue is decreased. Taken together, our results lead us to conclude that THS toxicants delay and impair wound healing by disrupting the sequential processes that lead to normal healing. In addition, the lack of elastin results in loss of wound plasticity, which may be responsible for reopening of wounds.

A Health Threat to Bystanders Living in the Homes of Smokers: How Smoke Toxins Deposited on Surfaces Can Cause Insulin Resistance.

Thirdhand smoke (THS) is the accumulation of secondhand smoke on environmental surfaces. THS is found on the clothing and hair of smokers as well as on surfaces in homes and cars of smokers. Exposure occurs by ingestion, inhalation and dermal absorption. Children living in homes of smokers are at highest risk because they crawl on the floor, touch parents’ clothing/hair and household objects. Using mice exposed to THS under conditions that mimic exposure of humans, we show that THS increases cellular oxidative stress by increasing superoxide dismutase (SOD) activity and hydrogen peroxide (H2O2) levels while reducing the activity of antioxidant enzymes catalase and glutathione peroxidase (GPx) that break down H2O2 into H2O and O2. This results in lipid peroxidation, protein nitrosylation and DNA damage. Consequences of these cell and molecular changes are hyperglycemia and insulinemia. Indeed, we found reduced levels of insulin receptor, PI3K, AKT, all important molecules in insulin signaling and glucose uptake by cells. To determine whether these effects on THS-induced insulin resistance are due to increase in oxidative stress, we treated mice exposed to THS with the antioxidants N-acetyl cysteine (NAC) and alpha-tocopherol (alpha-toc) and showed that the oxidative stress, the molecular damage, and the insulin resistance, were significantly reversed. Conversely, feeding the mice with chow that mimics “western diet”, which is known to increase oxidative stress, while exposing the mice to THS, further increased the oxidative stress and aggravated hyperglycemia and insulinemia. In conclusion, THS exposure results in insulin resistance in the form of non-obese type II diabetes (NODII) through oxidative stress. If confirmed in humans, these studies could have a major impact on how people view exposure to environmental tobacco toxins, in particular to children, elderly and workers in environments where tobacco smoke has taken place.

Thirdhand smoke contamination in hospital settings: assessing exposure risk for vulnerable paediatric patients

BackgroundTobacco has regained the status of the world's number two killer behind heart/vascular disease. Thirdhand smoke (THS) residue and particles from secondhand smoke (SHS) are suspected health hazards (eg, DNA...

Third-hand smoke exposure and health hazards in children

Smoking still represents a huge public health problem. Millions of children suffer the detrimental effects of passive smoking. An increasing number of countries have recently issued laws to regulate smoking in public places. Instead, homes remain a site where children are dangerously exposed to environmental tobacco smoke (ETS). The combination of tobacco smoke pollutants which remain in an indoor environment, the so-called 'third-hand smoke' (THS), represent a new concept in the field of tobacco control. THS consists of pollutants that remain on surfaces and in dust after tobacco has been smoked, are re-emitted into the gas-phase, or react with other compounds in the environment to form secondary pollutants. Indoor surfaces can represent a hidden reservoir of THS constituents that could be re-emitted long after the cessation of active smoking. Human exposure to THS pollutants has not yet been thoroughly studied. Infants and children are more prone to the risks related to THS exposure than adults because they typically spend more time indoors and have age-specific behaviours that may expose them to potential health hazards from THS. Further investigations are warranted to study the health effects of THS relevant to different exposure pathways and profiles. It would also be very important to evaluate how THS may affect the lung development through the in utero exposure during the pre-natal life. We aimed at reviewing recent findings published about THS, with special reference to the effects on children's health.

Inflammatory Diseases of the Lung Induced by Conventional Cigarette Smoke: A Review

Smoking-induced lung diseases were extremely rare prior to the 20th century. With commercialization and introduction of machine-made cigarettes, worldwide use skyrocketed and several new pulmonary diseases have been recognized. The majority of pulmonary diseases caused by cigarette smoke (CS) are inflammatory in origin. Airway epithelial cells and alveolar macrophages have altered inflammatory signaling in response to CS, which leads to recruitment of lymphocytes, eosinophils, neutrophils, and mast cells to the lungs-depending on the signaling pathway (nuclear factor-κB, adenosine monophosphate-activated protein kinase, c-Jun N-terminal kinase, p38, and signal transducer and activator of transcription 3) activated. Multiple proteins are upregulated and secreted in response to CS exposure, and many of these have immunomodulatory activities that contribute to disease pathogenesis. In particular, metalloproteases 9 and 12, surfactant protein D, antimicrobial peptides (LL-37 and human β defensin 2), and IL-1, IL-6, IL-8, and IL-17 have been found in higher quantities in the lungs of smokers with ongoing inflammation. However, many underlying mechanisms of smoking-induced inflammatory diseases are not yet known. We review here the known cellular and molecular mechanisms of CS-induced diseases, including COPD, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, acute eosinophilic pneumonia, chronic rhinosinusitis, pulmonary Langerhans cell histiocytosis, and chronic bacterial infections. We also discuss inflammation induced by secondhand and thirdhand smoke exposure and the pulmonary diseases that result. New targeted antiinflammatory therapeutic options are currently under investigation and hopefully will yield promising results for the treatment of these highly prevalent smoking-induced diseases.

Third-Hand Smoke: Old Smoke, New Concerns.

While the effects of active smoking and second-hand smoke (SHS) are well documented, the concept of third-hand smoke (THS) is a relatively new phenomenon in the environmental and public health field. This notion was coined in 2009 (Winickoff et al. in Pediatrics 123(1):e74-e79, 2009) but was not really brought to light until the New York Times published an article on the topic (Rabin in A new cigarette hazard: 'third-hand smoke'. The New York Times, http://www.nytimes.com/2009/01/03/health/research/03smoke.html?_r=0 , 2009). Research on THS is fairly new and currently only limited animal studies have been performed that explore the health impacts associated with an individual THS-specific component. The public at large has a limited understanding of this new concept. As such, attitudes and beliefs surrounding THS exposure are still immature. Future research must be conducted to facilitate hazard identification, exposure and risk assessment to address its health impact on susceptible populations and to differentiate THS versus active smoking and SHS. In addition, policies and laws concerning tobacco smoke will need to be reviewed, possibly revised with the role of THS considered as an indispensable component of a broader tobacco control strategy.

PO-0896 Consequences Of Second – And Thirdhand Smoke Exposure For Newborns At The Neonatal Intensive Care Unit

Background and aims Smoking is consuming the smoke of smouldering tobacco. Inhaling harmful substances from tobacco and a higher risk for disorders, is general knowledge. Less well known are the possible effects of second- and thirdhand smoke. Secondhand smoking is the involuntary inhalation of tobacco smoke in the ambient air. Inhaling the smoke residues from walls, furniture, clothes, toys and other objects or absorbing it through the skin is referred to as thirdhand smoking. The aim is to provide a scientifically based advice on dealing with this issue in a hospital setting. Methods A literature-study is performed. A PICO (patient-intervention-comparison-outcome) question is formulated to guide a literature search in scientific databases. Articles will be critically appraised. Results Four studies (two reviews, one cohort, one descriptive) were found all pointing out that exposure to second- and thirdhand smoking may adversely affect young children, especially in the age up to 1 year including preterm or otherwise respiratory compromised newborn infants in the NICU. Also addressed is the lack of knowledge of parents and staff on the consequences of second-and thirdhand smoke. Hospital staff has an opportunity to educate parents about the effects of smoking on their newborn baby. Additional steps as changing clothes and wearing gloves after smoking would be appropriate. Conclusions Healthcare professionals should take their responsibilities in preventing harm to fragile newborn infants as a result of tobacco smoke more serious.

Exposure to nitrosamines in thirdhand tobacco smoke increases cancer risk in non-smokers

In addition to passive inhalation, non-smokers, and especially children, are exposed to residual tobacco smoke gases and particles that are deposited to surfaces and dust, known as thirdhand smoke (THS). However, until now the potential cancer risks of this pathway of exposure have been highly uncertain and not considered in public health policy. In this study, we estimate for the first time the potential cancer risk by age group through non-dietary ingestion and dermal exposure to carcinogen N-nitrosamines and tobacco-specific nitrosamines (TSNAs) measured in house dust samples. Using a highly sensitive and selective analytical approach we have determined the presence of nicotine, eight N-nitrosamines and five tobacco-specific nitrosamines in forty-six settled dust samples from homes occupied by both smokers and non-smokers. Using observations of house dust composition, we have estimated the cancer risk by applying the most recent official toxicological information. Calculated cancer risks through exposure to the observed levels of TSNAs at an early life stage (1 to 6years old) exceeded the upper-bound risk recommended by the USEPA in 77% of smokers' and 64% of non-smokers' homes. The maximum risk from exposure to all nitrosamines measured in a smoker occupied home was one excess cancer case per one thousand population exposed.The results presented here highlight the potentially severe long-term consequences of THS exposure, particularly to children, and give strong evidence of its potential health risk and, therefore, they should be considered when developing future environmental and health policies.

Pediatric Asthma – do we need more innovation for treatment?

Pediatric Asthma – do we need more innovation for treatment?

Position Statement on Tobacco Exposures in Children and Families

Tobacco use was declared a “pediatric disease” in 1995 by the US Food and Drug Administration due to the strong connection between tobacco use/exposure in children (Kessler et al., 1997). Tobacco use and exposure are the single most preventable causes of morbidity and mortality in the United States and worldwide. The health consequences during childhood have been clearly documented, and the US Surgeon General stated in 2006 there are no safe levels of tobacco exposure (US Department of Health and Human Services, 2010a). The first position statement on tobacco exposures was developed by the Society of Pediatric Nurses (SPN) Public Policy Committee in 2004. Tobacco use, particularly among childbearing and childrearing families, has decreased slightly since 2004, though tobacco use and exposure remains a critical health issue for vulnerable populations of children and families. SPN is dedicated to supporting its members in their practice, as well as promoting the health and wellbeing of children and families. Pediatric nurses can play a pivotal role in reducing tobacco use and children’s tobacco exposure. Interventions to reduce tobacco use and exposure can include clinical advice, counseling, referral to smoking cessation, and policy changes. While most pediatric nurses may conduct these interventions in health-related settings, attention must be directed to other settings that serve children, such as preschool programs, schools, recreational programs, community settings, and others. Working together we, as pediatric nurses, can strive for the goal that all children have the right to grow up in a smokefree and healthy environment. Tobacco exposures—that is, tobacco use, secondhand smoke, or thirdhand smoke exposure—are highly prevalent

Pediatric Emergency Department Is a Promising Venue for Adult Tobacco Cessation Interventions

Pediatric Emergency Department Is a Promising Venue for Adult Tobacco Cessation Interventions

Second- and third-hand smoke exposure: Selected literature for healthcare professionals providing home-based services to the severely mentally ill

Purpose: To develop recommendations for healthcare professionals at risk for exposure to secondhand (SHS) and thirdhand smoke (THS) while providing home-based services to patients with severe mental illnesses (SMIs), such as schizophrenia. Summary: Healthcare professionals who provide services to those with SMIs have the potential to be exposed to SHS and THS. Smoking rates in persons diagnosed with schizophrenia are significantly higher compared to the general population (up to 90% versus approximately 30%). According to one study, only 31.5% of patients with SMIs are likely to have smoke-free homes. Currently there are no guidelines available for minimizing the effects of SHS and THS on healthcare professionals. Strategies for minimizing the effects are proposed. Conclusion: Literature dealing with the effects of SHS, potential occupational hazards of exposure, and the results of anti-public smoking laws to address the problem were reviewed. The health hazards of THS exposure are an emerging area. Data are limited on alternative strategies for healthcare professionals to minimize SHS and THS exposure. Suggestions to minimize exposure are provided.

Environmental Tobacco Smoke Exposure and Respiratory Complaints in Children Aged 0-13 Years: A Cross-sectional Study in South-Limburg, The Netherlands

Background: Two forms of environmental tobacco smoke (ETS) exposure have been described: second-hand smoke (SHS), which is the direct exposure to tobacco smoke; and third-hand smoke (THS), which is the exposure to residuals from tobacco smoke after the cigarette has been extinguished. The effects of SHS exposure on children’s respiratory health are known, but not of THS exposure. We evaluated the association between both exposures and respiratory complaints in children aged 0-13 years, and assessed whether the risk of respiratory complaints due to these exposures was higher in children with genetic predisposition for asthma compared to those without. Methods: A cross-sectional survey (91 items) was performed in 10,000 families with a child aged 0-13 years living in South-Limburg, the Netherlands, assessing child and family characteristics, child’s respiratory health, and parental smoking behaviour. Data were analyzed with (adjusted) multiple logistic regressions. Results: 1899 families responded. SHS exposure was not associated with an increased risk of respiratory complaints in children. THS exposure was associated with respiratory tract infections in the past 12 months (ORadjusted: 2.13; 95% CI: 1.04-4.36; p=0.04) and recent wheezing (ORadjusted: 2.61; 95%CI: 1.19-5.71; p=0.02) in children. There was no interaction between genetic predisposition for asthma and ETS exposure. Conclusions: Unlike previous studies, our study could not reveal a significant association between SHS exposure and an increased risk of respiratory complaints in children, most likely due to study limitations concerning cross-sectional design, response rate, selection bias and parental underreporting of SHS exposure to their children. THS exposure was significantly associated with an increased risk of respiratory complaints in children. This adds to the limited knowledge about the health effects of THS exposure in children and suggests that more research on this topic is needed. A genetic predisposition for asthma combined with ETS exposure did not increase the risk of respiratory complaints in children.

Protecting the Vulnerable: The Importance of Effective Parental Tobacco-Dependence Treatment During Prenatal and Newborn Care.

Tobacco use among pregnant women, as well as second- and third-hand smoke exposure of their infants, translates into the startling fact that more than one third of American children live with at least one parent who smokes cigarettes daily. Maternal smoking or second-hand smoke exposure during pregnancy is deleterious to the mother's health and contributes to prematurity, low birth-weight infants, and increased risk of sudden infant death syndrome (SIDS) and recurrent wheezing during the first year of life. Pregnant women who stop tobacco use during pregnancy are at high risk for postpartum relapse frequently associated with a partner who smokes tobacco, stress, poverty, and lack of social and medical support to remain tobacco free. Enhanced efforts to identify and support pregnant women who smoke, and to implement strategies to prevent exposure of their fetus and newborn to the hazards of tobacco-smoke exposure, are paramount in our public health efforts to eliminate health disparities in the United States. We discuss the critical elements of programs to assist mothers to stop smoking during pregnancy and toward family efforts to maintain a smoke-free environment for their infant. Postpartum interventions, whether in the neonatal intensive care unit (NICU), newborn nursery, or postnatal care setting, can provide assistance that women need to remain smoke free, to educate spouses or significant others and their families, and to aide in establishing goals of maintaining a tobacco smoke-free home and car. Physicians and other perinatal healthcare providers have a duty to identify pregnant women who smoke for "meaningful use" in the electronic medical record, and to provide advice and assistance in evidence-based smoking interventions in obstetrical care settings. Pediatricians, neonatologists, and others providing postpartum, "normal" nursery or NICU care have an opportunity to protect infants and young children from second- and third-hand smoke exposure by assisting their parents and family members in maintaining a tobacco-free environment to improve the health of infants, toddlers, and young children.

Thirdhand Smoke Exposure: An Emerging Threat from an Old Foe

Thirdhand Smoke Exposure: An Emerging Threat from an Old Foe

The New Danger of Thirdhand Smoke: Why Passive Smoking Does Not Stop at Secondhand Smoke

Passive smoking exposure is a topic of great concern for public health because of its well-known adverse effects on human health (International Agency for Research on Cancer 2004). Two news articles on this topic were published in the February 2011 issue of Environmental Health Perspectives (Burton 2011; Lubick 2011). Lubick (2011) discussed the global health burden of secondhand smoke, and Burton (2011) emphasized a new and alarming consequence of smoking in indoor environments—“thirdhand smoke”—a term first coined in 2006 (Szabo 2006). Secondhand smoke is defined as “the combination of smoke emitted from the burning end of a cigarette or other tobacco products and smoke exhaled by the smoker” (World Health Organization 2007). Thus, secondhand smoke exposure consists of an unintentional inhalation of smoke that occurs close to people smoking and/or in indoor environments where tobacco was recently used. Thirdhand smoke is a complex phenomenon resulting from residual tobacco smoke pollutants that adhere to the clothing and hair of smokers and to surfaces, furnishings, and dust in indoor environments. These pollutants persist long after the clearing of secondhand smoke. They are reemitted into the gas phase or react with oxidants or other compounds present in the environment to form secondary contaminants, some of which are carcinogenic or otherwise toxic for human health (Matt et al. 2011). Thus, thirdhand smoke exposure consists of unintentional intake (mainly through inhalation but also via ingestion and dermal routes) of tobacco smoke and other related chemicals that occurs in the absence of concurrent smoking. Exposure can even take place long after smoking has ceased, through close contact with smokers and in indoor environments in which tobacco is regularly smoked. Lubick (2011) considers secondhand smoke synonymous with passive smoking, as do the majority of the authors publishing on this topic. However, in light of new evidence about thirdhand smoke (Matt et al. 2011), it is no longer appropriate to use the term “secondhand smoke” as a synonym for passive smoking or environmental tobacco smoke, because it represents a pars pro toto. In other words, using the term “secondhand smoke” mistakes one part of the problem for the whole. Instead, we propose that “passive smoking” or “environmental tobacco smoke” be used as a more inclusive term to describe any tobacco smoke exposure outside of active smoking. This question of terminology is of particular concern for researchers evaluating passive smoking exposure in indoor settings, especially in domestic environments. Since numerous countries have introduced smoking bans in enclosed public places, domestic environments have become the main sources of passive smoking exposure (World Health Organization 2007). We believe researchers should determine the independent contributions of secondhand and thirdhand smoke when they assess the magnitude of pollutant intake due to passive smoking exposure.

Thirdhand Smoke in Review: Research Needs and Recommendations

Studies over the last half-century have clearly demonstrated that cigarette smoking is associated with adverse health effects both for smokers and for individuals exposed to secondhand smoke (SHS). Now a new level of exposure has been identified: thirdhand smoke (THS), or residual tobacco smoke pollutants that remain on surfaces and in dust and that are reemitted in the gas phase and interact with other compounds. In a new review, researchers offer a descriptive analysis of THS constituents and dynamics and argue for the establishment of a programmatic research agenda to close gaps in our understanding of the nature and effects of THS [EHP 119(9):1218–1226; Matt et al.]. THS exposure is the result of inhalation, ingestion, or dermal uptake of THS pollutants in the air, in dust, and on surfaces. The authors point out that THS and SHS are closely related, and in fact coexist as THS is first formed and in settings where smoking recurs regularly. But whereas SHS is removed by ventilation, THS pollutants may persist in environments for several hours or days after tobacco has been smoked. THS components—such as nicotine and carcinogenic polycyclic aromatic hydrocarbons, including benzo[a]pyrene—are sorbed and reemitted from indoor surfaces over varying periods of time after tobacco sources have been extinguished. Some THS components react with other environmental compounds to produce secondary pollutants. For instance, chemical reactions between nicotine and nitrous acid lead to the formation of additional tobacco-specific nitrosamines, and ozone can react with certain volatile organic compounds to form formaldehyde, acetaldehyde, and benzaldehyde. Thirdhand smoke lingers after secondhand smoke has cleared from the room. THS constituents have been measured in indoor spaces months after smoking last occurred. Given the U.S. Surgeon General’s conclusion that there appears to be no risk-free level of exposure to SHS, this raises the possibility that THS could lead to potentially harmful exposures, particularly for vulnerable populations such as children. The investigators recommend that future studies further define the chemistry and toxicology of THS, which will aid in establishing, enhancing, and enforcing public policies and personal practices that limit tobacco smoke exposure. The authors note that voluntary public and private policies enacted over the last decade—including an increase in smoke-free workplaces, public areas, and lodging—have effectively addressed THS exposure in some settings. They argue that stronger public health policies can be developed through an interdisciplinary research agenda that combines basic and applied risk assessment research with studies on tobacco use and cessation.

Second- and third-hand opium smoke exposure in the women and children of Afghanistan

Second- and third-hand opium smoke exposure in the women and children of Afghanistan

Thirdhand tobacco smoke: emerging evidence and arguments for a multidisciplinary research agenda.

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.

Thirdhand smoke: a new dimension to the effects of cigarette smoke on the developing lung

The underlying mechanisms and effector molecules involved in mediating in utero smoke exposure-induced effects on the developing lung are only beginning to be understood. However, the effects of a newly discovered category of smoke, i.e., thirdhand smoke (THS), on the developing lung are completely unknown. We hypothesized that, in addition to nicotine, other components of THS would also affect lung development adversely. Fetal rat lung explants were exposed to nicotine, 1-(N-methyl-N-nitrosamino)-1-(3-pyridinyl)-4-butanal (NNA), or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), the two main tobacco-specific N-nitrosamine constituents of THS, for 24 h. We then determined key markers for alveolar paracrine signaling [epithelial differentiation markers surfactant phospholipid and protein synthesis; mesenchymal differentiation markers peroxisome proliferator-activated receptor γ (PPAR-γ), fibronectin and calponin], the BCL-2-to-Bax ratio (BCL-2/Bax), a marker of apoptosis and the involvement of nicotinic acetylcholine receptors (nAChR)-α3 and -α7 in mediating NNA's and NNK's effects on the developing lung. Similar to the effects of nicotine, exposure of the developing lung to either NNK or NNA resulted in disrupted homeostatic signaling, indicated by the downregulation of PPAR-γ, upregulation of fibronectin and calponin protein levels, decreased BCL-2/Bax, and the accompanying compensatory stimulation of surfactant phospholipid and protein synthesis. Furthermore, nAChR-α3 and -α7 had differential complex roles in mediating these effects. NNK and NNA exposure resulted in breakdown of alveolar epithelial-mesenchymal cross-talk, reflecting lipofibroblast-to-myofibroblast transdifferentiation, suggesting THS constituents as possible novel contributors to in utero smoke exposure-induced pulmonary damage. These data are particularly relevant for designing specific therapeutic strategies, and for formulating public health policies to minimize THS exposure.