Altered microbiomes in thirdhand smoke-exposed children and their home environments.
TL;DR: In this article, the authors investigated if THS-polluted homes differed in children's human and built-environment microbiomes as compared to THS -free homes and found that THS exposure is associated with changes in the microbiomes of the home environment and of the children living in these homes.
Abstract: INTRODUCTION Tobacco smoke contains numerous toxic chemicals that accumulate in indoor environments creating thirdhand smoke (THS). We investigated if THS-polluted homes differed in children's human and built-environment microbiomes as compared to THS-free homes. METHODS Participants were n = 19 THS-exposed children and n = 10 unexposed children (≤5 years) and their caregivers. Environmental and biological samples were analyzed for THS pollutants and exposure. Swab samples were collected from the built-environment (floor, table, armrest, bed frame) and child (finger, nose, mouth, and ear canal), and 16S ribosomal RNA genes were analyzed for bacterial taxa using high-throughput DNA sequencing. RESULTS Phylogenetic α-diversity was significantly higher for the built-environment microbiomes in THS-polluted homes compared to THS-free homes (p < 0.014). Log2-fold comparison found differences between THS-polluted and THS-free homes for specific genera in samples from the built-environment (e.g., Acinetobacter, Bradyrhizobium, Corynebacterium, Gemella, Neisseria, Staphylococcus, Streptococcus, and Veillonella) and in samples from children (esp. Corynebacterium, Gemella, Lautropia, Neisseria, Rothia, Staphylococcus, and Veillonella). CONCLUSION When exposed to THS, indoor and children microbiomes are altered in an environment-specific manner. Changes are similar to those reported in previous studies for smokers and secondhand smoke-exposed persons. THS-induced changes in child and built-environmental microbiomes may play a role in clinical outcomes in children. IMPACT Despite smoking bans, children can be exposed to tobacco smoke residue (i.e., thirdhand smoke) that lingers on surfaces and in settled house dust. Thirdhand smoke exposure is associated with changes in the microbiomes of the home environment and of the children living in these homes. Thirdhand smoke is associated with increased phylogenetic diversity of the home environment and changes in the abundances of several genera of the child microbiome known to be affected by active smoking and secondhand smoke (e.g., Corynebacterium, Staphylococcus, Streptococcus). Thirdhand smoke exposure by itself may induce alterations in the microbiome that play a role in childhood pathologies.
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TL;DR: In this paper, the authors compared the different roles of urinary cotinine as a biomarker of recent overall tobacco smoke exposure and hand nicotine as a marker of children's contact with nicotine pollution in their environments.
17 citations
TL;DR: A review of the current literature related to cigarette and e-cigarette contamination in the context of environmental sources and impacts, with a focus on the documented influences on biota, ranging from bacteria to mammals, is presented in this paper.
Abstract: While the impacts of cigarette smoking on human health are widely known, a less recognized impact of tobacco product use and disposal is environmental pollution. This review discusses the current literature related to cigarette and e-cigarette contamination in the context of environmental sources and impacts, with a focus on the documented influences on biota, ranging from bacteria to mammals. Cigarette butts and electronic cigarette components can leach contaminants into soil, water, and air. Cellulose acetate cigarette filters comprising the butts are minimally degradable and are a source of bulk plastic and microplastic pollution, especially in aquatic ecosystems where they tend to accumulate. Cigarette combustion and aerosol production during e-cigarette use result in air contamination from sidestream, exhaled, and thirdhand pathways. The chemical byproducts of tobacco product use contaminate wastewater effluents, landfill leachates, and urban storm drains. The widespread detection of nicotine and cotinine in the environment illustrates the potential for large-scale environmental impacts of tobacco product waste. Studies show that cigarette butt leachate and nicotine are toxic to microbes, plants, benthic organisms, bivalves, zooplankton, fish, and mammals; however, there remain critical knowledge gaps related to the environmental impacts of tobacco product waste on environmental health and ecosystem functioning.
8 citations
TL;DR: In this article , the prevalence of and income-related disparities associated with exposure to thirdhand smoke among children were examined, and a cross-sectional study was conducted to examine the impact of exposure to smoke on children.
Abstract: This cross-sectional study examines the prevalence of and income-related disparities associated with exposure to thirdhand smoke among children.
8 citations
TL;DR: The significant association of hand nicotine with urinary cotinine suggests that THS pollution should be assessed in evaluating children's Overall TSE to cigars and other tobacco products, and hand nicotine may be a proxy for overall TSE.
Abstract: Objectives Past research has not examined secondhand and thirdhand smoke (THS) exposure in children of cigar smokers. We examined hand nicotine and cotinine levels in children of cigar smokers to explore the contribution of cigar smoke to tobacco smoke exposure (TSE). Methods Participants were children (N = 24; mean (SD) age = 6.5 (3.6) years) whose parents smoked cigars only or poly-used cigars and/or cigarettes. Primary outcomes were hand nicotine and urinary cotinine levels. Results All children had detectable hand nicotine (range: 7.6-312.5ng/wipe) and cotinine (range: 0.3-100.3ng/ml). Positive correlations were found between hand nicotine and cotinine (r = 0.693, p = .001), hand nicotine and parents who also smoked cigarettes (r = 0.407, p = .048), and hand nicotine and number of smokers around the child (r = 0.436, p = .03). Hand nicotine (r = -0.464, p = .02), but not cotinine (r = -0.266, p = .26), was negatively correlated with child age. Multiple regression results indicated a positive association between hand nicotine and cotinine (p = .002; semi-partial r2 = 0.415), irrespective of child age. Conclusions The significant association of hand nicotine with urinary cotinine suggests that THS pollution should be assessed in evaluating children's overall TSE to cigars and other tobacco products, and hand nicotine may be a proxy for overall TSE. Younger children may have increased THS pollutant uptake.
5 citations
TL;DR: A recent review as discussed by the authors suggests that Microbiome First medical approaches to human health and wellness could both aid the fight against non-communicable diseases and conditions (NCDs) and help to usher in sustainable healthcare.
Abstract: The is a sequential article to an initial review suggesting that Microbiome First medical approaches to human health and wellness could both aid the fight against noncommunicable diseases and conditions (NCDs) and help to usher in sustainable healthcare. This current review article specifically focuses on public health programs and initiatives and what has been termed by medical journals as a catastrophic record of recent failures. Included in the review is a discussion of the four priority behavioral modifications (food choices, cessation of two drugs of abuse, and exercise) advocated by the World Health Organization as the way to stop the ongoing NCD epidemic. The lack of public health focus on the majority of cells and genes in the human superorganism, the microbiome, is highlighted as is the “regulatory gap” failure to protect humans, particularly the young, from a series of mass population toxic exposures (e.g., asbestos, trichloroethylene, dioxin, polychlorinated biphenyls, triclosan, bisphenol A and other plasticizers, polyfluorinated compounds, herbicides, food emulsifiers, high fructose corn syrup, certain nanoparticles, endocrine disruptors, and obesogens). The combination of early life toxicity for the microbiome and connected human physiological systems (e.g., immune, neurological), plus a lack of attention to the importance of microbial rebiosis has facilitated rather than suppressed, the NCD epidemic. This review article concludes with a call to place the microbiome first and foremost in public health initiatives as a way to both rescue public health effectiveness and reduce the human suffering connected to comorbid NCDs.
3 citations
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TL;DR: The Human Microbiome Project Consortium reported the first results of their analysis of microbial communities from distinct, clinically relevant body habitats in a human cohort; the insights into the microbial communities of a healthy population lay foundations for future exploration of the epidemiology, ecology and translational applications of the human microbiome as discussed by the authors.
Abstract: The Human Microbiome Project Consortium reports the first results of their analysis of microbial communities from distinct, clinically relevant body habitats in a human cohort; the insights into the microbial communities of a healthy population lay foundations for future exploration of the epidemiology, ecology and translational applications of the human microbiome.
8,410 citations
University of Pittsburgh1, University of Colorado Denver2, University of Michigan3, University of Washington4, Veterans Health Administration5, University of California, San Francisco6, George Washington University7, University of California, Los Angeles8, Washington University in St. Louis9, Indiana University10, Michigan State University11
TL;DR: This study is the largest to examine composition of the lower respiratory tract microbiome in healthy individuals and the first to use the neutral model to compare the lung to the mouth, demonstrating that the lung microbiome does not derive entirely from the mouth.
Abstract: Rationale: Results from 16S rDNA-encoding gene sequence–based, culture-independent techniques have led to conflicting conclusions about the composition of the lower respiratory tract microbiome. Objectives: To compare the microbiome of the upper and lower respiratory tract in healthy HIV-uninfected nonsmokers and smokers in a multicenter cohort. Methods: Participants were nonsmokers and smokers without significantcomorbidities.Oralwashesandbronchoscopicalveolarlavages were collected in a standardized manner. Sequence analysis of bacterial 16S rRNA-encoding genes was performed, and the neutral modelincommunityecologywasusedtoidentifybacteriathatwere the most plausible members of a lung microbiome. Measurements and Main Results: Sixty-four participants were enrolled. Mostbacteriaidentifiedinthelungwerealsointhemouth,butspecific bacteria such as Enterobacteriaceae, Haemophilus, Methylobacterium, and Ralstonia species were disproportionally represented in the lungs compared with values predicted by the neutral model. Tropheryma was
648 citations
TL;DR: Infants of smokers are at risk of ETS exposure in their homes through dust, surfaces, and air as well as in households of non-smokers who expose their children to ETS.
Abstract: Objectives: To examine (1) whether dust and surfaces in households of smokers are contaminated with environmental tobacco smoke (ETS); (2) whether smoking parents can protect their infants by smoking outside and away from the infant; and (3) whether contaminated dust, surfaces, and air contribute to ETS exposure in infants. Design: Quasi-experiment comparing three types of households with infants: (1) non-smokers who believe they have protected their children from ETS; (2) smokers who believe they have protected their children from ETS; (3) smokers who expose their children to ETS. Setting: Homes of smokers and non-smokers. Participants: Smoking and non-smoking mothers and their infants ⩽ 1 year. Main outcome measures: ETS contamination as measured by nicotine in household dust, indoor air, and household surfaces. ETS exposure as measured by cotinine levels in infant urine. Results: ETS contamination and ETS exposure were 5–7 times higher in households of smokers trying to protect their infants by smoking outdoors than in households of non-smokers. ETS contamination and exposure were 3–8 times higher in households of smokers who exposed their infants to ETS by smoking indoors than in households of smokers trying to protect their children by smoking outdoors. Conclusions: Dust and surfaces in homes of smokers are contaminated with ETS. Infants of smokers are at risk of ETS exposure in their homes through dust, surfaces, and air. Smoking outside the home and away from the infant reduces but does not completely protect a smoker’s home from ETS contamination and a smoker’s infant from ETS exposure.
408 citations
TL;DR: The existing evidence on thirdhand smoke (THS) provides strong support for pursuing a programmatic research agenda to close gaps in current understanding of the chemistry, exposure, toxicology, and health effects of THS, as well as its behavioral, economic, and sociocultural considerations and consequences.
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.
375 citations
TL;DR: The hypothesis that the subgingival biofilm is compositionally different in current and never-smokers is tested by using an open-ended molecular approach for bacterial identification, with significant differences in the prevalence and abundance of disease-associated and health-compatible organisms.
Abstract: The subgingival microbiome is largely uncultivated, and therefore, cultivation-based and targeted molecular approaches have limited value in examining the effect of smoking on this community. We tested the hypothesis that the subgingival biofilm is compositionally different in current and never-smokers by using an open-ended molecular approach for bacterial identification. Subgingival plaque from deep sites of current and never-smokers matched for disease was analyzed by 16S sequencing. Smokers demonstrated greater abundance of Parvimonas, Fusobacterium, Campylobacter, Bacteroides, and Treponema and lower levels of Veillonella, Neisseria, and Streptococcus. Several uncultivated Peptostreptococci, Parvimonas micra, Campylobacter gracilis, Treponema socranskii, Dialister pneumosintes, and Tannerella forsythia were elevated in this group, while Veillonella sp. oral clone B2, Neisseria sp. oral clone 2.24, Streptococcus sanguinis, and Capnocytophaga sp. clone AH015 were at lower levels. The microbial profile of smoking-associated periodontitis is distinct from that of non-smokers, with significant differences in the prevalence and abundance of disease-associated and health-compatible organisms.
218 citations