Health Risks of Secondhand and Thirdhand Smoke

A special issue of Atmosphere (ISSN 2073-4433). This special issue belongs to the section "Air Quality and Human Health".

Deadline for manuscript submissions: closed (18 October 2022) | Viewed by 6629

Special Issue Editors

Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
Interests: thirdhand smoke; secondhand smoke; environmental toxicology and genotoxicology; carcinogenesis; biomarker development; DNA damage and repair; cancer biology; translational medicine

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Guest Editor
Biological Systems and Engineering Division, Lawrence Berkeley National Laboratory, Berkeley, CA 94720, USA
Interests: cancer biology; cancer genetics; environmental toxicology; thirdhand smoke; biomarker development; translational medicine
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Special Issue Information

Dear Colleagues,

Exposure to secondhand and thirdhand smoke (SHS and THS, respectively) remains widespread in many countries and affects a large population of adult and young non-smokers. Based on the U.S. Surgeon General, there is no risk-free level of SHS exposure. SHS exposure has well been documented as a risk factor for many human diseases. THS, a newly emerged smoke hazard, is defined by “the four Rs”: tobacco chemicals that remain, react, re-emit, and/or resuspended long after active smoking has ceased. Recently, its health impact has been increasingly recognized. The concept of THS as a distinct entity that poses health risks for small children has developed. We first reported that THS exposure caused significant DNA damage in human cells, and further demonstrated that early exposure to THS not only affects development, but also induces persistent changes to the immune system and lung cancer in mouse models. An increasing number of studies from many other groups have been reported using cellular and animal models as well as human subjects, which began to fill the knowledge gap in our understanding of the health risks of THS.

As found above, passive cigarette smoking causes complex biological and health responses and the mechanisms underlying them are not fully elucidated. Therefore, future in vitro and in vivo studies are needed to better understand their effects on biological systems. We believe that efforts should be made to identify and characterize novel chemical compounds in aged SHS and THS; the identification and measurement of biomarkers for SHS and/or THS exposure is also a key research area. We propose that an integrative systems biology approach will provide a comprehensive evaluation of the health effects of smoking exposure. As direct human studies linking THS to human risks and diseases are virtually impossible, model systems may serve as valuable tools. Etiological factors and genomic properties of lung cancer in never smokers is another intriguing area. It is also interesting to see what would be the potential impact of the current COVID-19 pandemic would be on SHS/THS exposure and related health issues. Ultimately, accumulating data from existing and future studies will help reduce the tobacco-related disease incidence through changes in lifestyle and tobacco control policies.

The aim of this Special Issue is to present new research articles, reviews and perspectives on the health risks of SHS and THS, with focuses on basic pathological and mechanistic findings, identification and development of exposure biomarkers, and translational studies involving   implementation of monitoring and preventive measures for such risks.

Dr. Bo Hang
Dr. Jian-Hua Mao
Guest Editors

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Keywords

  • Secondhand smoke exposure
  • Environmental smoke exposure
  • Thirdhand smoke exposure
  • Environmental toxicology
  • Health risk assessment
  • Cancer development
  • Genetic susceptibility
  • Children susceptibility
  • Risk in never-smokers
  • Biomarker development
  • Translational study
  • Tobacco control policy

Published Papers (1 paper)

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Research

19 pages, 2384 KiB  
Article
Nicotine Affects Multiple Biological Processes in EpiDermTM Organotypic Tissues and Keratinocyte Monolayers
by Giovanna L. Pozuelos, Matine Rubin, Samantha Vargas, Erik Ramirez, Dhiresh Bandaru, Jihui Sha, James Wohlschlegel and Prue Talbot
Atmosphere 2022, 13(5), 810; https://doi.org/10.3390/atmos13050810 - 16 May 2022
Cited by 3 | Viewed by 5907
Abstract
Dermal exposure to nicotine is common due to the widespread use of tobacco products. Here, we assessed the effects of nicotine at concentrations found in thirdhand smoke (THS) contaminated environments and electronic cigarette (EC) spills or leaks on a 3D human skin model [...] Read more.
Dermal exposure to nicotine is common due to the widespread use of tobacco products. Here, we assessed the effects of nicotine at concentrations found in thirdhand smoke (THS) contaminated environments and electronic cigarette (EC) spills or leaks on a 3D human skin model (EpiDermTM) and on submerged keratinocyte cultures. Air liquid interface treatment of EpiDermTM with 10 or 400 μg/mL of nicotine for 24 h followed by proteomics analysis showed altered pathways related to inflammation, protein synthesis, cell–cell adhesion, apoptosis, and mitochondrial function. Submerged cultured keratinocytes were used to validate the proteomics data and further characterize the response of skin cells to nicotine. Mitochondrial phenotype changed from networked to punctate in keratinocytes treated with 10 or 400 μg/mL of nicotine for 48 h and 24 h, respectively. After 72 h, all concentrations of nicotine caused a significant decrease in the networked phenotype. In Western blots, keratinocytes exposed to 400 μg/mL of nicotine had a significant decrease in mitofusin 2, while mitofusin 1 decreased after 72 h. The shift from networked to punctate mitochondria correlated with a decrease in mitofusin 1/2, a protein needed to establish and maintain the networked phenotype. Mitochondrial changes were reversible after a 24 h recovery period. Peroxisomes exposed to 400 μg/mL of nicotine for 24 h became enlarged and were fewer in number. Nicotine concentrations in THS and EC spills altered the proteome profile in EpiDermTM and damaged organelles including mitochondria and peroxisomes, which are involved in ROS homeostasis. These changes may exacerbate skin infections, inhibit wound healing, and cause oxidative damage to cells in the skin. Full article
(This article belongs to the Special Issue Health Risks of Secondhand and Thirdhand Smoke)
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