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Cited by 55Wound Healing and TreatmentsSmoking Behavior and CessationBurn Injury Management and Outcomes

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

Open access
Dhall, Sandeep, Alamat, Raquelle, Castro, Anthony, Sarker, Altaf H., Mao, Jian-Hua, Chan, Alex, Hang, Bo, Martins-Green, Manuela·2016·Clinical Science
DOI 10.1042/cs20160236
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Abstract

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 ≥3 years old living in homes of smokers are exposed to THS toxicants and show blood cotinine levels of ≥0.05 ng/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.

AI snapshot

Written from the paper’s full text.

TL;DR

In a mouse model of third hand smoke (THS) exposure, THS delayed wound closure by approximately 25% and impaired healing through oxidative stress, inflammatory dysregulation, reduced collagen/myofibroblasts, increased elastase, and defective angiogenesis with leaky vessels. The authors conclude that THS toxicants disrupt the sequential processes of normal healing and may help explain poor or reopening surgical wounds in exposed nonsmokers.

Key findings

  • THS-exposed mouse wounds closed more slowly: control wounds closed in approximately 12 days, whereas THS wounds took an average 25% more time to heal; THS wounds also had virtually no epithelial migration tongue, disrupted dermal–epidermal interactions, poorly developed granulation tissue, and significantly fewer αSMA-positive myofibroblasts at day 7 (P<0.001).
  • THS wounds showed a highly proteolytic environment: active MMP2 was significantly increased at day 1 then decreased at days 3–7, active MMP9 was higher up to day 3 then decreased by days 5 and 7, TIMP-1 was significantly reduced, and elastase activity was significantly increased.
  • Oxidative stress and molecular damage were elevated: SOD activity was significantly elevated by 4 h post-wounding and remained high during the first 7 days; H₂O₂ was elevated; GPx activity was greatly decreased during the first 3 days; catalase was unchanged; MDA increased particularly after 5 days; 3-nitrotyrosine was significantly higher after 2 days; 8-OH-dG was extremely high throughout healing; and LA-qPCR showed reduced amplification of 6.5-kb polβ and 8.7-kb β-globin fragments.
  • Inflammatory and angiogenic responses were disrupted: monocytes peaked at day 3 rather than day 1, macrophages were significantly reduced during the first 5 days, KC was lower while LIX was normal, GCSF was significantly decreased, MCP-1 was reduced, MIP-1α was normal, LIF was lower, insulin failed to elicit blood vessel sprouting in THS-exposed skin, and day 7 wounds showed fibrinogen around vessels suggesting leaky microvessels.

Methods

  • C57BL/6 mice were divided into control and THS-exposed groups starting after weaning until 24 weeks of age; THS exposure used household fabrics in cages smoked with 3R4F research cigarettes, two packs/day, 5 days/week, with total particulate matter maintained at 30 ± 5 μg/m³.
  • Full-thickness dorsal excision wounds were made with a 7 mm biopsy punch, and tissues were collected at various time points for histology, immunolabelling, zymography, ELISAs, oxidative stress assays, FACS, multiplex cytokine/chemokine analysis, in vivo angiogenesis assay, and LA-qPCR.
  • Statistical analysis used GraphPad Instat and SigmaPlot; ANOVA tested differences between two or more groups, and Student’s t test was used for two-group comparisons.

Limitations

  • Stated limitations: Not stated in the paper.
  • Evident limitations: the study is entirely in mice, and the authors only suggest that similar problems may occur in humans; no human wound-healing outcomes are reported.
  • Evident limitations: some experiments used small sample sizes, as reported in figure legends (e.g., n=3 for cytokine/chemokine arrays, n=4 for angiogenesis, n=5 for FACS/histology, n=6 for several other assays).

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1042/cs20160236

Cites

72 of 72 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

30 of 47 cited sources checked · 10 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    THS was shown to cause delayed healing.

    “Furthermore, THS was also shown to cause delayed healing [14].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [14] Martins-Green, 2014, Cigarette smoke toxins deposited on surfaces: implications for human health, PLoS One source
  • Premisecitation

    The animal model system mimics human exposure to THS.

    “We have recently developed an animal model system that mimics human exposure to THS.”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [14] Martins-Green, 2014, Cigarette smoke toxins deposited on surfaces: implications for human health, PLoS One source
  • Findingcitation

    The decrease in collagen deposition at day 7 in THS-exposed mouse wounds correlates with the reduced number of myofibroblasts.

    “The decrease in the level of collagen deposition observed at day 7 post-injury in the THSexposed mouse wounds correlates with the significantly reduced number of myofibroblasts, cells that effectively produce fibrillar collagen [39].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [39] Asakura, 2004, Leukotriene D4 stimulates collagen production from myofibroblasts transformed by TGF-beta, J. Allergy Clin. Immunol. source
  • Findingcitation

    Collagen deposition is decreased at day 7 post-injury in THS-exposed mouse wounds.

    “The decrease in the level of collagen deposition observed at day 7 post-injury in the THSexposed mouse wounds correlates with the significantly reduced number of myofibroblasts, cells that effectively produce fibrillar collagen [39].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [39] Asakura, 2004, Leukotriene D4 stimulates collagen production from myofibroblasts transformed by TGF-beta, J. Allergy Clin. Immunol. source
  • Findingcitation

    Elastase is overall increased in THS-exposed mouse wounds.

    “Additionally, the overall increase in elastase suggest a more proteolytic environment in the granulation tissue [30], which leads to elastin breakdown, a protein that is critical for elasticity of the healed tissue [47,48].”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [30] McCarty, 2012, The role of endogenous and exogenous enzymes in chronic wounds: a focus on the implications of aberrant levels of both host and bacterial proteases in wound healing, Wound Repair. Regen. source
    • cites [47] Raghunath, 1996, Fibrillin and elastin expression in skin regenerating from cultured keratinocyte autografts: morphogenesis of microfibrils begins at the dermo-epidermal junction and precedes elastic fiber formation, J. Invest. Dermatol. source

      The Patients section describes biopsies from children with burn wounds, and the elastin-formation section reports when elastin appeared after grafting; neither addresses elastase levels in THS-exposed mouse wounds. A search for elastase, THS, and mouse wounds found no supporting passage. In the citing sentence, the elastase increase is followed by [30], while [47,48] follow the separate statement about elastin and elasticity. Page numbers were not available in our copy. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [48] Almine, 2012, Elastin signaling in wound repair, Birth Defects Res. C Embryo Today source
  • Classified as probably not a substantial claim. 7
  • May combine two claims. 20

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    THS exposure causes significant damage to liver, lung and cognitive behaviour.

    “Our studies showed significant damage to liver, lung and cognitive behaviour [14].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [14] Martins-Green, 2014, Cigarette smoke toxins deposited on surfaces: implications for human health, PLoS One source

      The Introduction and Results and Discussion report liver and lung damage in THS-exposed mice, along with significantly increased activity in behavioral tests. The paper reports hyperactivity, not demonstrated damage to cognition; the claim also omits that these findings are from mice. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    THS has deleterious effects on multiple organs and delays healing of skin wounds.

    “We have recently shown that THS has deleterious effects on multiple organs and also delays healing of skin wounds [14].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [14] Martins-Green, 2014, Cigarette smoke toxins deposited on surfaces: implications for human health, PLoS One source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Significantly elevated SOD activity gives rise to increases in H2O2.

    “Significantly elevated SOD activity gives rise to increases in H 2 O 2 that if not broken down to H 2 O and O 2 by the antioxidant enzymes, GPx and catalase, lead to increase in oxidative stress [53].”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [53] Buettner, 2011, Superoxide dismutase in redox biology: the roles of superoxide and hydrogen peroxide, Anticancer Agents Med. Chem. source

  • May combine two claims.

    Interpretationcitation

    The increase in elastase suggests a more proteolytic environment in the granulation tissue, leading to elastin breakdown.

    “Additionally, the overall increase in elastase suggest a more proteolytic environment in the granulation tissue [30], which leads to elastin breakdown, a protein that is critical for elasticity of the healed tissue [47,48].”
    Quote in the paperSubstantial claim1 of 3 sources checked
    • cites [30] McCarty, 2012, The role of endogenous and exogenous enzymes in chronic wounds: a focus on the implications of aberrant levels of both host and bacterial proteases in wound healing, Wound Repair. Regen. source
    • cites [47] Raghunath, 1996, Fibrillin and elastin expression in skin regenerating from cultured keratinocyte autografts: morphogenesis of microfibrils begins at the dermo-epidermal junction and precedes elastic fiber formation, J. Invest. Dermatol. source

      The section on elastin deposition describes elastin appearing in regenerating skin and associating with fibrillin-containing microfibrils. Searches for elastase, granulation-tissue proteolysis, and elastin breakdown found no passage addressing the proteolytic environment attributed to this source. No page number was available in our copy. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [48] Almine, 2012, Elastin signaling in wound repair, Birth Defects Res. C Embryo Today source

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Doctors avoid performing surgery on patients who smoke due to known complications in clot formation, healing times and the quality of healing.

    “Doctors avoid performing surgery on patients who smoke due to known complications in clot formation, healing times and the quality of healing [12,38].”
    Quote in the paperNot a substantial claim1 of 2 sources checked
    • cites [12] Sorensen, 2003, Abstinence from smoking reduces incisional wound infection: a randomized controlled trial, Ann. Surg. source

      The Discussion (page unavailable) reports more incisional wound infections and ruptures in smokers than in never-smokers, supporting the claim that smoking compromises surgical wound healing. The paper does not establish that doctors avoid operating on smokers, or report complications in clot formation or healing times. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [38] Hunt, 2000, Physiology of wound healing, Adv. Skin Wound Care

  • May combine two claims.

    Premisecitation

    LIF is critical for monocyte maturation into macrophage and for proper formation of granulation tissue.

    “Furthermore, we show that there is an overall reduced level of the interleukin 6 class protein LIF; this cytokine is critical for monocyte maturation into macrophage and for proper formation of the granulation tissue [64].”
    Quote in the paperSubstantial claim1 of 1 sources checked
    • cites [64] Nicola, 2015, Leukemia inhibitory factor (LIF), Cytokine Growth Factor Rev source

      The hemopoietic-system section discusses LIF’s limited effects on blood-forming cells but does not address monocyte maturation into macrophages. The neuromuscular-system section describes muscle regeneration after injury, not granulation-tissue formation. Searches for monocyte-to-macrophage maturation and granulation tissue found no passage supporting either attributed role. (LLM, conf=0.73)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Findingown data

    Active MMP2 levels in THS-exposed mouse wounds are increased significantly at day 1 but then decrease at days 3-7.

    “We found that the levels of active MMP2 in the THSexposed mouse wounds is increased significantly at day 1 but then decreases at days 3-7 (Figure 3A, arrowhead).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    SOD activity in THS-exposed mouse wounds is significantly elevated by 4 h post-wounding and remains high during the first 7 days.

    “SOD activity, an enzyme that is critical in the dismutation of superoxide anions to H 2 O 2 , was already greatly significantly elevated by 4 h post-wounding when compared with the control wounds (Figure 4A).These levels remained high during the first 7 days post-wounding.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Injection of insulin subcutaneously resulted in development of many sprouting microvessels in control mice but was unable to elicit sprouting of blood vessels in THS-exposed mouse skin.

    “We found that injection of insulin subcutaneously resulted in the development of many sprouting microvessels in the skin of control mice but that insulin was unable to elicit sprouting of the blood vessels in the THS-exposed mouse skin (Figures 8A and 8B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    THS-exposed mice display delayed wound closure, with wounds taking on average 25% more time to heal than control wounds (which closed in approximately 12 days).

    “We show that mice living under conditions that mimic THS exposure in humans display delayed wound closure”
    • Also stated in: § Impaired healing in THS-exposed mouse wounds · plain
      “The control wounds closed in approximately 12 days whereas the THS mouse wounds took an average 25 % more time to heal (Figures 1A and 1B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    In THS-exposed mice, epidermal cells do not form the normal epidermal tongue that moves over granulation tissue to cover the wound and do not form adhesions with underlying dermis or proper basement membrane deposition.

    “The epidermal cells do not form the normal epidermal tongue that moves over the granulation tissue to cover the wound and does not form adhesions with the underlying dermis as well as proper deposition of the basement membrane to establish firm connections.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    THS increases blood vessel leakage and clot formation.

    “In the present study we show that THS delays wound healing by delaying wound closure, increasing oxidative stress and its associated tissue damages, causing an imbalance in chemokines and cytokines that result in decreasing/delaying the inflammatory response, decreasing collagen deposition, decreasing angiogenesis and increasing blood vessel leakage and clot formation.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    Lack of elastin results in loss of wound plasticity, which may be responsible for reopening of wounds.

    “In addition, the lack of elastin results in loss of wound plasticity, which may be responsible for reopening of wounds.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    The granulation tissue of THS-exposed wounds has lower elastic properties than normal and might be susceptible to reopening.

    “THS-exposed wound has lower elastic properties than normal and therefore might therefore be susceptible to reopening.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    THS toxicants affect the normal physiology of the skin and elevate stress levels even in the absence of wounding.

    “suggesting that the toxicants of THS affect the normal physiology of the skin and elevate stress levels even in the absence of wounding (Figure 4B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    The microenvironment of THS-exposed mouse wounds does not promote monocyte to macrophage differentiation, and the macrophage inflammatory phase is defective.

    “These results strongly suggest that the microenvironment of the THS-exposed mouse wounds does not promote monocyte to macrophage differentiation, a critical aspect of the inflammatory response and that the macrophage inflammatory phase is defective.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    THS becomes more toxic and potentially more harmful than fresh SHS with time.

    “This causes THS to become more toxic and potentially more harmful than fresh SHS with time [6].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [6] Sleiman, 2010, Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards, Proc. Natl. Acad. Sci. U.S.A. source

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    First hand smoke (FHS) and second hand smoke (SHS) cause impaired healing.

    “First hand smoke (FHS) and second hand smoke (SHS) have previously been reported to cause impaired healing [34][35][36][37].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [34][35][36][37]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationcitation

    ROS increases could inhibit pro-peptide cleavage by reacting with cysteine in the pro-peptide.

    “Furthermore, it is also possible that the increases in ROS levels we observe during the inflammatory phase of the THS-exposed mouse wounds could inhibit the pro-peptide cleavage by reacting with cysteine in the pro-peptide [44][45][46].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [44][45][46]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationown data

    Other TIMPs not included in the experiments might explain the low levels of MMP2 and 9 in THS-exposed mice.

    “However, the low levels of active MMP2 and 9 did not correlate with the lower levels of TIMP-1 we observed, suggesting that other TIMPs not included in our experiments might explain the low levels of MMP2 and 9.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Short term cessation of smoking does not effectively reduce the risk and complications during wound healing after surgery.

    “reports have also suggested that short term cessation of smoking does not effectively reduce the risk and complications during wound healing after surgery [13].”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [13] Sorensen, Short-term pre-operative smoking cessation intervention does not affect postoperative complications in colorectal surgery: a randomized clinical trial, Color Dis source

  • May combine two claims.

    Interpretationown data

    THS toxins deposited on the skin lead to detrimental effects and predispose the tissue to initiate improper healing after injury.

    “The significant increases in tissue damage observed in unwounded skin suggests that the THS toxins deposited on the skin lead to detrimental effects and also predispose the tissue to initiate a course of improper healing after injury.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    Elastase levels are elevated which reduces elastin, decreasing wound plasticity, which may be responsible for reopening of wounds.

    “Moreover, elastase levels are elevated which reduces elastin, decreasing wound plasticity, which may be responsible for reopening of wounds.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    Lower levels of macrophages could result in impairment of clearance of dead neutrophils and debris and altered production of factors that stimulate proper healing.

    “These lower levels of macrophages could result in impairment of the clearance of dead neutrophils and of debris from the wound tissue and in altered production of factors that stimulate proper healing.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationown data

    The mechanisms involved in THS-induced poor wound healing include delayed rate of healing, increased oxidative stress, impaired inflammation, improper cytokine/chemokine balance and abnormal angiogenesis.

    “We delineate for the first time the mechanisms involved in THS-induced poor wound healing.They involve delayed rate of healing, increased oxidative stress, impaired inflammation, improper cytokine/chemokine balance and abnormal angiogenesis, driving the pathogenesis of impaired wound healing.”
    Quote in the paperSubstantial claim
25 of 25

  • The paper relies on this without support.

    The cell and molecular mechanisms associated with the development of impaired wounds have not been studied.

    “However, the cell and molecular mechanisms associated with the development of impaired wounds has not been studied.”

  • The paper relies on this without support.

    Mouse wound healing responses are representative of human wound healing responses.

    “Our findings in the present study delineate the impact of THS on wound healing processes in mice and suggest the occurrence of similar problems in humans exposed to THS.”

  • The paper relies on this without support.

    THS is a stealth 'toxin' that permeates the homes of smokers and affects infants, children, spouses of smokers and elderly living in that environment.

    “This is particularly important because THS is a stealth 'toxin' that permeates the homes of smokers and affects infants, children, spouses of smokers and elderly living in that environment.”

  • The paper relies on this without support.

    The effects of THS on healing are not well known.

    “However, the effects of THS on healing are not well known.”

  • The paper relies on this without support.

    The underlying cell and molecular mechanisms that lead to THS-induced impaired healing are not known.

    “However, the underlying cell and molecular mechanisms that lead to THS-induced impaired healing are not known.”
5 of 5

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Hydrogen peroxide assay has two reported emission wavelengths

    Minor

    The methods say fluorescence was measured at an emission wavelength of 590 nm, whereas Figure 4 reports 605 nm for the same assay.

  • TBARS is described as measuring 8-OH-dG despite its stated lipid-peroxidation target

    Minor

    The discussion says the TBARS assay detected 8-OH-dG. The methods instead describe TBARS as a lipid-peroxidation assay quantified against an MDA standard curve; 8-OH-dG is measured with a separate assay.

  • Monocyte-marker antibody has conflicting fluorophore labels

    Minor

    The methods specify CD11c PE-eFluor®610 for monocyte analysis, but the Figure 6 caption specifies CD11c Alexa Fluor®532.

  • The same chemokine is assigned two different identifiers

    Minor

    The results identify MIP-1α as CCL3, then refer to it as CXCL2 in the same paragraph.

4 of 4

Cites

Flagged first, then by citations

Research works printed but not linked: 1

  1. Guo, 2010, Factors affecting wound healing, J. Dent. Res., 89, 219, 10.1177/0022034509359125 · DOI · Paper page

Cited by

Sorted by citations

Related

Authors
Dhall, S., Alamat, R., Castro, A., Sarker, A. H., Mao, J.-H., Chan, A., Hang, B., & Martins-Green, M.
Affiliations
  • University of California, Riverside (US)
  • Lawrence Berkeley National Laboratory (US)
  • Department of Cell Biology and Neuroscience, University of California at Riverside, Riverside, CA 92521, U.S.A.
Corresponding author
  • Dhall, Sandeep
  • Alamat, Raquelle
  • Castro, Anthony
  • Chan, Alex
ORCID
Venue
Clinical Science
Publisher
Portland Press Ltd.
Published
2016-06-13
Volume
130
Issue
14
Pages
1269-1284
ISSN
  • 0143-5221 (ISSN-L)
  • 1470-8736
DOI
10.1042/cs20160236
OpenAlex
W2344368835
Semantic Scholar
6ec5434680fb09f8af9911803c3814fc35e75839
Cited by
55
References
71
Citations by year
2026: 5 · 2025: 1 · 2024: 6 · 2023: 4 · 2022: 8 · 2021: 7 · 2020: 9 · 2019: 5 · 2018: 5 · 2017: 4 · 2016: 1
FWCI
4.49
Type
journal article
Language
en
Open access
Locations
  • Clinical Science (publishedVersion)
  • PubMed (publishedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
University of California, Riverside
Topics
  • Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
  • Health Sciences › Medicine › Physiology › Smoking Behavior and Cessation
  • Health Sciences › Medicine › Epidemiology › Burn Injury Management and Outcomes
Keywords
thirdhand smoke, wound healing, collagen deposition, oxidative stress, protein nitration, lipid peroxidation, DNA damage, elastase, elastin degradation, angiogenesis, inflammation, fibrin, cotinine, non-smokers
MeSH terms
Animals, Capillary Permeability, Collagen, Mice, Inbred C57BL, Nicotiana, Tobacco Smoke Pollution, Wound Healing, Oxidative Stress, Neovascularization, Physiologic, Chemokines, Tissue Inhibitor of Metalloproteinase-1, Mice

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