Environmental factors, such as exposure to chemical toxins (e.g. second-hand and third-hand smoke, pollution, pesticides, toxic metals, food toxins) or medical x-rays (e.g. mammograms, CT-scans) and infection by some bacteria and viruses (e.g. Helicobacter pylori, HIV, human papillomavirus) have been shown to impact your DNA damage levels. Below are select lists of online references and scientifiic peer-reviewed articles showing just a few examples. Please note that Exogen does not endorse any specific diet, activity, or product that may be listed.

 

Selected Online References

  • Negritto, M. C. (2010) Repairing Double-Strand DNA Breaks. Nature Education 3(9):26. http://www.nature.com/scitable/topicpage/repairing-double-strand-dna-breaks-14432332.
    “The genome of a cell is continuously damaged, which is inevitable because DNA damage often arises as a result of normal cellular processes. By-products of the cell’s own metabolism such as reactive oxygen species can damage DNA bases and cause lesions that can block progression of replication. The result is double-strand breaks (DSBs) in the chromosome. A DSB can also be caused by environmental exposure to irradiation, other chemical agents, or ultraviolet light (UV).”
 
 

Selected Scientific Peer-Reviewed Articles

  • Hang et al., “Thirdhand smoke causes DNA damage in humans.Mutagenesis, 2013.
    “Exposure to thirdhand smoke (THS) is a newly described health risk. Evidence supports its widespread presence in indoor environments… 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.”
  • Toyooka et al., “Cigarette sidestream smoke induces phosphorylated histone H2AX.Mutat Res, 2009.
    “CSS (Cigarette sidestream smoke) in fact induced DSBs (DNA double-strand breaks), which was also inhibited by NAC (N-acetylcysteine – antioxidant). DSBs are the worst type of DNA damage, related to genomic instability and carcinogenesis. Our results would increase the evidence of the strong genotoxicity of passive smoking.”
  • Urcan et al., “Induction of DNA double-strand breaks in primary gingival fibroblasts by exposure to dental resin composites.Biomaterials, 2010.
    “Our results for the first time show that exposure to dental resin monomers can induce DSBs (DNA double-strand breaks) in primary human oral cavity cells, which underscores their genotoxic capacity.”
  • Msiska et al., “DNA double-strand breaks by asbestos, silica, and titanium dioxide.” Am J Respir Cell Mol Biol, 2010.
    “A study was undertaken to compare the induction of DNA DSBs (double-strand breaks) in normal (small airway epithelial) cells and cancer cells (A549) after exposure to asbestos (crocidolite), a proven carcinogen, silica, a suspected carcinogen, and titanium dioxide (TiO(2)), an inert particle recently reported to be carcinogenic in animals. The results indicate that crocidolite induced greater DNA DSBs than silica and TiO(2), regardless of cell type… Cell viability assay indicated that crocidolite caused the greatest cytotoxicity in both cell types… The results of this study indicate that crocidolite has a greater carcinogenic potential than silica and TiO(2), judged by its ability to cause sustained genomic instability in normal lung cells.”
  • Woźniak et al., “In vitro genotoxicity of lead acetate: induction of single and double DNA strand breaks and DNA-protein cross-links.Mutat Res, 2003.
    “Lead is a ubiquitous environmental pollutant that can induce toxic effects in several biological systems… The results obtained suggest that lead acetate may induce single-strand breaks (SSB) and double-strand breaks (DSB) in DNA as well as DNA–protein cross-links.”
  • Calderón-Garcidueñas et al., “DNA damage in nasal respiratory epithelium from children exposed to urban pollution.Environ Mol Mutagen, 1997.
    “The present study documents the results of the single cell gel electrophoresis assay in detecting DNA damage in nasal respiratory epithelium of two groups of elementary school children, a group from a low-polluted Pacific coastal area and a highly exposed group from Southwest Metropolitan Mexico City… In our study, children living in a low-polluted environment had significantly less DNA nasal damage than SWMMC children.”
  • Mondal et al., “Micronucleus formation, DNA damage and repair in premenopausal women chronically exposed to high level of indoor air polution exposed from biomass fuel use in rural India.Mutat Res, 2010.
    “Thus, chronic exposure to biomass smoke causes chromosomal and DNA damage and upregulation of DNA repair mechanism.”
  • Toller et al., “Carcinogenic bacterial pathogen Helicobacter pylori triggers DNA double-strand breaks and a DNA damage response in its host cells.PNAS, 2011.
    “The bacterial pathogen Helicobacter pylori chronically infects the human gastric mucosa and is the leading risk factor for the development of gastric cancer. In this study, we examined the possibility that H. pylori directly compromises the genomic integrity of its host cells. We provide evidence that the infection introduces DNA double-strand breaks (DSBs) in primary and transformed murine and human epithelial and mesenchymal cells.
  • Pickering et al., “Rb inactivation leads to E2F1-mediated DNA double-strand break accumulation.” Oncogene, 2006.
    “Expressing the E7 protein of the human papillomavirus (HPV) inactivates the RB family of proteins and induces genomic instability.” “We found that specifically depleting pRb using RNAi, or inactivating RB family members by expressing E7, resulted in DSB (double-strand break) accumulation in normal human cells.
  • Tachiwana et al., “HIV-1 Vpr induces DNA double-strand breaks.Cancer Res, 2006.

    Here, we report that HIV-1 infection causes double-strand breaks in chromosomal DNA. We further found that Vpr, an accessory gene product of HIV-1, is a major factor responsible for HIV-1–induced double-strand breaks.”
  • Colin et al., “DNA double-strand breaks induced by mammographic screening procedures in human mammary epithelial cells.Int J Radiat Biol, 2011.
    “This study highlights the existence of DSB (DNA double-strand breaks) induced by mammography and revealed by γH2AX assay with two major radiobiological effects occurring: A low-dose effect, and a Low and Repeated Dose (LORD) effect”.
  •  Beels et al., ”
    γ-H2AX Foci as a Biomarker for Patient X-Ray Exposure in Pediatric Cardiac Catheterization. are we underestimating radiation risks?Circulation, 2009.
    ” In each patient, a net increase in gamma-H2AX foci, representing DNA double-strand breaks induced by interventional x-rays, was observed.”