A study1 has found that active smokers and those who are exposed to secondhand smoke are more likely to get bacterial infections. Tobacco use increases a woman’s susceptibility to bacterial vaginosis and sexually transmitted infections like chlamydia and gonorrhoea, among many other infections that are not covered in this article. It is understood that tobacco smoke reduces the function of leukocytes, allowing for the increased risk of infection.

Tobacco smoking has been significantly correlated with bacterial vaginosis, being twice as likely as in non-smokers.

     Why are smokers more susceptible to bacterial vaginosis and STIs?
Tobacco smoking can (in theory) increase infection risks via three mechanisms – causing physiological and structural changes in tissue, increasing bacterial virulence (strength), and dysregulation of the immune system. The three can occur at the same time.

Tobacco smoke, as it relates to the vagina and urinary tract, may:

  • Smoking changes the behaviour of blood vessels, tending to reduce blood flow to certain areas, including the skin. This reduces the effectiveness of the response of the body to a pathogen, giving it more of a head start.
  • Trace amounts of of a certain compound are present in vaginal secretions of women who smoke were found to promote viruses that parasitise a bacteria (bacteriophages), primarily lactobacilli. This can lead to a reduction in lactobacilli and promote the growth of anaerobes, thus facilitating bacterial vaginosis.
  • Tobacco use may be capable of affecting neutrophil and monocyte function directly and indirectly. Multiple effector functions are compromised by tobacco smoke, for example the smoke and/or nicotine have been demonstrated to reduce key antimicrobial activities such as phagocytosis, the killing of bacteria to kill phagocytosed bacteria, and thus the ability to kill certain bacteria.
  • Tobacco smoke suppresses responsiveness of cells to bacteria and lipopolysaccharide as demonstrated in the downregulation of surface pathogen recognition receptors.
  • Dendritic cells (which process antigens) are negatively affected by tobacco smoke and its constituents.
  • IgE levels are increased in smokers compared to non-smokers, with concentrations of antibacterial IgG levels reduced. This may be a key underlying mechanism of susceptibility to bacterial infection in smokers.
  1. Bagaitkar J, Demuth DR, Scott DA. Tobacco use increases susceptibility to bacterial infectionTobacco Induced Diseases. 2008;4(1):12. doi:10.1186/1617-9625-4-12.

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