Passive smoking by humans sensitizes circulating neutrophils

Am Rev Respir Dis. 1991 Sep;144(3 Pt 1):570-4. doi: 10.1164/ajrccm/144.3_Pt_1.570.

Abstract

The proinflammatory effects of passive inhalation of cigarette smoke were investigated by exposing a total of 16 healthy, young nonsmokers (mean age 29 +/- 1.4 yr, 11 women and five men) to actively smoking individuals in a poorly-ventilated room. Neutrophil functions were measured before and after 3 h of exposure to cigarette smoke. Passive cigarette smoking was associated with increased leukocyte counts (mean increase 33%, p less than 0.005), chemotaxis (57%, p less than 0.001), and release of reactive oxidants (71%, p less than 0.005) by stimulated neutrophils. These results were confirmed in a second study designed to eliminate the possible complicating effects of serial venepuncture. Plasma concentrations of the proinflammatory cytokines interleukin-1 (IL-1) alpha, IL-1 beta, IL-6, and tumor necrosis factor alpha (TNF alpha) were not affected by passive smoking. These results indicate that inhalation of sidestream tobacco smoke promotes systemic priming of neutrophils. These potentially proinflammatory events may induce oxidant-mediated tissue damage and carcinogenesis in the lungs of passive smokers.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Chemotaxis, Leukocyte / drug effects
  • Cotinine / urine
  • Cytochalasin B / pharmacology
  • Female
  • Humans
  • Leukocyte Count
  • Luminescent Measurements
  • Luminol / pharmacology
  • Male
  • N-Formylmethionine Leucyl-Phenylalanine / pharmacology
  • Neutrophils / immunology*
  • Neutrophils / physiology
  • Smoking / blood
  • Smoking / immunology
  • Tetradecanoylphorbol Acetate / pharmacology
  • Tobacco Smoke Pollution*
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Tobacco Smoke Pollution
  • Tumor Necrosis Factor-alpha
  • Cytochalasin B
  • N-Formylmethionine Leucyl-Phenylalanine
  • Luminol
  • Cotinine
  • Tetradecanoylphorbol Acetate