Leukotriene B4 (LTB4), an arachidonic acid metabolite released by neutrophils, is involved in the regulation of the host immune response to antigenic stimulation. Furthermore, LTB4 affects the chemokinesis, aggregation, and enzyme release of neutrophils and stimulates activity of cytotoxic T cells, natural killer cells and suppressor T cells.
On the other hand, smoking typically results in inflammatory stimulation of the lung, and long-term smoking can cause chronic stimulation.
In this paper, we report the measurement of LTB4, IgG, IgA, IgM, IgD and IgE in sera of cigarette smokers who did not have an allergic reaction (group 1), non-smokers who also had no history of allergy (group 2) and non-smokers who had delicate allergic conditions (group 3). The mean LTB4 concentration in serum of group 1 was nearly 3.3-fold greater than in group 2 and 2-fold greater than in group 3, being 430±55 (Mean±S. D.), 130±22 and 220±14pg/ml, respectively. Concentrations of IgG, IgA, IgM, IgD and IgE of all volunteers were in the normal healthy range. The mean concentration of IgE in the serum of group 1 did not change significantly within one day. It was 35±4IU/ml in the morning, 34±4IU/ml in the afternoon, 31±2IU/ml in the evening and 32±4IU/ml the next morning. But in group 3 the IgE concentration changed significantly within one day, being<25IU/ml in the morning, 97±7IU/ml in the afternoon, 97±7IU/ml in the evening and 25±14IU/ml the next morning. The IgE concentration in the serum of group 2 showed the same tendency as group 3. For all groups the LTB4 concentration in the serum changed during the day, that is LTB4 in the afternoon was higher than LTB4 in the morning. But the LTB4 in the evening was almost the same as in the morning, and remained so until the next morning.
We also measured nicotine and its metabolites in each volunteer's urine. We could detect nicotine and its metabolite, cotinine in urine of group 1, and a slight quantity of nocotine in urine of group 2 and group 3.
Thus, it appears that the production and release of LTB4 are promoted by antigens which are inhaled through smoking and that LTB4 can be increased in serum by passive smoking as can IgE.
