Eicosanoid levels in bronchoalveolar lavage fluid of young female smokers and non‐smokers

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Abstract
To evaluate indicators of inflammatory changes in the airways of young smokers we have measured the levels of several eicosanoids in bronchoalveolar lavage (BAL) fluid of 18 female smokers (age 33 ±2 years) and 9 female non‐smokers (age 29 ± 2 years) who were hospitalized for treatment not related to any pulmonary disease. In each BAL specimen the following eicosanoids were determined by radioimmunoassay: prostaglandin (PG) E2; PGF2x; 9α, 1 lβ‐PGF2, a metabolite of PGD2; 6‐keto PGF1x, a metabolite of prostacyclin; thromboxane (Tx) B2, a metabolite of TxA2; the 5‐lipoxygenase products 5‐hydroxy‐eicosa‐tetraenoic acid (HETE), leukotriene (LT) B4 and LTC4; the 12‐lipoxygenase product 12‐HETE; and the 15‐lipoxygenase product 15‐HETE. The concentrations of the cyclooxygenase products (pg ml‐1) in the BAL fluid of the non‐smokers were: PGE2 15.4±1.9, PGF2x, 7.6±1.0, 9α,11β‐PGF2 8.7±1.8, TxB2 8.8 ± 1.3, and 6‐keto PGF1α only 1.5±0.8. The concentration of the lipoxygenase products were: 15‐HETE 781 ± 200,12‐HETE 193 ± 33,5‐HETE 14.0 ± 3.1, LTC49.5±3.1, LTB46.2± 1.4. BAL fluid from smokers contained two‐ to three‐fold higher levels of TxB2 and PGF2α (P < 0.05). The levels of TxB2 and PGF2α were positively correlated to the number of package years (rs= 0.55 and rs= 0.65, P<0.02). The concentrations of 5‐, 12‐ and 15‐HETE tended to be higher in BAL fluid from smokers, but this was not significant. We conclude that in BAL fluid from females who denied pulmonary symptoms, the concentration of 12‐ and 15‐lipoxygenase products is 15 — 100‐fold higher than that of 5‐lipoxygenase or cyclooxygenase products. In these subjects smoking is associated with higher concentrations of bronchoconstrictive cyclooxygenase products and a tendency towards higher levels of 5‐, 12‐ and 15‐HETE, probably reflecting inflammatory changes in the airways. Therefore, these results indicate that smoking induces formation of the metabolites that may play a role in the development of chronic airways obstruction especially when inflammatory changes become more pronounced after greater exposure to tobacco smoke.

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