Abstract
To investigate the mechanism of bronchoconstriction by formaldehyde (FA), we examined the effect of FA on airway epithelial ion transport in guinea pigs. We investigated the mechanism by which formaldehyde induces bronchoconstriction and increases airway hyperreactivity in guinea pigs with experimental asthma, and evaluated the efficacy of several drugs. As a clinical study, we also investigated the effect of formaldehyde inhalation on respiratory function and airway hyperreactivity in students practing dissection, and evaluated the efficacy of disodium cromoglycate (DSCG, IntalTM).
The increment of short circuit current (Isc) was 9.42±2.84 μA/cm2 after a FA challenge of 12.5 mg/m3. DPC, DSCG, Ouabain and H-89 attenuated this increase in Isc. After a challenge with FA of 12.5 mg/m3, cAMP increased significantly. FA also activated PKA, but this activation was inhibited by PKA inhibitor H-89. Inhalation of 10 ppm of formaldehyde caused a significant increase in lung resistance. Pretreatment with DPC, H-89 and DSCG led to significant inhibition of the increase in lung resistance.
The student's PEF on leaving the anatomical laboratory was decreased by 8.9% as compared with that on entering the laboratory. Inhalation of DSCG significantly ameliorated the decrease of PEF to 2.7%. Students with asthma showed increased airway hyperreactivity after the dissection classes, but this increase in hyperreactivity could be prevented by inhalation of DSCG from the sixth week.
These findings suggest that formaldehyde induces activation of intracellular cAMP and PKA, and stimulates irritant receptors in the airways through electrophysiologic changes due to activation of the Cl channel, and that bronchoconstriction is caused by a response mediated via neurotransmitters such as acetylcholine, substance P, and neurokinin A.
These results suggest that DSCG is effective against bronchoconstriction and enhanced airway hyperreactivity due to inhalation of formaldehyde.
