Water-Soluble Cooling Lubricants Induce Airway Hyper- responsiveness in Rabbits

Abstract

Airway hyperresponsiveness (AHR) to water-soluble cooling lubricants (CL) induced by aerosol administered by tracheal tube was studied in a rabbit model of occupational lung disease. Two commercial CL were examined: the first was of the boric acid amine ester type without biozide (CL-BAE), the second was of the sulfonate type with biozide (CL-SB). 50, 5.0 or 0.5 mg/m³ CL was administered over a period of twice 2 h to six different groups of rabbits. Airway responsiveness (AR) to aerosols of 0.2% and 2.0% acetylcholine solution (ACH) was measured before and after each exposure to CL. A control group A of nine animals not exposed to CL showed no significant respiratory responses following inhalation of 0.2% ACH for 1 min. Conversely, inhalation of 2.0% ACH almost doubled the dynamic elastance (E_dyn) in the ACH challenge test in this animal group. Airway resistance (R_I), E_dyn, slope of inspiratory pressure generation (ΔP_es/t_I), arterial pressure (P_a) and arterial blood gas tensions (P_aO₂, P_aCO₂) were not significantly altered during and after exposures to CL. However, after CL-BAE inhalation of 50 and 5 mg/m³ over 4 h, the amplitude of the ACH-induced airway obstruction indicated by the changes in E_dyn rose significantly to almost five times the control response before exposure (group C, D, p < 0.005). Similar changes in R_I and ΔP_es/t_I were obtained. After inhalation of 0.5 mg/m³ CL-BAE (group D), no significant changes in AR were observed. Similar to CL-BAE inhalation of 50 mg/m³, CL-SB caused enlarged AR in the ACH challenge test (group E), whereas no significant changes were found after exposure to 5.0 and 0.5 mg/m³ in groups F and G. In summary, CL aerosols with and without biozide in the range of 50 and 5 mg/m³ applied via tracheal tubes increased AR to ACH within 4 h of exposure in a time- and concentration-dependent manner. It has to be assumed that this augmented AR indicates an increased risk of developing lubricant-induced obstructive lung diseases.