Abstract

Background: Oxidative stress, inflammation, and hypoxia, which are associated with chronic obstructive pulmonary disease (COPD) may contribute to auditory impairment. Aims and Objectives: The present study was undertaken to assess the brainstem auditory evoked potential (BAEP) of smokers and non-smokers with or without COPD.
Materials and Methods: The study comprised smokers with (n = 25) or without COPD (n = 15) and also healthy non-smokers (n = 30). Oxidative stress was assessed by malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP). Pulmonary functions were determined. Data were analyzed using ANOVA and Pearson’s correlation tests. P < 0.05 was considered statistically significant.
Results: Spirometric values were significantly lower in COPD group in comparison with other two groups. Oxidant/antioxidant imbalance was more in smokers with COPD. BAEP result (both right and left ear) showed no significant difference between non-smokers and smokers without COPD in Wave I (P = 0.885 and 0.085, respectively) and in wave II (P = 0.554 and 0.396, respectively). Significant difference (both ears) was found between non-smokers and smokers with and without COPD in waves III, IV, V, and IPL I-V. MDA showed significant negative and positive correlations with FRAP, wave latencies, and IPL. Significant negative correlation was found between pack years and FRAP. However, non-significant positive correlation was found with MDA. Significant positive correlation was found between pack years and wave latencies III, IV, and V and interpeak latency I-V in both ears. Conclusion: Smoking-induced oxidative stress as well as increased susceptibility to COPD, which in turn led to hypoxia and effects the auditory mechanisms and these are responsible for BAEP abnormalities.