Longitudinal Assessment of Hearing Loss in World Trade Center-Exposed Responders
- Institution
- ALBERT EINSTEIN COLLEGE OF MEDICINE, NY
- Principal investigator
- David G Goldfarb
- Funding
- $251K
- Duration
- 2025–2027
Moonbase score
Still being scored
Abstract
Project Summary The World Trade Center (WTC) disaster exposed responders to extreme noise from collapsing structures and prolonged recovery operations, with limited hearing protection.1,2 This exposure was further intensified by toxic dust and chemicals, which may have triggered metabolic and inflammatory responses, potentially affecting both lung function and sensorineural hearing loss (HL).3,4 While noise exposure is a well-established cause of HL, emerging evidence suggests that other factors, such as obstructive airways disease (OAD),5 a condition strongly associated with WTC dust exposure, may also contribute to hearing impairment.6-11 Previous research has shown that Fire Department of the City of New York (FDNY) responders who were heavily involved in rescue and recovery efforts exhibited increased HL, with reductions in hearing sensitivity persisting for 15 years post- disaster, affecting both low and high frequencies.12 These changes extend beyond the typical impacts of noise exposure,13 suggesting a unique pattern of hearing damage linked to complex exposures at the WTC site.14 Moreover, the observed HL involves frequencies not usually affected by noise alone, indicating that chemical and inflammatory factors may play a significant role. The proposed research aims to investigate HL among WTC- exposed FDNY responders, specifically focusing on the relationship between lung function and HL progression. To date, investigations have been limited by the absence of data on other WTC-related health conditions, such as OAD and lung function decline, and by the lack of an external comparison group. This proposal seeks to overcome these limitations by leveraging comprehensive spirometry and audiometry datasets to examine the relationship between pulmonary function decline and HL. WTC exposure is known to cause both immediate and chronic declines in lung function due to toxic exposures that trigger oxidative stress and inflammation.4,15-17 This study will explore whether these pulmonary function changes are associated with progressive HL among WTC responders. Additionally, we will strengthen our findings by comparing the WTC-exposed cohort with a large non- WTC-exposed, high-risk occupational cohort with longitudinal audiometry data. This comparison will help to distinguish the effects of WTC-specific exposures from industry-related risk factors and the healthy worker effect.18 We will also explore if FDNY responders with abnormal spirometry, indicative of OAD, are at higher risk for HL compared to those in the external cohort, enhancing our understanding of the interplay between lung health and auditory outcomes. The primary goal of this research is to elucidate a key mechanism contributing to HL in WTC-exposed responders and to identify specific subgroups that may benefit from targeted interventions. While there are no current pharmacologic treatments to reverse HL, managing lung function decline could potentially delay its onset. If a link is found between a reduced rate of pulmonary function decline and better hearing outcomes, early monitoring and intervention for lung health could help prevent HL, potentially reducing the future need for hearing aids among WTC responders.
Research team
- Jaeun ChoiPI
- David G GoldfarbPI
- Rachel Zeig-OwensPI
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