Association of volatile aromatic compounds in blood with hearing impairment

By Pooja Toshniwal PahariaMar 1 2024Reviewed by Lily Ramsey, LLM

In a recent study published in BMC Public Health, researchers evaluated the impact of benzene, ethylbenzene, and xylene (BEX) exposure on auditory health among United States (US) adults.

Study: Association between blood volatile organic aromatic compound concentrations and hearing loss in US adults. Image Credit: Ground Picture/Shutterstock.com

Background

Hearing loss (HL) is associated with financial hardships, an increased risk of diseases such as Alzheimer's disease and dementia, and communication difficulties.

There are few effective hearing loss (HL) treatments, highlighting the need for developing prevention strategies. Ototoxic processes and trace heavy metals are HL risk factors. The link between environmental contaminants in human blood and HL is unclear.

The concentration of polycyclic aromatic hydrocarbons (PAHs) in urine correlates with HL frequency across ages. However, using organic solvents in urine as HL biomarkers has limitations due to their short biological half-lives and varied metabolism.

BEX chemicals, a significant component of volatile-type organic aromatic compounds (VOACs), are recognized as carcinogens by the International Agency for Research on Cancer, causing reproductive dysfunction, asthma, leukemia, benzene poisoning, immune suppression, splenic damage, and premature birth.

About the study

The present study researchers comprehensively explored the link between BEX concentration in blood and hearing impairment among US adults.

The researchers analyzed the National Health and Nutrition Examination Survey (NHANES) data for 2003-2004, 2011-2012, and 2015-2016, including demographics, VOAC exposure, and audiometry measurements.

They performed weighted multivariable logistic regression modeling to determine the odds ratios (ORs) for the relationship between BEX concentration in blood with high-frequency HL (HFHL) and speech-frequency HL (SFHL).

Study covariates included age, sex, race, ethnicity, body mass index (BMI), marital status, education level, smoking habits, drinking status, diabetes, hypertension, and household income.

The team used the Linden and Jerger classification to define peak middle ear pressures as type C (<99 daPa), type B (0.2 compliance value), and other pressures as type A.

They analyzed participant blood samples at mobile examination centers (MECs) using mass spectrometry (MS), capillary gas chromatography (GC), selected ion monitoring (SIM), and isotope dilution methods.

Trained examiners conducted audiometry examinations, defining hearing loss as pure-tone averages exceeding 25 dB in both ears.

They conducted SFHL assessments at frequencies of 500, 1,000, 2,000, and 4,000 Hz and HFHL evaluations at 3,000, 4,000, 6,000, and 8,000 Hz.

The team conducted sensitivity analyses to examine the relationship between BEX and hearing loss, reclassifying individuals into three levels based on average hearing threshold, excluding those aged >40 years, and extracting serum cotinine data from NHANES to quantify tobacco smoke exposure.

The team excluded individuals below 20 or above 60 years with tympanometric type B or C in one or both ears.

They also excluded individuals with missing data for VOACs such as benzene, ethylbenzene, o-xylene, m/p-xylene, family income-poverty ratio (PIR), and marital status.

Further, they excluded individuals prescribed hydrocodone, acetaminophen, phenytoin, ciprofloxacin, rifampin, levofloxacin, aspirin, minocycline, bumetanide, nitroglycerin, or metronidazole from the study.

Study participants did not suffer from cerumen or collapsing external ear canals, did not use hearing aids, or suffered from Parkinson’s disease.

Results

The study included 2,174 participants with a mean age of 39 years and weighted prevalences of HL, HFHL, and SFHL, being 47% (n=995), 46% (n=973), and 25% (n=513), respectively.

Individuals with advanced age, male gender, married status, higher BMI, educational attainment, occupational noise exposure, smoking history, alcohol use, diabetes, and hypertension had higher hearing impairment prevalence than those with no impairment.

However, the dose-response assessments indicated increased risk among older females with weight in the normal range.

Benzene, ethylbenzene, ortho-xylene, and para/meta-xylene exposures and cumulative BEX concentrations elevated hearing impairment risk with ORs of 1.4, 1.2, 1.2, 1.4, and 1.3, respectively). 

Concerning the SFHL endpoint, benzene, ethylbenzene, ortho-xylene, para/meta-xylene, and cumulative BEX concentrations elevated the risk with ORs of 1.2, 1.3, 1.3, 1.2, and 1.3, respectively.

For HFHL, benzene, ethylbenzene, ortho-xylene, para/meta-xylene, and cumulative BEX exposures increased hearing impairment risk with ORs of 1.2, 1.4, 1.4, 1.2, and 1.3, respectively.

Surprisingly, the correlation between HL severity and BEX concentration was positive for HL and HFHL, not SFHL. Sensitivity analyses yielded similar findings, indicating the robustness of the primary results.

Low doses of benzene can activate cellular oxidative stress, contributing to hearing loss. Obesity may lower the risk of hearing impairment induced by BEX by altering insulin-like growth factor (IGF-1) levels.

Prolonged progesterone and estrogen stimulation in females can elevate hearing thresholds and negatively impact hearing. The team hypothesizes that BEX may disrupt the female endocrine system, with compensatory increases in estrogen outweighing the protective benefits.

Conclusions

The study findings showed a positive association between BEX exposure and hearing impairment (HL, HFHL, and SFHL) risk among American adults.

Future studies could elucidate the mechanisms underlying BEX-related hearing impairment and validate findings from longitudinal environmental research.