Chemicals, noise and occupational hearing health in South Africa: A mapping study.

BACKGROUND: Chemical exposure leading to ototoxicity is a fresh challenge for occupational healthcare in South Africa. OBJECTIVES: The critical question is: 'what is known about occupational ototoxic chemicals with or without noise exposure in South Africa?' METHOD: This qualitative, mapping study was completed with published (peer-reviewed) and grey literature from 1979-2019. Data was analysed using the Preferred Reporting Items for Systematic reviews and Meta-Analyses: extension for Scoping Reviews and the Nursing and Allied Health Resources Section subcommittee on Mapping the Literature of Nursing and Allied Health (adapted). Numerical analysis of article type was completed, but the primary focus was on capturing patterns/trends using thematic analysis and ideology critique. RESULTS: The African Journal of Disability, African Journal of Primary Health Care and Family Medicine, South African Medical Journal, The South African Journal of Communication Disorders [SAJCD] and Health SA Gesondheid) were included with the SAJCD containing one relevant item and seventeen other items were analysed. Research focusses on the mining sector (gold) in Gauteng, and ototoxic medication (tuberculosis and/or human immunodeficiency virus) take precedence. In KwaZulu-Natal, the focus is on commerce and industry across formal and informal sectors. There are no governmental policies that refer to chemical ototoxicity. Occupational hearing loss is configured exclusively on the meme that noise exposure is the only toxin. CONCLUSION: Chemical exposures are only just beginning to be recognised as ototoxic in South Africa. Hearing conservation programmes should always serve the workers' interests and never bow down to the econometric interests of employers.

Disruption of Gap Junction-Mediated Intercellular Communication in the Spiral Ligament Causes Hearing and Outer Hair Cell Loss in the Cochlea of Mice.

It is well-known that outer hair cell (OHC) loss occurs in the cochlea of animal models of permanent hearing loss induced by intense noise exposure. Our earlier studies demonstrated the production of hydroxynonenal and peroxynitrite, as well as the disruption of gap junction-mediated intercellular communication (GJIC), in the cochlear spiral ligament prior to noise-induced sudden hearing loss. The goal of the present study was to evaluate the mechanism underlying cochlear OHC loss after sudden hearing loss induced by intense noise exposure. In organ of Corti explant cultures from mice, no significant OHC loss was observed after in vitro exposure to 4-hydroxynonenal (a product of lipid peroxidation), H2O2, SIN-1 (peroxynitrite generator), and carbenoxolone (a gap junction inhibitor). Interestingly, in vivo intracochlear carbenoxolone injection through the posterior semicircular canal caused marked OHC and hearing loss, as well as the disruption of gap junction-mediated intercellular communication in the cochlear spiral ligament. However, no significant OHC loss was observed in vivo in animals treated with 4-hydroxynonenal and SIN-1. Taken together, our data suggest that disruption of GJIC in the cochlear lateral wall structures is an important cause of cochlear OHC loss in models of hearing loss, including those induced by noise.

Assessing ototoxicity due to chronic lead and cadmium intake with and without noise exposure in the mature mouse.

Exposure to heavy metals may lead to hearing impairment. However, experimental studies have not explored this issue with and without noise exposure in mature animals with environmentally relevant doses. The aim of this study was to investigate ototoxicity produced by lead (Pb) and cadmium (Cd) and noise, singly and in combination, in the adult CBA/CaJ mouse. Metals were delivered via drinking water (0.03 mM, 1 mM, and 3 mM Pb; or 30, 100, and 300 µM Cd) for 12 weeks, resulting in environmentally- and occupationally relevant mean (± standard deviations) blood levels of Pb (2.89 ± 0.44, 38.5 ± 4.9, and 60.1 ± 6.6 µg/dl, respectively) and Cd (1.3 ± 0.23, 6.37 ± 0.87, 27.2 ± 4.1 µg/L, respectively). Metal treatment was also combined with a noise exposure consisting of a 105 dB broadband (2-20 kHz) stimulus for 2 hr or a sham exposure. Auditory performance was determined by comparing auditory brainstem responses (ABR) and distortion product otoacoustic emissions (DPOAE) at baseline and after 11 weeks of metal treatment. Metal-exposed animals did not develop significant auditory deficits and did not exhibit morphological damage to cochlear hair cells. In contrast, noise-exposed animals, including those exposed to combinations of metals and noise, demonstrated significant hair cell loss, reduced DPOAE amplitudes, and ABR threshold shifts of 42.2 ± 13 dB at 32 kHz (105 dB noise alone). No significant potentiation or synergistic effects were found in groups exposed to multiple agents. This study establishes a highly reproducible adult mouse model that may be used to evaluate a variety of environmental exposure mixtures.

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss.

Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8-12 dB and 11-25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18-30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways.

CDK2 inhibitors as candidate therapeutics for cisplatin- and noise-induced hearing loss.

Hearing loss caused by aging, noise, cisplatin toxicity, or other insults affects 360 million people worldwide, but there are no Food and Drug Administration-approved drugs to prevent or treat it. We screened 4,385 small molecules in a cochlear cell line and identified 10 compounds that protected against cisplatin toxicity in mouse cochlear explants. Among them, kenpaullone, an inhibitor of multiple kinases, including cyclin-dependent kinase 2 (CDK2), protected zebrafish lateral-line neuromasts from cisplatin toxicity and, when delivered locally, protected adult mice and rats against cisplatin- and noise-induced hearing loss. CDK2-deficient mice displayed enhanced resistance to cisplatin toxicity in cochlear explants and to cisplatin- and noise-induced hearing loss in vivo. Mechanistically, we showed that kenpaullone directly inhibits CDK2 kinase activity and reduces cisplatin-induced mitochondrial production of reactive oxygen species, thereby enhancing cell survival. Our experiments have revealed the proapoptotic function of CDK2 in postmitotic cochlear cells and have identified promising therapeutics for preventing hearing loss.

The glucocorticoid antagonist mifepristone attenuates sound-induced long-term deficits in auditory nerve response and central auditory processing in female rats.

Systemic corticosteroids have been the mainstay of treatment for various hearing disorders for more than 30 yr. Accordingly, numerous studies have described glucocorticoids (GCs) and stressors to be protective in the auditory organ against damage associated with a variety of health conditions, including noise exposure. Conversely, stressors are also predictive risk factors for hearing disorders. How both of these contrasting stress actions are linked has remained elusive. Here, we demonstrate that higher corticosterone levels during acoustic trauma in female rats is highly correlated with a decline of auditory fiber responses in high-frequency cochlear regions, and that hearing thresholds and the outer hair cell functions (distortion products of otoacoustic emissions) are left unaffected. Moreover, when GC receptor (GR) or mineralocorticoid receptor (MR) activation was antagonized by mifepristone or spironolactone, respectively, GR, but not MR, inhibition significantly and permanently attenuated trauma-induced effects on auditory fiber responses, including inner hair cell ribbon loss and related reductions of early and late auditory brainstem responses. These findings strongly imply that higher corticosterone stress levels profoundly impair auditory nerve processing, which may influence central auditory acuity. These changes are likely GR mediated as they are prevented by mifepristone.-Singer, W., Kasini, K., Manthey, M., Eckert, P., Armbruster, P., Vogt, M. A., Jaumann, M., Dotta, M., Yamahara, K., Harasztosi, C., Zimmermann, U., Knipper, M., Rüttiger, L. The glucocorticoid antagonist mifepristone attenuates sound-induced long-term deficits in auditory nerve response and central auditory processing in female rats.

Hearing loss, lead (Pb) exposure, and noise: a sound approach to ototoxicity exploration.

To determine the state of the research on ototoxic properties of Pb, evaluate possible synergistic effects with concurrent noise exposure, and identify opportunities to improve future research, we performed a review of the peer-reviewed literature to identify studies examining auditory damage due to Pb over the past 50 years. Thirty-eight studies (14 animal and 24 human) were reviewed. Of these, 24 suggested potential ototoxicity due to Pb exposure, while 14 found no evidence of ototoxicity. More animal studies are needed, especially those investigating Pb exposure levels that are occupationally and environmentally relevant to humans. Further investigations into potential interactions of Pb in the auditory system with other hazards and compounds that elicit ototoxicity are also needed in animal models. To better assess the effects of Pb exposure on the human auditory system and the possibility of a synergism with noise, future epidemiological studies need to carefully consider and address four main areas of uncertainty: (1) hearing examination and quantification of hearing loss, (2) Pb exposure evaluation, (3) noise exposure evaluation, and (4) the personal characteristics of those exposed. Two potentially confounding factors, protective factors and mixtures of ototoxicants, also warrant further exploration.

Chemical-Induced Hearing Loss in Shipyard Workers.

OBJECTIVE: The aim of this study was to determine the effect of lead, cadmium, arsenic, toluene, and xylene exposure on hearing compared with noise exposures alone. METHODS: Personnel at a shipyard (n = 1266) were divided into four exposure groups on the basis of concentrations: low metals/low solvents/high noise (reference group), high metals/high solvents/low noise, high metals/low solvents/high noise, and high metals/high solvents/high noise. Hearing changes occurring from the years 2004 to 2015 were analyzed. RESULTS: Hearing changes were significantly worse at 1000 Hz (P = 0.007), averaged across 2000 to 4000 Hz (P = 0.014), and averaged across 500 to 6000 Hz (P = 0.014) for the high metals/high solvent/high noise group compared with the low metals/low solvents/high noise only reference group. CONCLUSION: Simultaneous exposures classified as high for metals/solvents/noise appear to damage hearing more than exposure to noise alone. Hearing conservation programs should take into consideration combined exposures to metals, solvents, and noise, not simply exposure to noise.

[Role of green tea polyphenols in noise-induced hearing loss].

Objective: To investigate the role and mechanism of action of green tea polyphenols in noise-induced hearing loss. Methods: Male specific pathogen-free guinea pigs were randomly divided into normal control group with 9 guinea pigs, noise exposure group with 36 guinea pigs, and green tea polyphenol intervention group with 36 guinea pigs. Auditory brainstem response (ABR) threshold shift was examined before noise exposure and at 1, 3, 7, and 14 days of noise exposure. The surface preparation of cochlear basilar membrane was used for hair cell count and the morphology of hair cells was also observed. Western blot was used to observe the expression of cysteinyl aspartate-specific protease-9 (caspase-9) and cysteinyl aspartate-specific protease-3 (caspase-3) in cochlear tissue. Results: Both the noise exposure group and the green tea polyphenol intervention group had an increase in ABR threshold after noise exposure, and the green tea polyphenol intervention group had a significantly lower ABR threshold shift than the noise exposure group at all time points (P<0.05). Both groups had enlargement, atrophy, or loss of hair cells after noise exposure, and at 7 and 14 days of noise exposure, the noise exposure group had a significantly higher rate of abnormal hair cells than the green tea polyphenol intervention group (P<0.05). Both groups had an increase in the expression of caspase-9 and caspase-3 after noise exposure, and the noise exposure group had a significantly greater increase than the green tea polyphenol intervention group (P<0.05). Conclusion: Green tea polyphenols can reduce noise-induced hearing loss and hair cell injury, possibly by regulating the expression of caspase-9 and caspase-3.

The risk of hearing loss associated with occupational exposure to organic solvents mixture with and without concurrent noise exposure: A systematic review and meta-analysis.

This study is a meta-analysis of the previous epidemiological studies which investigated the quantitative estimates of the association between independent or combined exposure to noise and mixed organic solvents and hearing loss until October 2014. Overall, 15 studies with information on 7530 individuals (6% female) were included. Having assessed - by puretone audiometry - the adjusted odds ratio estimates for the association between solvents mixture exposure and the risk of developing hearing loss stood at 2.05 (95% confidence interval (CI): 1.44-2.9). Similarly, for subjects who were concurrently exposed to noise and solvents mixture, an OR of 2.95 (95% CI: 2.1-4.17) was obtained. There was some evidence of heterogeneity within each of the 2 exposure groups (p heterogeneity < 0.001). This heterogeneity was not explained by differences in strength of effect between duration of exposure, the number of solvent and exposure index in subgroups of solvents mixture exposure. Based on the available data, our analysis has provided the evidence of increased risk of developing hearing loss for workers exposed to organic solvents even at quite low concentration. Moreover, if such exposure is accompanied by noise, it will exacerbate the extent of hearing loss. Int J Occup Med Environ Health 2017;30(4):521-535.

Comprehensive Audiometric Analysis of Hearing Impairment and Tinnitus After Cisplatin-Based Chemotherapy in Survivors of Adult-Onset Cancer.

PURPOSE: Cisplatin is widely used but highly ototoxic. Effects of cumulative cisplatin dose on hearing loss have not been comprehensively evaluated in survivors of adult-onset cancer. PATIENTS AND METHODS: Comprehensive audiological measures were conducted on 488 North American male germ cell tumor (GCT) survivors in relation to cumulative cisplatin dose, including audiograms (0.25 to 12 kHz), tests of middle ear function, and tinnitus. American Speech-Language-Hearing Association criteria defined hearing loss severity. The geometric mean of hearing thresholds (0.25 to 12 kHz) summarized overall hearing status consistent with audiometric guidelines. Patients were sorted into quartiles of hearing thresholds of age- and sex-matched controls. RESULTS: Increasing cumulative cisplatin dose (median, 400 mg/m(2); range, 200 to 800 mg/m(2)) was significantly related to hearing loss at 4, 6, 8, 10, and 12 kHz (P trends, .021 to < .001): every 100 mg/m(2) increase resulted in a 3.2-dB impairment in age-adjusted overall hearing threshold (4 to 12 kHz; P < .001). Cumulative cisplatin doses > 300 mg/m(2) were associated with greater American Speech-Language-Hearing Association-defined hearing loss severity (odds ratio, 1.59; P = .0066) and worse normative-matched quartiles (odds ratio, 1.33; P = .093) compared with smaller doses. Almost one in five (18%) patients had severe to profound hearing loss. Tinnitus (40% patients) was significantly correlated with reduced hearing at each frequency (P < .001). Noise-induced damage (10% patients) was unaffected by cisplatin dose (P = .59). Hypertension was significantly related (P = .0066) to overall hearing threshold (4 to 12 kHz) in age- and cisplatin dose-adjusted analyses. Middle ear deficits occurred in 22.3% of patients but, as expected, were not related to cytotoxic drug dosage. CONCLUSION: Follow-up of adult-onset cancer survivors given cisplatin should include routine inquiry for hearing status and tinnitus, referral to audiologists as clinically indicated, and hypertension control. Patients should be urged to avoid noise exposure, ototoxic drugs, and other factors that further damage hearing.

Oxidative stress biomarkers and otoacoustic emissions in humans exposed to styrene and noise.

OBJECTIVE: Evaluating the correlation between otoacoustic emission levels, styrene exposure, and oxidative stress biomarkers concentration in styrene-exposed subjects, to investigate the role of oxidative stress in outer hair cell damage. DESIGN: Distortion product otoacoustic emissions were measured in the exposed workers and in a control group. Separation between the distortion and reflection otoacoustic components was performed by time-frequency-domain filtering. The urinary concentration of the DNA and RNA oxidation products, namely 8-oxo-7,8-dihydroguanine (oxoGua), 8-oxo-7,8-dihydro-2'-deoxyguanosine (oxodGuo), and 8-oxo-7,8-dihydroguanosine (oxoGuo), were evaluated. STUDY SAMPLE: Nine subjects exposed to styrene in a fiberglass factory, eight control subjects. The two groups were statistically equivalent in mean age. RESULTS: Statistically significant differences were found in the distortion component levels between the exposed and the control group. High levels of the oxidative damage biomarkers were found in the workers exposed to high levels of styrene. Significant negative correlation was found between the otoacoustic emission distortion component levels and the concentration of the oxoGuo biomarker. CONCLUSIONS: Exposure-induced damage of the cochlear amplifier is shown in the mid-frequency range, confirming animal experiments, in which hair cells in the cochlear middle turn were damaged. Hearing damage is consistent with the outer hair cell apoptosis pathway associated with oxidative stress.

'Ecstasy' enhances noise-induced hearing loss.

'Ecstasy' or 3,4-methylenedioxy-N-methamphetamine (MDMA) is an amphetamine abused for its euphoric, empathogenic, hallucinatory, and stimulant effects. It is also used to treat certain psychiatric disorders. Common settings for Ecstasy use are nightclubs and "rave" parties where participants consume MDMA and dance to loud music. One concern with the club setting is that exposure to loud sounds can cause permanent sensorineural hearing loss. Another concern is that consumption of MDMA may enhance such hearing loss. Whereas this latter possibility has not been investigated, this study tested the hypothesis that MDMA enhances noise-induced hearing loss (NIHL) by exposing rats to either MDMA, noise trauma, both MDMA and noise, or neither treatment. MDMA was given in a binge pattern of 5 mg/kg per intraperitoneal injections every 2 h for a total of four injections to animals in the two MDMA-treated groups (MDMA-only and Noise + MDMA). Saline injections were given to the animals in the two non-MDMA groups (Control and Noise-only). Following the final injection, noise trauma was induced by a 10 kHz tone at 120 dB SPL for 1 h to animals in the two noise trauma-treated groups (Noise-only and Noise + MDMA). Hearing loss was assessed by the auditory brainstem response (ABR) and cochlear histology. Results showed that MDMA enhanced NIHL compared to Noise-only and that MDMA alone caused no hearing loss. This implies that "clubbers" and "rave-goers" are exacerbating the amount of NIHL when they consume MDMA and listen to loud sounds. In contrast to earlier reports, the present study found that MDMA by itself caused no changes in the click-evoked ABR's wave latencies or amplitudes.

Metalloproteinases and their associated genes contribute to the functional integrity and noise-induced damage in the cochlear sensory epithelium.

Matrix metalloproteinases (MMPs) and their related gene products regulate essential cellular functions. An imbalance in MMPs has been implicated in various neurological disorders, including traumatic injuries. Here, we report a role for MMPs and their related gene products in the modulation of cochlear responses to acoustic trauma in rats. The normal cochlea was shown to be enriched in MMP enzymatic activity, and this activity was reduced in a time-dependent manner after traumatic noise injury. The analysis of gene expression by RNA sequencing and qRT-PCR revealed the differential expression of MMPs and their related genes between functionally specialized regions of the sensory epithelium. The expression of these genes was dynamically regulated between the acute and chronic phases of noise-induced hearing loss. Moreover, noise-induced expression changes in two endogenous MMP inhibitors, Timp1 and Timp2, in sensory cells were dependent on the stage of nuclear condensation, suggesting a specific role for MMP activity in sensory cell apoptosis. A short-term application of doxycycline, a broad-spectrum inhibitor of MMPs, before noise exposure reduced noise-induced hearing loss and sensory cell death. In contrast, a 7 d treatment compromised hearing sensitivity and potentiated noise-induced hearing loss. This detrimental effect of the long-term inhibition of MMPs on noise-induced hearing loss was further confirmed using targeted Mmp7 knock-out mice. Together, these observations suggest that MMPs and their related genes participate in the regulation of cochlear responses to acoustic overstimulation and that the modulation of MMP activity can serve as a novel therapeutic target for the reduction of noise-induced cochlear damage.

A weight of evidence approach for the assessment of the ototoxic potential of industrial chemicals.

There is accumulating epidemiological evidence that exposure to some solvents, metals, asphyxiants and other substances in humans is associated with an increased risk of acquiring hearing loss. Furthermore, simultaneous and successive exposure to certain chemicals along with noise can increase the susceptibility to noise-induced hearing loss. There are no regulations that require hearing monitoring of workers who are employed at locations in which occupational exposure to potentially ototoxic chemicals occurs in the absence of noise exposure. This project was undertaken to develop a toxicological database allowing the identification of possible ototoxic substances present in the work environment alone or in combination with noise exposure. Critical toxicological data were compiled for chemical substances included in the Quebec occupational health regulation. The data were evaluated only for noise exposure levels that can be encountered in the workplace and for realistic exposure concentrations up to the short-term exposure limit or ceiling value (CV) or 5 times the 8-h time-weighted average occupational exposure limit (TWA OEL) for human data and up to 100 times the 8-h TWA OEL or CV for animal studies. In total, 224 studies (in 150 articles of which 44 evaluated the combined exposure to noise and a chemical) covering 29 substances were evaluated using a weight of evidence approach. For the majority of cases where potential ototoxicity was previously proposed, there is a paucity of toxicological data in the primary literature. Human and animal studies indicate that lead, styrene, toluene and trichloroethylene are ototoxic and ethyl benzene, n-hexane and p-xylene are possibly ototoxic at concentrations that are relevant to the occupational setting. Carbon monoxide appears to exacerbate noise-induced hearing dysfunction. Toluene interacts with noise to induce more severe hearing losses than the noise alone.

Ambient noise levels in the chemotherapy clinic.

Many of the drugs used for chemotherapy treatments are known to be ototoxic, and can result in permanent hearing threshold shifts. The degree of ototoxic damage can be influenced by many factors including dosage, duration of exposure, genetics, and coadministration with other ototoxic agents. Cisplatin is known for its ototoxic effects on hearing thresholds, particularly in the high frequencies. Recent studies have indicated a synergistic relationship between Cisplatin administration and moderate to high noise level exposure starting between 70-85 dB SPL. This study measured the noise levels in the Portland Veteran's Affairs Medical Center's outpatient chemotherapy clinic. Average (LAeq) and peak (LCpeak) noise measures were recorded every minute from 7 am until 6 pm on the two busiest clinic days. Patients, visitors, and staff members filled out anonymous surveys regarding their reactions to noise levels. Cumulative noise levels were not at levels known to interact with Cisplatin for a significant period of time. Noise measurement analysis indicated that levels were at or above 70 dB SPL for less than ten minutes during the 11-hour recording window. The patient and visitor surveys indicated that both groups were unbothered by noise in the clinic. However, most staff members were bothered by or concerned about noise levels, and many felt that it caused stress and difficulty communicating on the phone.

Interaction of tamoxifen and noise-induced damage to the cochlea.

Tamoxifen has been used extensively in the treatment of breast cancer and other neoplasms. In addition to its well-known action on estrogen receptors it is also known to acutely block chloride channels that participate in cell volume regulation. Tamoxifen's role in preventing cochlear outer hair cell (OHC) swelling in vitro suggested that OHC swelling noted following noise exposure could potentially be a therapeutic target for tamoxifen in its role as a chloride channel blocker to help prevent noise-induced hearing loss. To investigate this possibility, the effects of exposure to tamoxifen on physiologic measures of cochlear function in the presence and absence of subsequent noise exposure were studied. Male Mongolian gerbils (2-4 months old) were randomly assigned to different groups. Tamoxifen at ∼10 mg/kg was administered to one of the groups. Five hours later they were exposed to a one-third octave band of noise centered at 8 kHz in a sound-isolation chamber for 30 min at 108 dB SPL. Compound action potential (CAP) thresholds and distortion product otoacoustic emission (DPOAE) levels were measured 30-35 days following noise exposure. Tamoxifen administration did not produce any changes in CAP thresholds and DPOAE levels when administered by itself in the absence of noise. Tamoxifen causes a significant increase in CAP thresholds from 8 to 15 kHz following noise exposure compared to CAP thresholds in animals exposed to noise alone. No significant differences were seen in the DPOAE levels in the f(2) = 8-15 kHz frequency range where maximum noise-induced increases in CAP thresholds were seen. Contrary to our original expectation, it is concluded that tamoxifen potentiates the degree of damage to the cochlea resulting from noise exposure.

A multicenter study on the audiometric findings of styrene-exposed workers.

OBJECTIVE: The objective of this study was to evaluate hearing loss among workers exposed to styrene, alone or with noise. DESIGN: This cross-sectional study was conducted as part of NoiseChem, a European Commission 5th Framework Programme research project, by occupational health institutes in Finland, Sweden, and Poland. STUDY SAMPLE: Participants' ages ranged from 18-72 years (n = 1620 workers). Participants exposed to styrene, alone or with noise, were from reinforced fiberglass products manufacturing plants (n = 862). Comparison groups were comprised of workers noise-exposed (n = 400) or controls (n = 358). Current styrene exposures ranged from 0 to 309 mg/m(3), while mean current noise levels ranged from 70-84 dB(A). Hearing thresholds of styrene-exposed participants were compared with Annexes A and B from ANSI S3.44, 1996. RESULTS: The audiometric thresholds of styrene exposed workers were significantly poorer than those in published standards. Age, gender, and styrene exposure met the significance level criterion in the multiple logistic regression for the binary outcome 'hearing loss' (P = 0.0000). Exposure to noise (<85 dBA p = 0.0001; ≥85 dB(A) p = 0.0192) interacted significantly with styrene exposure. CONCLUSIONS: Occupational exposure to styrene is a risk factor for hearing loss, and styrene-exposed workers should be included in hearing loss prevention programs.

The association between low levels of lead in blood and occupational noise-induced hearing loss in steel workers.

As the use of leaded gasoline has ceased in the last decade, background lead exposure has generally been reduced. The aim of this study was to examine the effect of low-level lead exposure on human hearing loss. This study was conducted in a steel plant and 412 workers were recruited from all over the plant. Personal information such as demographics and work history was obtained through a questionnaire. All subjects took part in an audiometric examination of hearing thresholds, for both ears, with air-conducted pure tones at frequencies of 500, 1000, 2000, 3000, 4000, 6000 and 8000 Hz. Subjects' blood samples were collected and analyzed for levels of manganese, copper, zinc, arsenic, cadmium and lead with inductive couple plasma-mass spectrometry. Meanwhile, noise levels in different working zones were determined using a sound level meter with A-weighting network. Only subjects with hearing loss difference of no more than 15 dB between both ears and had no congenital abnormalities were included in further data analysis. Lead was the only metal in blood found significantly correlated with hearing loss for most tested sound frequencies (p<0.05 to p<0.0001). After adjustment for age and noise level, the logistic regression model analysis indicated that elevated blood lead over 7 microg/dL was significantly associated with hearing loss at the sound frequencies of 3000 through 8000 Hz with odds ratios raging from 3.06 to 6.26 (p<0.05-p<0.005). We concluded that elevated blood lead at level below 10 microg/dL might enhance the noise-induced hearing loss. Future research needs to further explore the detailed mechanism.

Audiological findings in individuals exposed to organic solvents: case studies.

Millions of people around the world are exposed to industrial organic solvents such as toluene and xylene in the manufacturing sectors. Solvents are neurotoxic substances that are detrimental to the functioning of the nervous system, including the central auditory nervous system (CANS). This study investigated hearing and auditory processing in seven individuals with a history of exposure to industrial solvents. A battery of audiological tests was administered to all subjects: pure tone, speech, and impedance audiometry, otoacoustic emissions tests, auditory brainstem responses, middle latency responses, as well as the SCAN-A and R-SPIN tests with low predictability sentence lists. All individuals in this study exhibited findings consistent with retrocochlear and/or central abnormality. Two of the seven subjects in this study had normal pure tone thresholds at all frequencies bilaterally, yet showed abnormal retrocochlear/central results on one or more tests. The auditory test battery approach used in this study appears to be valuable in evaluating the pathological conditions of the CANS in solvent-exposed individuals.