Recall the reported effects of exposure to styrene and noise on the cochlear hair cells and hearing function in rats. Describe which possible confounding factors were and were not controlled for in this study, and what the results indicate about the respective ototoxic effects on humans of exposure to styrene and noise. Characterize the effects in humans of isolated and combined exposure to styrene and noise. Ototoxicity of styrene and the synergistic action of styrene and noise have been shown in rats. The respective data in humans are scarce and equivocal. This study evaluated the effects of occupational exposure to styrene and combined exposures to styrene and noise on hearing. The study group, comprised of 290-yacht yard and plastic factory workers, was exposed to a mixture of organic solvents, having styrene as its main compound. The reference group, totaling 223 subjects, included (1) white-collar workers, exposed neither to solvents nor noise and (2) metal factory workers, exposed exclusively to noise. All subjects were assessed by means of a detailed questionnaire and underwent otorhinolaryngological and audiometric examinations. Multiple logistic regression analysis revealed almost a 4-fold (or 3.9; 95% CI = 2.4–6.2) increase in the odds of developing hearing loss related to styrene exposure. The factors adjusted for were: age, gender, current occupational exposure to noise, and exposure to noise in the past. In cases of the combined exposures to styrene and noise, the odds ratios were two to three times higher than the respective values for styrene-only and noise-only exposed subjects. The mean hearing thresholds—adjusted for age, gender, and exposure to noise—were significantly higher in the solvent-exposed group than in the unexposed reference group at all frequencies tested. A positive linear relationship existed between an averaged working life exposure to styrene concentration and a hearing threshold at the frequencies of 6 and 8 kHz. This study provides the epidemiological evidence that occupational exposure to styrene is related to an increased risk of hearing loss. Combined exposures to noise and styrene seem to be more ototoxic than exposure to noise alone.

The World Health Organization (WHO) and the International Labour Organization (ILO) are developing joint estimates of the work-related burden of disease and injury (WHO/ILO Joint Estimates), with contributions from a large number of individual experts. Evidence from mechanistic data suggests that occupational exposure to noise may cause cardiovascular disease (CVD). In this paper, we present a systematic review and meta-analysis of parameters for estimating the number of deaths and disability-adjusted life years from CVD that are attributable to occupational exposure to noise, for the development of the WHO/ILO Joint Estimates. We aimed to systematically review and meta-analyse estimates of the effect of any (high) occupational exposure to noise (≥85 dBA), compared with no (low) occupational exposure to noise (<85 dBA), on the prevalence, incidence and mortality of ischaemic heart disease (IHD), stroke, and hypertension. A protocol was developed and published, applying the Navigation Guide as an organizing systematic review framework where feasible. We searched electronic academic databases for potentially relevant records from published and unpublished studies up to 1 April 2019, including International Trials Register, Ovid MEDLINE, PubMed, Embase, Lilacs, Scopus, Web of Science, and CISDOC. The MEDLINE and Pubmed searches were updated on 31 January 2020. We also searched grey literature databases, Internet search engines and organizational websites; hand-searched reference lists of previous systematic reviews and included study records; and consulted additional experts. We included working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State but excluded children (<15 years) and unpaid domestic workers. We included randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of the effect of any occupational exposure to noise on CVD prevalence, incidence or mortality, compared with the theoretical minimum risk exposure level (<85 dBA). At least two review authors independently screened titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. We prioritized evidence from cohort studies and combined relative risk estimates using random-effect meta-analysis. To assess the robustness of findings, we conducted sensitivity analyses (leave-one-out meta-analysis and used as alternative fixed effects and inverse-variance heterogeneity estimators). At least two review authors assessed the risk of bias, quality of evidence and strength of evidence, using Navigation Guide tools and approaches adapted to this project. Seventeen studies (11 cohort studies, six case-control studies) met the inclusion criteria, comprising a total of 534,688 participants (39,947 or 7.47% females) in 11 countries in three WHO regions (the Americas, Europe, and the Western Pacific). The exposure was generally assessed with dosimetry, sound level meter and/or official or company records. The outcome was most commonly assessed using health records. We are very uncertain (low quality of evidence) about the effect of occupational exposure to noise (≥85 dBA), compared with no occupational exposure to noise (<85 dBA), on: having IHD (0 studies); acquiring IHD (relative risk (RR) 1.29, 95% confidence interval (95% CI) 1.15 to 1.43, two studies, 11,758 participants, I² 0%); dying from IHD (RR 1.03, 95% CI 0.93-1.14, four studies, 198,926 participants, I² 26%); having stroke (0 studies); acquiring stroke (RR 1.11, 95% CI 0.82-1.65, two studies, 170,000 participants, I² 0%); dying from stroke (RR 1.02, 95% CI 0.93-1.12, three studies, 195,539 participants, I² 0%); having hypertension (0 studies); acquiring hypertension (RR 1.07, 95% CI 0.90-1.28, three studies, four estimates, 147,820 participants, I² 52%); and dying from hypertension (0 studies). Data for subgroup analyses were missing. Sensitivity analyses supported the main analyses. For acquiring IHD, we judged the existing body of evidence from human data to provide "limited evidence of harmfulness"; a positive relationship is observed between exposure and outcome where chance, bias, and confounding cannot be ruled out with reasonable confidence. For all other included outcomes, the bodies of evidence were judged as "inadequate evidence of harmfulness". Producing estimates for the burden of CVD attributable to occupational exposure to noise appears to not be evidence-based at this time. 10.1016/j.envint.2018.09.040. CRD42018092272.

Industrial noise in the working environment has adverse effects on human hearing; literature and private studies confirm that. It has been determined that significant changes in the hearing threshold level occur in the high frequency audiometry, i.e., in the 8-20 kHz frequency range. Therefore, it is important to determine the effect of ultrasonic noise (10-40 kHz) on the human body in the working environment. This review describes hearing and nonhearing effects (thermal effects, subjective symptoms and functional changes) of the exposure to noise emitted by ultrasound devices. Many countries have standard health exposure limits to prevent effects of the exposure to ultrasonic noise in the working environment.

Questionnaire and audiometric data of 701 dockyard workers (517 noise and organic solvent mixture-exposed and 184 noise-only-exposed) were referred to 205 control subjects not exposed to either noise or solvents. The odds ratio (OR) of hearing loss was significantly increased by approximately 3 times in the noise-only group and by almost 5 times in the noise and solvent group. A moderate effect of solvent ototoxicity, in addition to noise, was observed on hearing threshold at a frequency 8 kHz. ORs for hearing loss were 1.12 for each increment of 1 year of age, 1.07 for every decibel of lifetime noise exposure (dB-A), and 1.004 for each increment of the index of lifetime exposure to solvents. The results suggest an additive damaging effect of coexposure to noise and organic solvents to the auditory organ.

Objectives It is known that some industrial organic solvents are ototoxic. This study was aimed at evaluating the hearing effects of a mixture of organic solvents alone or in combination with noise on employees in paint and lacquer enterprises. The concentration of solvents was below the occupational exposure limits (OEL) for most of the subjects. Methods Altogether 517 subjects were divided into the following three groups: persons with no risk due to noise or organic solvent exposure at the workplace, workers exposed to organic solvents only, and workers exposed to both organic solvents and noise. Results The relative risk (RR) of hearing loss in the solvent-only exposure group was significantly increased (RR 4.4 and RR 2.8 for noise exposure of <80 dB-A and <85 dB-A, respectively) in a wide range of frequencies (2-8 kHz). No additional risk in the solvent + noise exposure group was found (RR 2.8). Hearing thresholds were significantly poorer in a wide range of frequencies (1-8 kHz) for both groups exposed to solvents, when compared with the reference group. The mean hearing thresholds at frequencies of 2-4 kHz were poorer for workers exposed to solvents + noise than for the solvent-only group; this finding suggests an additional effect for noise. However, there was no correlation between hearing loss and the extent of solvent exposure. Conclusions The results indicate that occupational organic solvent exposure at moderate concentrations increases the risk of hearing loss, and the ototoxic effects should be considered when the health effects of exposed workers are monitored.

The World Health Organization (WHO) and the International Labour Organization (ILO) are developing a joint methodology for estimating the national and global work-related burden of disease and injury (WHO/ILO joint methodology), with contributions from a large network of experts. In this paper, we present the protocol for two systematic reviews of parameters for estimating the number of deaths and disability-adjusted life years from cardiovascular disease attributable to exposure to occupational noise, to inform the development of the WHO/ILO joint methodology. We aim to systematically review studies on exposure to occupational noise (Systematic Review 1) and systematically review and meta-analyse estimates of the effect of occupational noise on cardiovascular diseases (Systematic Review 2), applying the Navigation Guide systematic review methodology as an organizing framework, conducting both systematic reviews in tandem and in a harmonized way. Separately for Systematic Reviews 1 and 2, we will search electronic academic databases for potentially relevant records from published and unpublished studies, including Medline, EMBASE, Web of Science and CISDOC. We will also search electronic grey literature databases, Internet search engines and organizational websites; hand search reference list of previous systematic reviews and included study records; and consult additional experts. We will include working-age (≥15 years) workers in the formal and informal economy in any WHO and/or ILO Member State, but exclude children (<15 years) and unpaid domestic workers. The eligible risk factor will be occupational noise. Eligible outcomes will be hypertensive heart disease, ischaemic heart disease, stroke, cardiomyopathy, myocarditis, endocarditis and other circulatory diseases. For Systematic Review 1, we will include quantitative prevalence studies of exposure to occupational noise (i.e., low: <85 dB(A) and high: ≥85 dB(A)) stratified by country, sex, age and industrial sector or occupation. For Systematic Review 2, we will include randomized controlled trials, cohort studies, case-control studies and other non-randomized intervention studies with an estimate of the relative effect of high exposure to occupational noise on the prevalence of, incidence of or mortality due to cardiovascular disease, compared with the theoretical minimum risk exposure level (i.e., low exposure). At least two review authors will independently screen titles and abstracts against the eligibility criteria at a first stage and full texts of potentially eligible records at a second stage, followed by extraction of data from qualifying studies. At least two review authors will assess risk of bias and the quality of evidence, using the most suited tools currently available. For Systematic Review 2, if feasible, we will combine relative risks using meta-analysis. We will report results using the guidelines for accurate and transparent health estimates reporting (GATHER) for Systematic Review 1 and the preferred reporting items for systematic reviews and meta-analyses guidelines (PRISMA) for Systematic Review 2. PROSPERO registration number: CRD42018092272.