Description: Objectives Noise-induced hearing loss is one of the most serious occupational diseases worldwide. It is caused by interactions between environmental and genetic factors. The purpose of this study was to examine the association between the genetic susceptibility of the eye absent homolog 4 (EYA4) gene and the risk of developing noise-induced hearing loss in China. Methods A case–control association study was carried out with 326 hearing loss cases and 326 controls matched with age and duration of noise exposure, drawn from a cohort of steel workers. Five single nucleotide polymorphisms (SNPs) in the EYA4 were selected and genotyped. Logistic regression was performed to analyse the main effect of genotypes and interactions between genotypes and individual/environmental factors adjusted for confounding factors. Moreover, generalised multiple dimensionality reduction was applied to further detect interaction among the 5 selected SNPs. Results Analysis revealed that locus polymorphism of rs3813346 was associated with the risk of developing noise-induced hearing loss in the dominance model, the codominance model and the addictive model (p=0.004, 0.009 and 0.003, respectively). A significant interaction between rs9321402 and cumulative noise exposure was found (p=0.002). A significant main effect p value (p=0.006) was obtained in the high-level exposure group (cumulative noise exposure ≥98 dB(A)). Generalised multiple dimensionality reduction indicated that the combined interaction of the 2 loci—rs3813346 and rs9493627—significantly affected the incidence of noise-induced hearing loss. Conclusions The research suggests that EYA4 genetic variant and its interaction with noise levels may modify the susceptibility to develop noise-induced hearing loss in Chinese population.

Description: Objective Occupationally acquired noise-induced hearing loss (NIHL) is the most prevalent occupational disease in Austria and among the most common in many other countries. Because of the wide variation in hearing loss after equivalent exposures it has long been assumed that some individuals are more vulnerable to occupational NIHL than others. Earlier attempts to define predictors of NIHL before starting occupational noise exposure have largely failed. We present results of a prospective study evaluating the potential of temporary threshold shift (TTS) after a test exposure to predict NIHL. Methods Between 1982 and 1989, overall 311 apprentices were included into a prospective study during their initial health screening visit. At this occasion, a standardised noise exposure was applied (20 min, 200–500 Hz, 100 dBA) and the TTS at 4 kHz was determined during at least 10 min after exposure. Hearing loss was monitored at follow-up visits every 3–5 years. Follow-up was 13 years on average. Results Permanent threshold shift was predicted by duration of noise exposure, frequency of wearing noise protectors and especially by the initial TTS at 4 kHz. Using 14 dB TTS as a cut-off had 82% sensitivity and 53% specificity to predict 20 dB or higher levels of NIHL. Conclusions The TTS model can be successfully applied as a method to detect individuals at greater risk of occupational NIHL. It is recommended to routinely include such a procedure into initial workers’ examinations for suitability to work under occupational noise conditions and for counselling on the use of hearing protectors.

Description: Objectives The healthy worker effect usually leads to underestimation of the association between occupational exposure and asthma. The role of irritants in work-related asthma is disputed. We estimated the effect of occupational exposure on asthma expression in a longitudinal study, using marginal structural modelling to control for the healthy worker effect. Methods Analyses included 1284 participants (17–79 years, 48% men) from the follow-up (2003–2007) of the French Epidemiological study on the Genetics and Environment of Asthma (case-control study). Age at asthma onset, periods with/without attacks over lifetime and occupational history were recorded retrospectively. Exposures to known asthmagens, irritants or low level of chemicals/allergens were evaluated through a job-exposure matrix. The job history was reconstructed into 5-year intervals. Results Thirty-one per cent of subjects had ever been exposed to occupational asthmagens. Among the 38% of subjects who had asthma (ever), presence of attacks was reported in 52% of all time periods. Using standard analyses, no association was observed between exposure to known asthmagens (OR (95% CI): 0.99 (0.72 to 1.36)) or to irritants/low level of chemicals/allergens (0.82 (0.56 to 1.20)) and asthma attacks. Using a marginal structural model, all associations increased with suggestive evidence for known asthmagens (1.26 (0.90 to 1.76)), and reaching statistical significance for irritants/low level of chemicals/allergens (1.56 (1.02 to 2.40)). Conclusions The healthy worker effect has an important impact in risk assessment in work-related asthma studies. Marginal structural models are useful to eliminate imbalances in exposure due to disease-driven selection. Results support the role of irritants in work-related asthma.

Description: Objective Cleaning products may cause work-related asthma, but information regarding the specific exposures involved is scarce. We aimed to determine the associations between asthma and occupational exposure to cleaning agents in hospital workers. Methods Analyses were conducted in 179 (136 women) hospital workers and a reference population of 545 subjects (18–79 years) from the French case-control and familial Epidemiological study on the Genetics and Environment of Asthma (2003–2007). Exposures to cleaning agents were estimated using three methods: self-report, expert assessment and an asthma-specific job-exposure matrix (JEM). Associations between cleaning products and current asthma were evaluated by logistic regressions, stratified by sex and adjusted for age and smoking status. Results According to expert assessment, 55% of male and 81% of female hospital workers were exposed to cleaning/disinfecting tasks weekly (p〈0.001). No association was observed between cleaning/disinfecting tasks and current asthma in men or in women whatever the assessment method used. In women, exposure to decalcifiers (expert assessment) was associated with current asthma (OR (95% CI):2.38 (1.06 to 5.33)). In hospital workers classified as exposed according to both the expert assessment and the JEM, additional associations were observed for exposure to ammonia (3.05 (1.19 to 7.82)) and to sprays with moderate/high intensity (2.87 (1.02 to 8.11)). Conclusions Female hospital workers are often exposed to numerous cleaning products, some of which were markedly associated with current asthma. Low numbers prevented a meaningful analysis in men. Objective and more accurate estimates of occupational exposure to cleaning products are needed to better understand the adverse effects of cleaning products.

Description: Background There is limited information regarding the occupational exposures of subjects with a diagnosis of work-exacerbated asthma (WEA). Objectives To: (1) identify potential specific occupational, chemical, biological and physical agents associated with incident cases of WEA and (2) compare these agents with occupational exposures of occupational asthma (OA) and non-work-related asthma (NWRA) cases. Methods Subjects were workers with work-related asthma (WRA) or NWRA referred between 2005 and 2008 to two Quebec clinics specialised in the field of WRA. Specific inhalation challenges were performed to differentiate OA from WEA. Work exposures were assessed using a detailed occupational questionnaire. Exposures to 41 chemical and biological agents were coded in a semiquantitative way according to a combination of indices for concentration in workplace air, frequency and confidence of exposure by an occupational hygienist expert in occupational exposure coding. This expert was blind to the medical status of WEA, OA or NWRA. Five physical agents were coded on a yes/no scale. Results 153 subjects were enrolled (53 WEA, 67 OA and 33 NWRA). WEA cases were significantly more exposed to ammonia, engine exhaust fumes, silica, mineral fibres, aerosol propellants and solvents, and significantly less exposed to animal derived dust and enzymes than were OA cases. Exposure to physical conditions did not differ between WEA and OA. Conclusions Exposures associated with WEA differ from those associated with OA in this study. A proportion of subjects with WEA may suffer from low-dose irritant asthma, which remains a hypothesis to be tested.

Description: Objectives The authors had a unique opportunity to study the early impacts of occupational and recreational exposures on the development of noise-induced hearing loss (NIHL) in a cohort of 392 young workers. The objectives of this study were to estimate strength of associations between occupational and recreational exposures and occurrence of early-stage NIHL and to determine the extent to which relationships between specific noise exposures and early-stage NIHL were mitigated through the use of hearing protection. Methods Participants were young adults who agreed to participate in a follow-up of a randomised controlled trial. While the follow-up study was designed to observe long-term effects (up to 16 years) of a hearing conservation intervention for high school students, it also provided opportunity to study the potential aetiology of NIHL in this worker cohort. Study data were collected via exposure history questionnaires and clinical audiometric examinations. Results Over the 16-year study period, the authors documented changes to hearing acuity that exceeded 15 dB at high frequencies in 42.8% of men and 27.7% of women. Analyses of risk factors for NIHL were limited to men, who comprised 68% of the cohort, and showed that risks increased in association with higher levels of the most common recreational and occupational noise sources, as well as chemical exposures with ototoxic potential. Use of hearing protection and other safety measures, although not universal and sometimes modest, appeared to offer some protection. Conclusions Early-stage NIHL can be detected in young workers by measuring high-frequency changes in hearing acuity. Hearing conservation programmes should focus on a broader range of exposures, whether in occupational or non-occupational settings. Priority exposures include gunshots, chainsaws, power tools, smoking and potentially some chemical exposures.