Description: Objectives Healthcare workers have high rates of low back pain (LBP) related to handling patients. A large chain of nursing homes experienced reduced biomechanical load, compensation claims and costs following implementation of a safe resident handling programme (SRHP). The aim of this study was to examine whether LBP similarly declined and whether it was associated with relevant self-reported occupational exposures or personal health factors. Methods Worker surveys were conducted on multiple occasions beginning with the week of first SRHP introduction (baseline). In each survey, the outcome was LBP during the prior 3 months with at least mild severity during the past week. Robust Poisson multivariable regression models were constructed to examine correlates of LBP cross-sectionally at 2 years (F3) and longitudinally at 5–6 years (F5) post-SRHP implementation among workers also in at least one prior survey. Results LBP prevalence declined minimally between baseline and F3. The prevalence was 37% at F3 and cumulative incidence to F5 was 22%. LBP prevalence at F3 was positively associated with combined physical exposures, psychological job demands and prior back injury, while frequent lift device usage and ‘intense’ aerobic exercise frequency were protective. At F5, the multivariable model included frequent lift usage at F3 (relative risk (RR) 0.39 (0.18 to 0.84)) and F5 work–family imbalance (RR=1.82 (1.12 to 2.98)). Conclusions In this observational study, resident lifting device usage predicted reduced LBP in nursing home workers. Other physical and psychosocial demands of nursing home work also contributed, while frequent intense aerobic exercise appeared to reduce LBP risk.

Description: Objective Among the aetiological factors of chronic low back pain (CLBP), occupational factors are often suspected, but their contribution remains to be ascertained. This study aimed to determine the impact of a wide range of occupational factors on the incidence and persistence of CLBP. Method From the VISAT (VIeillissement SAnté Travail) study, 1560 workers were examined at baseline and 5 years later. CLBP was defined as having low back pain or specific treatment for at least 6 months. Participants newly affected with CLBP and those with persistent CLBP at follow-up were distinguished. In addition to individual factors, a broad panel of occupational factors were analysed, covering employment, physical, organisational and psychosocial factors. Multivariate analyses were used to determine predictive factors of incidence and persistence of CLBP. Receiver operating characteristic (ROC) curves were performed to analyse the contribution of occupational factors. Results 22.6% of participants without any CLBP initially presented with CLBP 5 years later, while 53.7% of participants with CLBP at baseline had CLBP at the second collection. Carrying heavy loads, the lack of recognition of completed work and productivity-related income predicted a higher risk of incidence of CLBP. However, no significant association between occupational factors and the risk for persistence of CLBP was observed, while the risk was multiplied by two for history of depression and rheumatological events. ROC curves confirmed the significant contribution of occupational factors to incidence of CLBP. Conclusions Occupational factors played a pivotal role in the incidence of CLBP, while individual factors were the main determinants of persistence of CLBP.

Description: Objectives To examine the longitudinal relationship between incidence of diagnosed chronic disease and work status and hours worked. Methods A dynamic cohort approach was taken to construct our study sample using the Canadian National Population Health Survey. Participant inclusion criteria included being employed and without a chronic health condition in the survey cycle prior to diagnosis, and participation in consecutive surveys following diagnosis. Each respondent was matched with up to 5 respondents without a diagnosed health condition. The direct and indirect associations between chronic disease and work status and hours worked following diagnosis were examined using probit and linear regression path models. Separate models were developed for arthritis, back problems, diabetes, hypertension and heart disease. Results We identified 799 observations with a diagnosis of arthritis, 858 with back pain, 178 with diabetes, 569 with hypertension and 163 with heart disease, which met our selection criteria. An examination of total effects at time 1 and time 2 showed that, excluding hypertension, chronic disease diagnosis was related to work loss. The time 2 effect of chronic disease diagnosis on work loss was mediated through time 1 work status. With the exception of heart disease, an incident case of chronic disease was not related to changes in work hours among observations with continuous work participation. Conclusions Chronic disease can result in work loss following diagnosis. Research is required to understand how modifying occupational conditions may benefit employment immediately after diagnosis.

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: Objectives There is evidence of adverse associations between short-term exposure to traffic-related pollution and health, but little is known about the relative contribution of the various sources and particulate constituents. Methods For each day for 2011–2012 in London, UK over 100 air pollutant metrics were assembled using monitors, modelling and chemical analyses. We selected a priori metrics indicative of traffic sources: general traffic, petrol exhaust, diesel exhaust and non-exhaust (mineral dust, brake and tyre wear). Using Poisson regression models, controlling for time-varying confounders, we derived effect estimates for cardiovascular and respiratory hospital admissions at prespecified lags and evaluated the sensitivity of estimates to multipollutant modelling and effect modification by season. Results For single day exposure, we found consistent associations between adult (15–64 years) cardiovascular and paediatric (0–14 years) respiratory admissions with elemental and black carbon (EC/BC), ranging from 0.56% to 1.65% increase per IQR change, and to a lesser degree with carbon monoxide (CO) and aluminium (Al). The average of past 7 days EC/BC exposure was associated with elderly (65+ years) cardiovascular admissions. Indicated associations were higher during the warm period of the year. Although effect estimates were sensitive to the adjustment for other pollutants they remained consistent in direction, indicating independence of associations from different sources, especially between diesel and petrol engines, as well as mineral dust. Conclusions Our results suggest that exhaust related pollutants are associated with increased numbers of adult cardiovascular and paediatric respiratory hospitalisations. More extensive monitoring in urban centres is required to further elucidate the associations.

Description: Background Welders are at risk for cardiovascular disease. Recent studies linked tobacco smoke exposure to hypomethylation of the F2RL3 (coagulation factor II (thrombin) receptor-like 3) gene, a marker for cardiovascular disease prognosis and mortality. However, whether welding fumes cause hypomethylation of F2RL3 remains unknown. Methods We investigated 101 welders (median span of working as a welder: 7 years) and 127 unexposed controls (non-welders with no obvious exposure to respirable dust at work), age range 23–60 years, all currently non-smoking, in Sweden. The participants were interviewed about their work history, lifestyle factors and diseases. Personal sampling of respirable dust was performed for the welders. DNA methylation of F2RL3 in blood was assessed by pyrosequencing of four CpG sites, CpG_2 (corresponds to cg03636183) to CpG_5, in F2RL3 . Multivariable linear regression analysis was used to assess the association between exposure to welding fumes and F2RL3 methylation. Results Welders had 2.6% lower methylation of CpG_5 than controls (p〈0.001). Higher concentrations of measured respirable dust among the welders were associated with hypomethylation of CpG_2, CpG_4 and CpG_5 (β=–0.49 to –1.4, p〈0.012); p〈0.029 adjusted for age, previous smoking, passive smoking, education, current residence and respirator use. Increasing the number of years working as a welder was associated with hypomethylation of CpG_4 (linear regression analysis, β=–0.11, p=0.039, adjusted for previous smoking). Previous tobacco smokers had 1.5–4.7% (p〈0.014) lower methylation of 3 of the 4 CpG sites in F2RL3 (CpG_2, CpG_4 and CpG_5) compared to never-smokers. A non-significant lower risk of cardiovascular disease with more methylation was observed for all CpG sites. Conclusions Welding fumes exposure and previous smoking were associated with F2RL3 hypomethylation. This finding links low-to-moderate exposure to welding fumes to adverse effects on the cardiovascular system, and suggests a potential mechanistic pathway for this link, via epigenetic effects on F2RL3 expression.

Description: Objectives To examine the benefit of a psychological Stage of Change (SOC) approach, relative to standard ergonomics advice, for the prevention of work-related musculoskeletal pain and discomfort (MSPD). Methods A cluster randomised trial was conducted in South Australia across a broad range of workplaces. Repeated face-to-face interviews were conducted onsite to assess MSPD, safety climate, job satisfaction and other factors. Changes in MSPD across intervention groups and time were investigated using Generalised Estimating Equation (GEE) methods. Results 25 workgroups (involving 242 workers) were randomly allocated to either a standard intervention or an intervention tailored according to SOC. The prevalence of MSPD increased for both groups, but was only significant for the standard group, in respect of lower back MSPD. Workers receiving tailored interventions were 60% less likely to experience lower back MSPD. After adjusting for age, gender and job satisfaction, it was found that company safety climate and length of employment were significantly correlated to the time-intervention effect. There was no correlation with workload. Conclusions Compared with standard ergonomics advice to management, there was evidence of a benefit of stage-matched intervention for MSPD prevention, particularly for low back pain. Organisational safety climate should be taken into account when planning prevention programmes.

Description: Objective To compare short-term effects of fine particles (PM 2.5 ; aerodynamic diameter 〈2.5 µm) from different sources on the blood levels of markers of systemic inflammation. Methods We followed a panel of 52 ischaemic heart disease patients from 15 November 2005 to 21 April 2006 with clinic visits in every second week in the city of Kotka, Finland, and determined nine inflammatory markers from blood samples. In addition, we monitored outdoor air pollution at a fixed site during the study period and conducted a source apportionment of PM 2.5 using the Environmental Protection Agency's model EPA PMF 3.0. We then analysed associations between levels of source-specific PM 2.5 and markers of systemic inflammation using linear mixed models. Results We identified five source categories: regional and long-range transport (LRT), traffic, biomass combustion, sea salt, and pulp industry. We found most evidence for the relation of air pollution and inflammation in LRT, traffic and biomass combustion; the most relevant inflammation markers were C-reactive protein, interleukin-12 and myeloperoxidase. Sea salt was not positively associated with any of the inflammatory markers. Conclusions Results suggest that PM 2.5 from several sources, such as biomass combustion and traffic, are promoters of systemic inflammation, a risk factor for cardiovascular diseases.

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 role of outdoor air pollution in the incidence of chronic obstructive pulmonary disease (COPD) remains unclear. We investigated this question using a large, nationally representative cohort based on primary care records linked to hospital admissions. Methods A cohort of 812 063 patients aged 40–89 years registered with 205 English general practices in 2002 without a COPD diagnosis was followed from 2003 to 2007. First COPD diagnoses recorded either by a general practitioner (GP) or on admission to hospital were identified. Annual average concentrations in 2002 for particulate matter with an aerodynamic diameter 〈10 µm (PM 10 ) and 〈2.5 µm (PM 2.5 ), nitrogen dioxide (NO 2 ), ozone and sulfur dioxide (SO 2 ) at 1 km 2 resolution were estimated from emission-based dispersion models. Hazard ratios (HRs) per interquartile range change were estimated from Cox models adjusting for age, sex, smoking, body mass index and area-level deprivation. Results 16 034 participants (1.92%) received a COPD diagnosis from their GP and 2910 participants (0.35%) were admitted to hospital for COPD. After adjustment, HRs for GP recorded COPD and PM 10 , PM 2.5 and NO 2 were close to unity, positive for SO 2 (HR=1.07 (95% CI 1.03 to 1.11) per 2.2 µg/m 3 ) and negative for ozone (HR=0.94 (0.89 to 1.00) per 3 µg/m 3 ). For admissions HRs for PM 2.5 and NO 2 remained positive (HRs=1.05 (0.98 to 1.13) and 1.06 (0.98 to 1.15) per 1.9 µg/m 3 and 10.7 µg/m 3 , respectively). Conclusions This large population-based cohort study found limited, inconclusive evidence for associations between air pollution and COPD incidence. Further work, utilising improved estimates of air pollution over time and enhanced socioeconomic indicators, is required to clarify the association between air pollution and COPD incidence.