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: Introduction The oxidative potential (OP) of particulate matter (PM) has been proposed as a health-relevant metric, but currently few epidemiological studies investigated associations of OP with health. Our main aim was to assess associations of long-term exposure to OP with respiratory health in children. Our second aim was to evaluate whether OP is more consistently associated with respiratory health than PM mass, PM composition or nitrogen dioxide (NO 2 ). Methods For 3701 participants of a prospective birth cohort, annual average concentrations of OP (assessed by spin resonance (OP ESR ) and dithiothreitol assay (OP DTT )), PM with an aerodynamic diameter of less than 2.5 µm (PM 2.5 ) mass, NO 2 , and PM 2.5 constituents at the home addresses at birth and at all follow-up addresses were estimated by land-use regression. Repeated questionnaire reports of asthma and hay fever until age 14 years, and measurements of allergic sensitisation, lung function and fractional exhaled nitric oxide at age 12 years were linked with air pollution concentrations. Results Asthma incidence, prevalence of asthma symptoms and rhinitis were positively associated with OP DTT (adjusted OR (95% CI) per IQR increase in exposure 1.10 (1.01 to 1.20), 1.08 (1.02 to 1.16), 1.15 (1.05 to 1.26), respectively). These associations persisted after adjustment for most co-pollutants. Forced expiratory volume in 1s and forced vital capacity were negatively associated with OP DTT . These associations were sensitive to adjustment for NO 2 . Respiratory health was not significantly associated with PM 2.5 mass and OP ESR . Conclusions Respiratory health was more strongly associated with OP DTT than with PM 2.5 mass; OP DTT associations with lung function, but not symptoms, were sensitive to adjustment for NO 2 .

Description: Objectives Several respirable hazards, including smoking and indoor air pollution from biomass, were suggested to increase the risk of tuberculosis. Few studies have been conducted on ambient air pollution and tuberculosis. We investigated the association between exposure to ambient air pollution and incidence of active tuberculosis. Methods We conducted a cohort study using 106 678 participants of a community-based screening service in Taiwan, 2005–2012. We estimated individual exposure to air pollution using data from the nearest air quality monitoring station and the road intensity within a 500 m buffer zone. The incidence of tuberculosis was ascertained from the national tuberculosis registry. Results After a median follow-up of 6.7 years, 418 cases of tuberculosis occurred. Exposure to fine particulate matter (PM 2.5 ) was associated with increased risk of active tuberculosis (adjusted HR: 1.39/10 μg/m 3 (95% CI 0.95 to 2.03)). In addition, traffic-related air pollution including nitrogen dioxide (adjusted HR: 1.33/10 ppb; 95% CI 1.04 to 1.70), nitrogen oxides (adjusted HR: 1.21/10 ppb; 95% CI 1.04 to 1.41) and carbon monoxide (adjusted HR: 1.89/ppm; 95% CI 0.78 to 4.58) was associated with tuberculosis risk. There was a non-significant trend between the length of major roads in the neighbourhood and culture-confirmed tuberculosis (adjusted HR: 1.04/km; 95% CI 0.995 to 1.09). Conclusions Our study revealed a possible link between ambient air pollution and risk of active tuberculosis. Since people from developing countries continue to be exposed to high levels of ambient air pollution and to experience high rates of tuberculosis, the impact of worsening air pollution on global tuberculosis control warrants further investigation.

Description: Background Asthma prevalence and acute exacerbations have been associated with endotoxin exposure. However, there are limited data on relations between acute asthma outcomes in children and personal exposure to endotoxin or whether this relation is modified by personal air pollution exposures. Methods We made repeated measurements of the fractional concentration of exhaled NO (F e NO ), forced expiratory volume in 1 s (FEV 1 ) and personal endotoxin exposures in patients with persistent asthma aged 9–18 years, each of whom was followed for 10 consecutive days in Riverside and Whittier, California. Endotoxin was measured in PM 2.5 , and simultaneously we measured personal exposure to air pollutants: NO 2 and PM 2.5 mass, elemental carbon and organic carbon. Endotoxin exposure–response relations and interactions between endotoxin and air pollutants were analysed with mixed models controlling for personal temperature, humidity and the 10-day period. Results Neither percent-predicted FEV 1 nor F e NO was associated with personal endotoxin overall; however, endotoxin was associated with FEV 1 among patients with average percent-predicted FEV 1 〈80%. When NO 2 was above its median, F e NO increased by 2.2% (95% CI –0.8% to 5.2%) for an interquartile increase in personal endotoxin, whereas F e NO was lower by –1.8% (95% CI –4% to 0.5%) when NO 2 was≤its median. However, this is out of 12 interaction tests between personal endotoxin and a binary air pollutant for each outcome (FEV 1 and F e NO ), and there were no interactions with any continuous-scaled pollutant. Conclusions Personal endotoxin exposure was not associated with acute daily changes in F e NO or FEV 1 in a cohort panel of schoolchildren with asthma, except for decreased FEV 1 among patients with more severe asthma (percent-predicted FEV 1 〈80%). There was limited evidence of effect modification of endotoxin by personal exposure to air pollution.

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: Background In several studies, exposure to fine particulate matter (PM) has been associated with inflammation, with inconsistent results. We used repeated measurements to examine the association of long-term fine and ultrafine particle exposure with several blood markers of inflammation and coagulation. Methods We used baseline (2000–2003) and follow-up (2006–2008) data from the Heinz Nixdorf Recall Study, a German population-based prospective cohort of 4814 participants. A chemistry transport model was applied to model daily surface concentrations of PM air pollutants (PM 10 , PM 2.5 ) and particle number on a grid of 1 km 2 . Applying mixed regression models, we analysed associations of long-term (mean of 365 days prior to blood draw) particle exposure at each participant's residence with the level of high-sensitivity C reactive protein (hs-CRP), fibrinogen, platelet and white cell count (WCC), adjusting for short-term PM exposure (moving averages of 1–7 days), personal characteristics, season, ambient temperature (1–5 days), ozone and time trend. Results We analysed 6488 observations: 3275 participants with baseline data and 3213 with follow-up data. An increase of 2.4 µg/m 3 in long-term PM 2.5 was associated with an adjusted increase of 5.4% (95% CI 0.6% to 10.5%) in hs-CRP and of 2.3% (95% CI 1.4% to 3.3%) in the platelet count. Fibrinogen and WCC were not associated with long-term particle exposure. Conclusions In this population-based cohort, we found associations of long-term exposure to PM with markers of inflammation (hs-CRP) and coagulation (platelets). This finding supports the hypothesis that inflammatory processes might contribute to chronic effects of air pollution on cardiovascular disease.

Description: Objectives Iron-ore miners are exposed to extremely dusty and physically arduous work environments. The demanding activities of mining select healthier workers with longer work histories (ie, the Healthy Worker Survivor Effect (HWSE)), and could have a reversing effect on the exposure–response association. The objective of this study was to evaluate an iron-ore mining cohort to determine whether the effect of respirable dust was confounded by the presence of an HWSE. Methods When an HWSE exists, standard modelling methods, such as Cox regression analysis, produce biased results. We compared results from g-estimation of accelerated failure-time modelling adjusted for HWSE with corresponding unadjusted Cox regression modelling results. Results For all-cause mortality when adjusting for the HWSE, cumulative exposure from respirable dust was associated with a 6% decrease of life expectancy if exposed ≥15 years, compared with never being exposed. Respirable dust continued to be associated with mortality after censoring outcomes known to be associated with dust when adjusting for the HWSE. In contrast, results based on Cox regression analysis did not support that an association was present. Conclusions The adjustment for the HWSE made a difference when estimating the risk of mortality from respirable dust. The results of this study, therefore, support the recommendation that standard methods of analysis should be complemented with structural modelling analysis techniques, such as g-estimation of accelerated failure-time modelling, to adjust for the HWSE.

Description: Background Combustion-generated fine particulate matter (PM 2.5 ) is associated with cardiovascular morbidity. Both traffic-related air pollution and residential wood combustion may be important, but few studies have compared their impacts. Objectives To assess and compare effects of traffic-related and woodsmoke PM 2.5 on endothelial function and systemic inflammation (C reactive protein, interleukin-6 and band cells) among healthy adults in Vancouver, British Columbia, Canada, using high efficiency particulate air (HEPA) filtration to introduce indoor PM 2.5 exposure gradients. Methods We recruited 83 healthy adults from 44 homes in traffic-impacted or woodsmoke-impacted areas to participate in this randomised, single-blind cross-over intervention study. PM 2.5 concentrations were measured during two consecutive 7-day periods, one with filtration and the other with ‘placebo filtration’. Endothelial function and biomarkers of systematic inflammation were measured at the end of each 7-day period. Results HEPA filtration was associated with a 40% decrease in indoor PM 2.5 concentrations. There was no relationship between PM 2.5 exposure and endothelial function. There was evidence of an association between indoor PM 2.5 and C reactive protein among those in traffic-impacted locations (42.1% increase in C reactive protein per IQR increase in indoor PM 2.5 , 95% CI 1.2% to 99.5%), but not among those in woodsmoke-impacted locations. There were no associations with interleukin-6 or band cells. Conclusions Evidence of an association between C reactive protein and indoor PM 2.5 among healthy adults in traffic-impacted areas is consistent with the hypothesis that traffic-related particles, even at relatively low concentrations, play an important role in the cardiovascular effects of the urban PM mixture. Trial registration number http://www.clinicaltrials.gov (NCT01570062).