Description: Background Between 2001 and 2010, six research groups conducted coordinated prospective studies of carpal tunnel syndrome (CTS) incidence among US workers from various industries to estimate exposure–response relationships. Objective This analysis examined the presence and magnitude of confounding between biomechanical and workplace psychosocial factors and incidence of dominant-hand CTS. Methods 1605 participants, without CTS at enrolment, were followed for up to 3.5 years (2471 person-years). Demographic information, medical history and workplace psychosocial stress measures were collected at baseline. Individual workplace biomechanical exposures were collected for each task and combined across the workweek using time-weighted averaging (TWA). CTS case criteria were based on symptoms and results of electrophysiological testing. HRs were estimated with Cox proportional hazard models. Confounding was assessed using causal diagrams and an empirical criterion of 10% or greater change in effect estimate magnitude. Results There were 109 incident CTS cases (IR=4.41/100 person-years; 6.7% cumulative incidence). The relationships between CTS and forceful repetition rate, % time forceful hand exertion and the Threshold Limit Value for Hand Activity Level (TLV-HAL) were slightly confounded by decision latitude with effect estimates being attenuated towards the null (10–14% change) after adjustment. The risk of CTS among participants reporting high job strain was attenuated towards the null by 14% after adjusting for the HAL Scale or the % time forceful hand exertions. Conclusions Although attenuation of the relationships between CTS and some biomechanical and work psychosocial exposures was observed after adjusting for confounding, the magnitudes were small and confirmed biomechanical and work psychosocial exposures as independent risk factors for incident CTS.

Description: Objectives Links between arrhythmias and particulate matter exposures have been found among sensitive populations. We examined the relationship between personal particulate matter ≤2.5 µm aerodynamic diameter (PM 2.5 ) exposures and ectopy in a panel study of healthy welders. Methods Simultaneous ambulatory ECG and personal PM 2.5 exposure monitoring with DustTrak Aerosol Monitor was performed on 72 males during work and non-work periods for 5–90 h (median 40 h). ECGs were summarised hourly for supraventricular ectopy (SVE) and ventricular ectopy (VE). PM 2.5 exposures both work and non-work periods were averaged hourly with lags from 0 to 7 h. Generalised linear mixed-effects models with a random participant intercept were used to examine the relationship between PM 2.5 exposure and the odds of SVE or VE. Sensitivity analyses were performed to assess whether relationships differed by work period and among current smokers. Results Participants had a mean (SD) age of 38 (11) years and were monitored over 2993 person-hours. The number of hourly ectopic events was highly skewed with mean (SD) of 14 (69) VE and 1 (4) SVE. We found marginally significant increases in VE with PM 2.5 exposures in the sixth and seventh hour lags, yet no association with SVE. For every 100 μg/m 3 increase in sixth hour lagged PM 2.5 , the adjusted OR (95% CI) for VE was 1.03 (1.00 to 1.05). Results persisted in work or non-work exposure periods and non-smokers had increased odds of VE associated with PM 2.5 as compared with smokers. Conclusions A small increase in the odds of VE with short-term PM 2.5 exposure was observed among relatively healthy men with environmental and occupational exposures.

Description: Objectives To investigate exposure–response relationships between measured movements and postures of the wrist and the incidence of carpal tunnel syndrome (CTS), and any modifications by sex. Methods In 2011, we established a historical cohort of 9364 members of the Painters’ Union in Denmark. Self-reported task distributions were obtained by questionnaire (53% responded) and combined with sex-specific task exposure matrices to get individual estimates of exposure intensity, that is, velocity of wrist flexion/extension, mean power frequency (MPF) and non-neutral wrist postures. Exposure duration was assessed from yearly working proportions. Registered first-time hospital discharge CTS diagnoses and CTS surgery were collected as outcomes. The cohort was followed from 1994 to 2010. Log-linear Poisson regression was used. Results For CTS diagnoses, the adjusted incidence rate ratios (IRRs) increased with increasing wrist velocity (IRR=1.37 (95% CI 1.10 to 1.71) per °/s) and MPF (IRR=1.53 (95% CI 1.21 to 1.91) per 0.01 Hz). For CTS surgery, the results were similar. The outcomes were not related to non-neutral postures or exposure duration. The adjusted IRRs for women were higher than those for men. There were no multiplicative interaction effects between exposure intensity, exposure duration and sex. However, the absolute incidence rates (IRs) increased at a steeper rate for women than for men, indicating an additive interaction. Conclusions The incidence of CTS increased with increasing velocity of wrist flexion/extension and MPF of wrist movements. The relative increase in incidence rates was the same for women and men, but the absolute incidence rates increased at a steeper rate for women than for men.

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: Objectives Many hairdressers leave their profession due to health problems, including occupational hand eczema, which has been associated with skin exposure to sensitising hair dye components such as paraphenylenediamine (PPD) and paratoluenediamine (PTD). Since the use of protective gloves is advised but without the short-term effect being known, our main goal was to attribute a significant biomarker reduction to adequate glove use, in a real work situation. Methods 11 hairdressers were studied over 2 weeks. In the first week, they worked as usual and (re)used their gloves. Thereafter, we intervened to improve glove use during the second week. In both weeks, workplace exposure data were collected through observations, and systemic exposure was quantified by biomonitoring of PPD and PTD. The effect of improved glove use and other exposure determinants was studied through mixed models analysis. Results We showed that improved glove use significantly reduced mean PTD concentrations from 24.1 before to 4.2 µg/g creatinine after the intervention (n=11, third day postshift). In addition, mean PTD concentrations increased during the first week (14 times elevated after three consecutive shifts), but not during the second week. For PPD, no effect of improved glove use and no accumulation effect were detected. Conclusions Our study is the first to deliver evidence for a significant reduction in systemic exposure to PTD through improved glove use. Disposable gloves should never be reused. PTD biomonitoring is shown to be a practical tool to quantify recent dermal exposure to oxidative hair dye components.

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: 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: 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.