Description: Objectives Occupational exposure to disinfectants is associated with work-related asthma, especially in healthcare workers. However, little is known about the specific products involved. To evaluate disinfectant exposures, we designed job-exposure (JEM) and job-task-exposure (JTEM) matrices, which are thought to be less prone to differential misclassification bias than self-reported exposure. We then compared the three assessment methods: self-reported exposure, JEM and JTEM. Methods Disinfectant use was assessed by an occupational questionnaire in 9073 US female registered nurses without asthma, aged 49–68 years, drawn from the Nurses' Health Study II. A JEM was created based on self-reported frequency of use (1–3, 4–7 days/week) of 7 disinfectants and sprays in 8 nursing jobs. We then created a JTEM combining jobs and disinfection tasks to further reduce misclassification. Exposure was evaluated in 3 classes (low, medium, high) using product-specific cut-offs (eg, 〈30%, 30–49.9%, ≥50%, respectively, for alcohol); the cut-offs were defined from the distribution of self-reported exposure per job/task. Results The most frequently reported disinfectants were alcohol (weekly use: 39%), bleach (22%) and sprays (20%). More nurses were classified as highly exposed by JTEM (alcohol 41%, sprays 41%, bleach 34%) than by JEM (21%, 30%, 26%, respectively). Agreement between JEM and JTEM was fair-to-moderate ( 0.3–0.5) for most disinfectants. JEM and JTEM exposure estimates were heterogeneous in most nursing jobs, except in emergency room and education/administration. Conclusions The JTEM may provide more accurate estimates than the JEM, especially for nursing jobs with heterogeneous tasks. Use of the JTEM is likely to reduce exposure misclassification.

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 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 Nurses are at increased risk of occupational asthma, an observation that may be related to disinfectants exposure. Whether asthma history influences job type or job changes among nurses is unknown. We investigated this issue in a large cohort of nurses. Methods The Nurses’ Health Study II is a prospective study of US female nurses enrolled in 1989 (ages 24–44 years). Job status and asthma were assessed in biennial (1989–2011) and asthma-specific questionnaires (1998, 2003). Associations between asthma history at baseline (diagnosis before 1989, n=5311) and job type at baseline were evaluated by multinomial logistic regression. The relations of asthma history and severity during follow-up to subsequent job changes were evaluated by Cox models. Results The analytic cohort included 98 048 nurses. Compared with nurses in education/administration (likely low disinfectant exposure jobs), women with asthma history at baseline were less often employed in jobs with likely high disinfectant exposure, such as operating rooms (odds ratio 0.73 (95% CI 0.63 to 0.86)) and emergency room/inpatient units (0.89 (0.82 to 0.97)). During a 22-year follow-up, nurses with a baseline history of asthma were more likely to move to jobs with lower exposure to disinfectants (HR 1.13 (1.07 to 1.18)), especially among those with more severe asthma (HR for mild persistent: 1.13; moderate persistent 1.26; severe persistent: 1.50, compared with intermittent asthma, p trend: 0.004). Conclusions Asthma history was associated with baseline job type and subsequent job changes among nurses. This may partly reflect avoidance of tasks involving disinfectant use, and may introduce bias in cross-sectional studies on disinfectant exposure and asthma in nurses.

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).

Description: Objectives Exposure to traffic-related air pollution (TRAP) has been associated with adverse respiratory and systemic outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and thereby health effects. The authors aimed to determine the short-term health effects of TRAP in healthy participants and any possible modifying effect of PA. Methods Crossover real-world exposure study comparing in 28 healthy participants pulmonary and inflammatory responses to four different exposure scenarios: 2 h exposure in a high and low TRAP environment, each at rest and in combination with intermittent moderate PA, consisting of four 15 min rest and cycling intervals. Data were analysed using mixed effect models for repeated measures. Results Intermittent PA compared to rest, irrespective of the TRAP exposure status, increased statistically significant (p≤0.05) pulmonary function (forced expiratory volume in 1 s (34 mL), forced vital capacity (29 mL), forced expiratory flow (FEF 25–75% ) (91 mL)), lung inflammation (fraction of exhaled nitric oxide, FeNO, (0.89 ppb)), and systemic inflammation markers interleukin-6 (52.3%), leucocytes (9.7%) and neutrophils count (18.8%). Interquartile increases in coarse particulate matter were statistically significantly associated with increased FeNO (0.80 ppb) and neutrophil count (5.7%), while PM 2.5 and PM 10 (particulate matter smaller than 2.5 and 10 µm in diameter, respectively) increased leucocytes (5.1% and 4.0%, respectively). We found no consistent evidence for an interaction between TRAP and PA for any of the outcomes of interest. Conclusions In a healthy population, intermittent moderate PA has beneficial effects on pulmonary function even when performed in a highly polluted environment. This study also suggests that particulate air pollution is inducing pulmonary and systemic inflammatory responses.

Description: Introduction Since 2000 a decline in the incidence of occupational asthma (OA) has been reported in the UK and Europe. We aimed to describe and account for trends in the incidence of OA in the West Midlands, UK using annual notification data from the SHIELD voluntary surveillance scheme over the period 1991–2011. Methods All notifications to the SHIELD database between January 1991 and December 2011 were identified, along with patients’ demographic data, occupations, causative agents and confirmatory tests. Annual notifications were scaled to give an annual count per million workers, giving a measure of incidence, and also standardised against those of bakers’ asthma. Non-parametric analyses were undertaken between annual incidence and time (years) for common causative agents using (1) a negative binomial regression univariate model and (2) a logistic regression model calculating annual reporting ORs. A step-change analysis was used to examine time points at which there were marked reductions in incidence. Results A decrease in annual incidence of OA was observed over the study period (incident rate ratio=0.945; 95% CI 0.933 to 0.957; p〈0.0001), an effect that was lost after standardising for bakers’ asthma. Decreases in incidence were seen for most common causative agents, with only cleaning product-related OA increasing over 21 years. Marked fall in incidence was seen in 2004 for isocyanates, and in 1995 for latex. Most notifications came from a regional specialist occupational lung disease unit, with notifications from other sites falling from 16 cases/million workers/annum in 1995 to 0 in 2004. Conclusions Reporter fatigue and increasing under-recognition of OA are both factors which contribute to the apparent fall in incidence of OA in the West Midlands. There is a future need for interventions that enable health professionals to identify potential cases of OA in the workplace and in healthcare settings.