Occupational exposure to inhaled pollutants and risk of airflow obstruction: a large UK population-based UK Biobank cohort

Thorax ◽  
2020 ◽  
Vol 75 (6) ◽  
pp. 468-475
Author(s):  
Steven S Sadhra ◽  
Nuredin Mohammed ◽  
Om P Kurmi ◽  
David Fishwick ◽  
Sara De Matteis ◽  
...  

BackgroundAlthough around 10% to 15% of COPD burden can be attributed to workplace exposures, little is known about the role of different airborne occupational pollutants (AOP). The main aim of the study was to assess the effect size of the relationship between various AOP, their level and duration of exposure with airflow obstruction (AFO).MethodsA cross-sectional analysis was conducted in 228 614 participants from the UK Biobank study who were assigned occupational exposure using a job exposure matrix blinded to health outcome. Adjusted prevalence ratios (PRs) and 95% CI for the risk of AFO for ever and years of exposure to AOPs were estimated using robust Poisson model. Sensitivity analyses were conducted for never-smokers, non-asthmatic and bi-pollutant model.ResultsOf 228 614 participants, 77 027 (33.7%) were exposed to at least one AOP form. 35.5% of the AFO cases were exposed to vapours, gases, dusts or fumes (VGDF) and 28.3% to dusts. High exposure to vapours increased the risk of occupational AFO by 26%. Exposure to dusts (adjusted PR=1.05; 95% CI 1.01 to 1.08), biological dusts (1.05; 1.01 to 1.10) and VGDF (1.04; 1.01 to 1.07) showed a significantly increased risk of AFO, however, statistically not significant following multiple testing. There was no significant increase in risk of AFO by duration (years) of exposure in current job. The results were null when restricted to never-smokers and when a bi-pollutant model was used. However, when data was analysed based on the level of exposure (low, medium and high) compared with no exposure, directionally there was increase in risk for those with high exposure to vapours, gases, fumes, mists and VGDF but statistically significant only for vapours.ConclusionHigh exposure (in current job) to airborne occupational pollutants was suggestive of higher risk of AFO. Future studies should investigate the relationship between lifetime occupational exposures and COPD.

2019 ◽  
Vol 54 (1) ◽  
pp. 1900186 ◽  
Author(s):  
Sara De Matteis ◽  
Deborah Jarvis ◽  
Andrew Darnton ◽  
Sally Hutchings ◽  
Steven Sadhra ◽  
...  

Occupational exposures are important, preventable causes of chronic obstructive pulmonary disease (COPD). Identification of COPD high-risk jobs is key to focus preventive strategies, but a definitive job-list is unavailable.We addressed this issue by evaluating the association of lifetime job-histories and lung function data in the population-based UK Biobank cohort, whose unprecedented sample size allowed analyses restricted to never-smokers to rule out the most important confounder, tobacco smoking. COPD was spirometrically defined as forced expiratory volume in 1 s/forced vital capacity ratio below the lower limit of normal. Lifetime job-histories were collected via OSCAR (Occupations Self-Coding Automatic Recording), a new validated online tool that automatically codes jobs into the UK Standard Occupational Classification v.2000. Prevalence ratios for COPD by employment duration in each job compared to lifetime office workers were estimated using robust Poisson regression adjusted for age, sex, centre and smoking. Only associations confirmed among never-smokers and never-asthmatics were considered reliable.From the 116 375 participants with complete job-histories, 94 551 had acceptable/repeatable spirometry data and smoking information and were included in the analysis. Six occupations showed an increased COPD risk among never-smokers and never-asthmatics; most of these also with positive exposure-response trends. Interesting new findings included sculptors, gardeners and warehouse workers.COPD patients, especially never-smokers, should be asked about their job-history for better disease management. Focussed preventive strategies in COPD high-risk jobs are warranted.


2018 ◽  
Vol 75 (5) ◽  
pp. 328-336 ◽  
Author(s):  
Régis Colin ◽  
Michel Grzebyk ◽  
Pascal Wild ◽  
Guy Hédelin ◽  
Ève Bourgkard

ObjectivesTo assess the relationship between occupational exposure to metalworking fluids (MWFs) in the steel-producing industry and bladder cancer incidence.MethodsA nested case–control study on bladder cancer was set up in a cohort of workers from six French steel-producing factories. Three controls were randomly selected for each incident bladder cancer case diagnosed from 2006 to 2012. Controls were matched to cases on age at diagnosis and counter-matched on a surrogate measure of exposure to MWFs derived from a job-exposure matrix. Cases (n=84) and controls (n=251) were face-to-face interviewed. Experts assessed occupational exposure to MWFs (straight, soluble and synthetic) using questionnaires and reports from factory visits. Occupational exposures were based on three metrics: duration, frequency-weighted duration and cumulative exposure index. Conditional multiple logistic regressions were used to determine ORs and 95% CIs, taking non-occupational and occupational exposure into account.ResultsIn the 25 years before diagnosis, ORs increased significantly with duration of exposure to straight MWFs (OR=1.13 (1.02–1.25)) and increased with frequency-weighted duration of exposure to straight MWFs (OR=1.44 (0.97–2.14)). These results remained valid after adjusting for duration of smoking, average number of cigarettes smoked per day, time since smoking cessation and exposure to polycyclic aromatic hydrocarbons (PAHs). ORs also increased with soluble MWFs but not significantly. No significant association was found with older exposures to MWFs or with exposure to synthetic MWFs.ConclusionThe increased risk of bladder cancer observed among workers exposed to straight MWFs and to a lesser extent to soluble MWFs may be explained by the presence of carcinogens (such as PAH) in mineral oils component of straight and soluble oils. Prevention therefore remains necessary in sectors using MWFs.


2019 ◽  
Vol 28 (15) ◽  
pp. 2477-2485 ◽  
Author(s):  
Diana A van der Plaat ◽  
Judith M Vonk ◽  
Natalie Terzikhan ◽  
Kim de Jong ◽  
Maaike de Vries ◽  
...  

Abstract Many workers are daily exposed to occupational agents like gases/fumes, mineral dust or biological dust, which could induce adverse health effects. Epigenetic mechanisms, such as DNA methylation, have been suggested to play a role. We therefore aimed to identify differentially methylated regions (DMRs) upon occupational exposures in never-smokers and investigated if these DMRs associated with gene expression levels. To determine the effects of occupational exposures independent of smoking, 903 never-smokers of the LifeLines cohort study were included. We performed three genome-wide methylation analyses (Illumina 450 K), one per occupational exposure being gases/fumes, mineral dust and biological dust, using robust linear regression adjusted for appropriate confounders. DMRs were identified using comb-p in Python. Results were validated in the Rotterdam Study (233 never-smokers) and methylation-expression associations were assessed using Biobank-based Integrative Omics Study data (n = 2802). Of the total 21 significant DMRs, 14 DMRs were associated with gases/fumes and 7 with mineral dust. Three of these DMRs were associated with both exposures (RPLP1 and LINC02169 (2×)) and 11 DMRs were located within transcript start sites of gene expression regulating genes. We replicated two DMRs with gases/fumes (VTRNA2-1 and GNAS) and one with mineral dust (CCDC144NL). In addition, nine gases/fumes DMRs and six mineral dust DMRs significantly associated with gene expression levels. Our data suggest that occupational exposures may induce differential methylation of gene expression regulating genes and thereby may induce adverse health effects. Given the millions of workers that are exposed daily to occupational exposures, further studies on this epigenetic mechanism and health outcomes are warranted.


Author(s):  
Lars-Gunnar Gunnarsson ◽  
Lennart Bodin

Objectives: To carry out an integrated and stratified meta-analysis on occupational exposure to electromagnetic fields (EMFs), metals and pesticides and its effects on amyotrophic lateral sclerosis (ALS) and Parkinson’s and Alzheimer’s disease, and investigate the possibility of publication bias. Methods: In the current study, we updated our recently published meta-analyses on occupational exposures in relation to ALS, Alzheimer’s and Parkinson’s disease. Based on 66 original publications of good scientific epidemiological standard, according to the Meta-analysis of Observational Studies in Epidemiology (MOOSE) and the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) guidelines, we analysed subgroups by carrying out stratified meta-analyses on publication year, statistical precision of the relative risk (RR) estimates, inspection of the funnel plots and test of bias. Results: Based on 19 studies the weighted RR for occupational exposure to EMFs was 1.26 (95% confidence interval (CI) 1.07–1.50) for ALS, 1.33 (95% CI 1.07–1.64) for Alzheimer’s disease and 1.02 (95% CI 0.83–1.26) for Parkinson’s disease. Thirty-one studies concerned occupational exposure to pesticides and the weighted RR was 1.35 (95% CI 1.02–1.79) for ALS, 1.50 (95% CI 0.98–2.29) for Alzheimer’s disease and 1.66 (95% CI 1.42–1.94) for Parkinson’s disease. Finally, 14 studies concerned occupational exposure to metals and only exposure to lead (five studies) involved an elevated risk for ALS or Parkinson’s disease and the weighted RR was 1.57 (95% CI 1.11–2.20). The weighted RR for all the non-lead exposures was 0.97 (95% CI 0.88–1.06). Conclusions: Exposure to pesticides increased the risk of getting the mentioned neurodegenerative diseases by at least 50%. Exposure to lead was only studied for ALS and Parkinson’s disease and involved 50% increased risk. Occupational exposure to EMFs seemed to involve some 10% increase in risk for ALS and Alzheimer’s disease only.


2019 ◽  
Vol 123 (5) ◽  
pp. 574-582 ◽  
Author(s):  
L. C. Stasinopoulos ◽  
A. Zhou ◽  
E. Hyppönen

AbstractExcessive Ca intakes have been proposed to associate with vascular calcification and a higher risk of prostate cancer. We investigated the associations of supplemental and dietary Ca intake with mortality using data from 497 828 UK Biobank participants. The average follow-up was 4·2 years and 14 255 participants died, 8297 from cancer, 2959 from CVD and 572 from respiratory disease. The use of Ca supplements and milk consumption were associated with differences in mortality in younger (≤65 years) but not in older participants (>65 years, Pinteraction ≤ 0·04 for all comparisons). Among participants <65 years, there was an inverse association between Ca supplementation (OR 0·91, 95 % CI 0·83, 0·99) and milk consumption (OR 0·93, 95 % CI 0·86, 1·00) with respect to all-cause mortality. In the same age group, milk drinkers had lower odds of cancer mortality (OR 0·89, 95 % CI 0·80, 0·98) but Ca supplement use was associated with increased odds of respiratory mortality (OR 1·69, 95 % CI 1·16, 2·74). All associations in participants aged ≥65 years were null after full adjustment. In sensitivity analyses stratified by hormone replacement therapy, Ca supplement use was associated with decreased odds of cancer mortality in users but increased risk in other women (OR 0·81, 95 % CI 0·69, 0·94 v. OR 1·17, 95 % CI 1·01, 1·35, respectively). To conclude, we saw little evidence for harm with dietary or supplemental Ca. Further studies are required to confirm the proposed interaction with hormone replacement therapy and to exclude reverse causation as a determinant in the association between Ca supplements and increased risk of respiratory diseases.


2019 ◽  
Vol 76 (9) ◽  
pp. 668-671
Author(s):  
Cheryl E Peters ◽  
Laura Bogaert ◽  
Lidija Latifovic ◽  
Linda Kachuri ◽  
Shelley A Harris ◽  
...  

ObjectivesThe causes of kidney cancer are not well understood though occupational exposures are thought to play a role. Crystalline silica is a known human carcinogen, and despite previous links with kidney disease, there have been few studies investigating its association with kidney cancer. We addressed this research gap using a population-based case-control study of Canadian men.MethodsQuestionnaire data were obtained from individuals with histologically confirmed kidney cancer, and population-based controls recruited from eight Canadian provinces (1994–1997). An industrial hygienist characterised participants’ lifetime occupational exposure, and their confidence in the assessment (possibly, probably or definitely exposed) to silica on three dimensions (intensity, frequency and duration), and cumulative exposure was estimated. Logistic regression was used to estimate ORs and 95% CIs, adjusting for potential confounders.ResultsNearly half of the 689 kidney cancer cases (49%) and 2369 controls (44%) had ever been occupationally exposed to crystalline silica. In a fully adjusted model, workers ever-exposed to silica had a slightly increased risk of kidney cancer relative to those who were unexposed (OR 1.10, 95% CI 0.92 to 1.32). Odds were modestly (and generally not statistically significantly) increased for models with duration of exposure and cumulative exposure, though exposure-response relationships were not evident.ConclusionsOur findings do not provide evidence that occupational exposure to crystalline silica increases risk of kidney cancer in men.


2019 ◽  
Vol 29 (12) ◽  
pp. 5217-5233 ◽  
Author(s):  
Lauren E Salminen ◽  
Rand R Wilcox ◽  
Alyssa H Zhu ◽  
Brandalyn C Riedel ◽  
Christopher R K Ching ◽  
...  

Abstract Secondhand smoke exposure is a major public health risk that is especially harmful to the developing brain, but it is unclear if early exposure affects brain structure during middle age and older adulthood. Here we analyzed brain MRI data from the UK Biobank in a population-based sample of individuals (ages 44–80) who were exposed (n = 2510) or unexposed (n = 6079) to smoking around birth. We used robust statistical models, including quantile regressions, to test the effect of perinatal smoke exposure (PSE) on cortical surface area (SA), thickness, and subcortical volumes. We hypothesized that PSE would be associated with cortical disruption in primary sensory areas compared to unexposed (PSE−) adults. After adjusting for multiple comparisons, SA was significantly lower in the pericalcarine (PCAL), inferior parietal (IPL), and regions of the temporal and frontal cortex of PSE+ adults; these abnormalities were associated with increased risk for several diseases, including circulatory and endocrine conditions. Sensitivity analyses conducted in a hold-out group of healthy participants (exposed, n = 109, unexposed, n = 315) replicated the effect of PSE on SA in the PCAL and IPL. Collectively our results show a negative, long term effect of PSE on sensory cortices that may increase risk for disease later in life.


2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Brett J. Green ◽  
Donald H. Beezhold

Occupational exposure to high-molecular-weight allergens is a risk factor for the development and pathogenesis of IgE-mediated respiratory disease. In some occupational environments, workers are at an increased risk of exposure to fungal enzymes used in industrial production. Fungal enzymes have been associated with adverse health effects in the work place, in particular in baking occupations. Exposure-response relationships have been demonstrated, and atopic workers directly handling fungal enzymes are at an increased risk for IgE-mediated disease and occupational asthma. The utilization of new and emerging fungal enzymes in industrial production will present new occupational exposures. The production of antibody-based immunoassays is necessary for the assessment of occupational exposure and the development of threshold limit values. Allergen avoidance strategies including personal protective equipment, engineering controls, protein encapsulation, and reduction of airborne enzyme concentrations are required to mitigate occupational exposure to fungal enzymes.


PLoS Medicine ◽  
2021 ◽  
Vol 18 (8) ◽  
pp. e1003767
Author(s):  
Xiang Li ◽  
Mengying Wang ◽  
Yongze Song ◽  
Hao Ma ◽  
Tao Zhou ◽  
...  

Background Air pollution has been related to incidence of type 2 diabetes (T2D). We assessed the joint association of various air pollutants with the risk of T2D and examined potential modification by obesity status and genetic susceptibility on the relationship. Methods and findings A total of 449,006 participants from UK Biobank free of T2D at baseline were included. Of all the study population, 90.9% were white and 45.7% were male. The participants had a mean age of 56.6 (SD 8.1) years old and a mean body mass index (BMI) of 27.4 (SD 4.8) kg/m2. Ambient air pollutants, including particulate matter (PM) with diameters ≤2.5 μm (PM2.5), between 2.5 μm and 10 μm (PM2.5–10), nitrogen oxide (NO2), and nitric oxide (NO) were measured. An air pollution score was created to assess the joint exposure to the 4 air pollutants. During a median of 11 years follow-up, we documented 18,239 incident T2D cases. The air pollution score was significantly associated with a higher risk of T2D. Compared to the lowest quintile of air pollution score, the hazard ratio (HR) (95% confidence interval [CI]) for T2D was 1.05 (0.99 to 1.10, p = 0.11), 1.06 (1.00 to 1.11, p = 0.051), 1.09 (1.03 to 1.15, p = 0.002), and 1.12 (1.06 to 1.19, p < 0.001) for the second to fifth quintile, respectively, after adjustment for sociodemographic characteristics, lifestyle factors, genetic factors, and other covariates. In addition, we found a significant interaction between the air pollution score and obesity status on the risk of T2D (p-interaction < 0.001). The observed association was more pronounced among overweight and obese participants than in the normal-weight people. Genetic risk score (GRS) for T2D or obesity did not modify the relationship between air pollution and risk of T2D. Key study limitations include unavailable data on other potential T2D-related air pollutants and single-time measurement on air pollutants. Conclusions We found that various air pollutants PM2.5, PM2.5–10, NO2, and NO, individually or jointly, were associated with an increased risk of T2D in the population. The stratified analyses indicate that such associations were more strongly associated with T2D risk among those with higher adiposity.


BMJ Open ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. e031953
Author(s):  
Yu Shi ◽  
Haifeng Xue ◽  
Yuanshuo Ma ◽  
Licheng Wang ◽  
Tian Gao ◽  
...  

ObjectivesThis study had three objectives: (1) describe the prevalence of occupational exposure among Chinese medical personnel in detail, (2) verify the partial mediating role of work environment satisfaction in the relationship between occupational exposure and job satisfaction, and (3) examine if stress symptoms moderate the relationship between occupational exposure and job satisfaction.DesignA large cross-sectional online survey was conducted in July 2018 in China.SettingA survey was conducted in 54 cities across 14 provinces of China.ParticipantsA total of 12 784 questionnaires were distributed, and 9924 healthcare workers (HCWs) completed valid questionnaires. The response rate was 77.63%.Outcome measuresA confidential questionnaire was distributed to HCWs. The relationships among and the mechanisms of the variables were explored using descriptive statistical analyses, Pearson’s correlation coefficient and multiple linear regression analysis.ResultsThe most common occupational exposures among HCWs in the past 12 months were psychosocial and organisational hazards (85.93%). Overall, physicians (93.7%) and nurses (89.2%) were the main victims of occupational exposure. Occupational exposure correlated negatively with work environment satisfaction and job satisfaction, and positively with stress symptoms. Moreover, work environment satisfaction fully mediated the relationship between occupational exposure and job satisfaction, and stress symptoms moderated the relationship between occupational exposure and job satisfaction.ConclusionThe incidence of occupational exposure among HCWs is generally high. The high frequency of psychosocial and organisational hazards among physicians and nurses should be taken seriously and dealt with in a timely manner by hospital managers. The negative impact of occupational exposure on job satisfaction must be buffered by measures to reduce stress symptoms and enhance working environment satisfaction, ultimately improving the overall quality of life of HCWs and promoting comprehensive development of the medical team.


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