Exposure to crystalline silica in Canadian workplaces and the risk of kidney cancer

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.

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 76 (Suppl 1) ◽  
pp. A19.2-A19
Author(s):  
Markku Sallmén ◽  
Sanni Uuksulainen ◽  
Christer Hublin ◽  
Aki Koskinen ◽  
Markku Sainio

Epidemiologic studies indicate that occupational exposure to solvents may increase risk of Parkinson disease (PD).We constructed a population-based case-control study of incident PD using a register of Reimbursement of medicine costs of the Social Insurance Institution of Finland, along with the Population Information System, including census records for all Finnish residents. PD cases were diagnosed between 1995–2014. Controls were randomly selected from the population while matching on diagnosis year, birth year (1930–1950), and sex. A total of 11,757 PD cases and 23 236 controls had data from the occupational census in 1990, ensuring ≥4 years exposure lagging and 21 years of occupational history data (5 censuses from 1970–1990). We used the Finnish Job Exposure Matrix to assess cumulative exposure (CE) to four groups of solvents (aliphatic/alicyclic hydrocarbon, aromatic hydrocarbon, chlorinated hydrocarbon, other). We estimated PD-solvent odds ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression, while adjusting for age, sex, socioeconomic status and smoking (a_OR), or additionally for CE to chromium and one of the other solvent groups (ab_OR).In total, 3758 cases (30.4%) and 7445 controls (32.0%) were potentially exposed to solvents (a_OR 0.99; CI: 0.94–1.05). Exposure to chlorinated hydrocarbons was associated with PD (a_OR 1.20; CI: 1.05–1.36; ab_OR 1.21 CI: 1.04–1.40) at the highest CE group (20–145 ppm-years, n=409 cases and 728 controls) but not at lower CE levels. Overall, CE to chlorinated hydrocarbons (n=1840 cases and 3693 controls) was associated with increased risk of PD (p-for-trend=0.01). There was no evidence of a positive association for any of the other solvent groups.We observed a positive association between occupational exposure to chlorinated hydrocarbons and risk of PD. This was especially true for greatest duration and/or level of exposure.


2019 ◽  
Vol 76 (7) ◽  
pp. 433-440 ◽  
Author(s):  
Catherine L Callahan ◽  
Melissa C Friesen ◽  
Sarah J Locke ◽  
Pamela J Dopart ◽  
Patricia A Stewart ◽  
...  

ObjectivesLead is a suspected carcinogen that has been inconsistently associated with kidney cancer. To clarify this relationship, we conducted an analysis of occupational lead exposure within a population-based study of kidney cancer using detailed exposure assessment methods.MethodsStudy participants (1217 cases and 1235 controls), enrolled between 2002 and 2007, provided information on their occupational histories and, for selected lead-related occupations, answered questions regarding workplace tasks, and use of protective equipment. Industrial hygienists used this information to develop several estimates of occupational lead exposure, including probability, duration and cumulative exposure. Unconditional logistic regression was used to compute ORs and 95% CIs for different exposure metrics, with unexposed subjects serving as the reference group. Analyses were also conducted stratifying on several factors, including for subjects of European ancestry only, single nucleotide polymorphisms in ALAD (rs1805313, rs1800435, rs8177796, rs2761016), a gene involved in lead toxicokinetics.ResultsIn our study, cumulative occupational lead exposure was not associated with kidney cancer (OR 0.9, 95% CI 0.7 to 1.3 for highest quartile vs unexposed; ptrend=0.80). Other lead exposure metrics were similarly null. We observed no evidence of effect modification for the evaluated ALAD variants (subjects of European ancestry only, 662 cases and 561 controls) and most stratifying factors, although lead exposure was associated with increased risk among never smokers.ConclusionsThe findings of this study do not offer clear support for an association between occupational lead exposure and kidney cancer.


2017 ◽  
Vol 75 (4) ◽  
pp. 303-309 ◽  
Author(s):  
Mengting Xu ◽  
Jack Siemiatycki ◽  
Jérôme Lavoué ◽  
Romain Pasquet ◽  
Javier Pintos ◽  
...  

ObjectivesTo determine whether occupational exposure to gasoline engine emissions (GEE) increased the risk of lung cancer and more specifically whether leaded or unleaded GEE increased the risk.MethodsTwo population-based case–control studies were conducted in Montreal, Canada. The first was conducted in the early 1980s and included many types of cancer including lung cancer. The second was conducted in the late 1990s and focused on lung cancer. Population controls were used in both studies. Altogether, there were 1595 cases and 1432 population controls. A comprehensive expert-based exposure assessment procedure was implemented and exposure was assessed for 294 agents, including unleaded GEE, leaded GEE and diesel engine emissions (DEE). Logistic regression analyses were conducted to estimate ORs between various metrics of GEE exposure and lung cancer, adjusting for smoking, DEE and other potential confounders.ResultsAbout half of all controls were occupationally exposed to GEE. Irrespective of the metrics of exposure (any exposure, duration of exposure and cumulative exposure) and the type of lung cancer, and the covariates included in models, none of the point estimates of the ORs between occupational exposure to leaded or unleaded GEE and lung cancer were above 1.0. Pooling two studies, the OR for any exposure to leaded GEE was 0.82 (0.68–1.00).ConclusionsOur results do not support the hypothesis that occupational exposure to GEE increases the risk of lung cancer.


Author(s):  
Grace X Chen ◽  
Andrea’t Mannetje ◽  
Jeroen Douwes ◽  
Leonard H Berg ◽  
Neil Pearce ◽  
...  

Abstract In a New Zealand population-based case-control study we assessed associations with occupational exposure to electric shocks, extremely low-frequency magnetic fields (ELF-MF) and motor neurone disease using job-exposure matrices to assess exposure. Participants were recruited between 2013 and 2016. Associations with ever/never, duration, and cumulative exposure were assessed using logistic regression adjusted for age, sex, ethnicity, socioeconomic status, education, smoking, alcohol consumption, sports, head or spine injury and solvents, and mutually adjusted for the other exposure. All analyses were repeated stratified by sex. An elevated risk was observed for having ever worked in a job with potential for electric shocks (odds ratio (OR)=1.35, 95% confidence interval (CI): 0.98, 1.86), with the strongest association for the highest level of exposure (OR=2.01, 95%CI: 1.31, 3.09). Analysis by duration suggested a non-linear association: risk was increased for both short-duration (<3 years) (OR= 4.69, 95%CI: 2.25, 9.77) and long-duration in a job with high level of electric shock exposure (>24 years; OR=1.88; 95%CI: 1.05, 3.36), with less pronounced associations for intermediate durations. No association with ELF-MF was found. Our findings provide support for an association between occupational exposure to electric shocks and motor neurone disease but did not show associations with exposure to work-related ELF-MF.


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.


Thorax ◽  
2019 ◽  
Vol 74 (7) ◽  
pp. 650-658 ◽  
Author(s):  
Sheikh M Alif ◽  
Shyamali Dharmage ◽  
Geza Benke ◽  
Martine Dennekamp ◽  
John Burgess ◽  
...  

RationaleWhile cross-sectional studies have shown associations between certain occupational exposures and lower levels of lung function, there was little evidence from population-based studies with repeated lung function measurements.ObjectivesWe aimed to investigate the associations between occupational exposures and longitudinal lung function decline in the population-based Tasmanian Longitudinal Health Study.MethodsLung function decline between ages 45 years and 50 years was assessed using data from 767 participants. Using lifetime work history calendars completed at age 45 years, exposures were assigned according to the ALOHA plus Job Exposure Matrix. Occupational exposures were defined as ever exposed and cumulative exposure -unit- years. We investigated effect modification by sex, smoking and asthma status.ResultsCompared with those without exposure, ever exposures to aromatic solvents and metals were associated with a greater decline in FEV1 (aromatic solvents 15.5 mL/year (95% CI −24.8 to 6.3); metals 11.3 mL/year (95% CI −21.9 to – 0.7)) and FVC (aromatic solvents 14.1 mL/year 95% CI −28.8 to – 0.7; metals 17.5 mL/year (95% CI –34.3 to – 0.8)). Cumulative exposure (unit years) to aromatic solvents was also associated with greater decline in FEV1 and FVC. Women had lower cumulative exposure years to aromatic solvents than men (mean (SD) 9.6 (15.5) vs 16.6 (14.6)), but greater lung function decline than men. We also found association between ever exposures to gases/fumes or mineral dust and greater decline in lung function.ConclusionsExposures to aromatic solvents and metals were associated with greater lung function decline. The effect of aromatic solvents was strongest in women. Preventive strategies should be implemented to reduce these exposures in the workplace.


2020 ◽  
Vol 77 (3) ◽  
pp. 172-178 ◽  
Author(s):  
Nynke Spinder ◽  
Lynn M Almli ◽  
Tania A Desrosiers ◽  
Kathryn E Arnold ◽  
Jorieke E H Bergman ◽  
...  

ObjectivesThe aim of this study was to assess the association between maternal occupational exposure to solvents and gastroschisis in offspring.MethodsWe used data from the National Birth Defects Prevention Study, a large population-based case-control study of major birth defects conducted in 10 US states from 1997 to 2011. Infants with gastroschisis were ascertained by active birth defects surveillance systems. Control infants without major birth defects were selected from vital records or birth hospital records. Self-reported maternal occupational histories were collected by telephone interview. Industrial hygienists reviewed this information to estimate exposure to aromatic, chlorinated and petroleum-based solvents from 1 month before conception through the first trimester of pregnancy. Cumulative exposure to solvents was estimated for the same period accounting for estimated exposure intensity and frequency, job duration and hours worked per week. ORs and 95% CIs were estimated to assess the association between exposure to any solvents or solvent classes, and gastroschisis risk.ResultsAmong 879 cases and 7817 controls, the overall prevalence of periconceptional solvent exposure was 7.3% and 7.4%, respectively. Exposure to any solvent versus no exposure to solvents was not associated with gastroschisis after adjusting for maternal age (OR 1.00, 95% CI 0.75 to 1.32), nor was an association noted for solvent classes. There was no exposure-response relationship between estimated cumulative solvent exposure and gastroschisis after adjusting for maternal age.ConclusionOur study found no association between maternal occupational solvent exposure and gastroschisis in offspring. Further research is needed to understand risk factors for gastroschisis.


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.


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