Sources of Discrepancies between a Job Exposure Matrix and a Case by Case Expert Assessment for Occupational Exposure to Formaldehyde and Wood-Dust

1993 ◽  
Vol 22 (Supplement 2) ◽  
pp. S113-S120 ◽  
Author(s):  
D. Luce ◽  
M. Gerin ◽  
F. Berrino ◽  
P. Pisani ◽  
A. Leclerc
Author(s):  
Eirini Dimakakou ◽  
Helinor J. Johnston ◽  
George Streftaris ◽  
John W. Cherrie

Human exposure to particulate air pollution (e.g., PM2.5) can lead to adverse health effects, with compelling evidence that it can increase morbidity and mortality from respiratory and cardiovascular disease. More recently, there has also been evidence that long-term environmental exposure to particulate air pollution is associated with type-2 diabetes mellitus (T2DM) and dementia. There are many occupations that may expose workers to airborne particles and that some exposures in the workplace are very similar to environmental particulate pollution. We conducted a cross-sectional analysis of the UK Biobank cohort to verify the association between environmental particulate air pollution (PM2.5) exposure and T2DM and dementia, and to investigate if occupational exposure to particulates that are similar to those found in environmental air pollution could increase the odds of developing these diseases. The UK Biobank dataset comprises of over 500,000 participants from all over the UK. Environmental exposure variables were used from the UK Biobank. To estimate occupational exposure both the UK Biobank’s data and information from a job exposure matrix, specifically developed for UK Biobank (Airborne Chemical Exposure–Job Exposure Matrix (ACE JEM)), were used. The outcome measures were participants with T2DM and dementia. In appropriately adjusted models, environmental exposure to PM2.5 was associated with an odds ratio (OR) of 1.02 (95% CI 1.00 to 1.03) per unit exposure for developing T2DM, while PM2.5 was associated with an odds ratio of 1.06 (95% CI 0.96 to 1.16) per unit exposure for developing dementia. These environmental results align with existing findings in the published literature. Five occupational exposures (dust, fumes, diesel, mineral, and biological dust in the most recent job estimated with the ACE JEM) were investigated and the risks for most exposures for T2DM and for all the exposures for dementia were not significantly increased in the adjusted models. This was confirmed in a subgroup of participants where a full occupational history was available allowed an estimate of workplace exposures. However, when not adjusting for gender, some of the associations become significant, which suggests that there might be a bias between the occupational assessments for men and women. The results of the present study do not provide clear evidence of an association between occupational exposure to particulate matter and T2DM or dementia.


AIHAJ ◽  
1989 ◽  
Vol 50 (11) ◽  
pp. 574-578 ◽  
Author(s):  
SUBODH K. RASTOGI ◽  
BRAHMA N. GUPTA ◽  
TANVEER HUSAIN ◽  
NEERAJ MATHUR

Author(s):  
Kathrine Pape ◽  
Cecile Svanes ◽  
Camilla S Sejbæk ◽  
Andrei Malinovschi ◽  
Byndis Benediktsdottir ◽  
...  

Abstract Background While direct effects of occupational exposures on an individual’s respiratory health are evident, a new paradigm is emerging on the possible effects of pre-conception occupational exposure on respiratory health in offspring. We aimed to study the association between parental occupational exposure starting before conception and asthma in their offspring (at 0–15 years of age). Methods We studied 3985 offspring participating in the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Their mothers or fathers (n = 2931) previously participated in the European Community Respiratory Health Survey (ECRHS). Information was obtained from questionnaires on parental job history pre- and post-conception which was linked to an asthma-specific job-exposure matrix (JEM). We assessed the association between parental occupational exposure and offspring asthma, applying logistic regression models, clustered by family and adjusted for study centre, offspring sex, parental characteristics (age, asthma onset, place of upbringing, smoking) and grandparents’ level of education. Results Parental occupational exposure to microorganisms, pesticides, allergens or reactive chemicals pre-conception or both pre- and post-conception was not related to offspring asthma; in general, subgroup analyses confirmed this result. However, maternal exposure both pre- and post-conception to allergens and reactive chemicals was associated with increased odds for early-onset asthma in offspring (0–3 years of age); odds ratio 1.70 (95% CI: 1.02–2.84) and 1.65 (95% CI: 0.98–2.77), respectively. Conclusions This study did not find evidence that parental occupational exposure, defined by an asthma JEM before conception only or during pre- and post-conception vs non-exposed, was associated with offspring asthma.


2020 ◽  
pp. oemed-2020-106738
Author(s):  
Angelo d’Errico ◽  
Jana Zajacova ◽  
Anna Cacciatore ◽  
Santo Alfonzo ◽  
Fabio Beatrice ◽  
...  

ObjectivesThere is sufficient evidence for a causal association of sinonasal epithelial cancers (SNEC) only for exposure to wood and leather dusts, nickel compounds and employment in isopropyl alcohol production. The aim of this study was to assess whether other occupational hazards are associated with the risk of SNEC for the main histologic types, namely adenocarcinoma (AD) and squamous cell carcinoma (SCC).MethodsThe study population included 375 incident SNEC cases collected from 1996 to 2014 (79% of all diagnosed SNEC) throughout the Piedmont region by the regional Sinonasal Cancer Registry, and 408 hospital controls. Exposure to 17 occupational agents was assigned through expert assessment based on interviews to the subjects on jobs held throughout their working life. The relationship of SNEC with ever and cumulative exposure to the hazards was assessed through unconditional logistic regression models adjusted for age, sex, area of residence, smoking habit, year of enrolment and coexposures.ResultsAD was associated with both ever and cumulative exposure to wood dust, leather dust and organic solvents, and with cumulative exposure to textiles dusts. SCC risk was significantly increased by ever exposure to nickel, chromium and welding fumes, as well as by cumulative exposure to welding fumes, arsenic and organic solvents. A mixed group of other histological types was associated with both ever and cumulative exposure to wood dust and textile dusts.ConclusionsThe associations of SNEC with wood dust, leather dust and nickel were confirmed, while some new associations were observed for other hazards, which merit further investigation.


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