Is Environmental and Occupational Particulate Air Pollution Exposure Related to Type-2 Diabetes and Dementia? A Cross-Sectional Analysis of the UK Biobank.

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.

Evaluation of the Suitability of an Existing Job-Exposure Matrix for the Assessment of Exposure of UK Biobank Participants to Dust, Fumes, and Diesel Exhaust Particulates.

Many epidemiological studies have shown an association between outdoor particulate air pollutants and increased morbidity and mortality. Inhalation of ambient aerosols can exacerbate or promote the development of cardiovascular and pulmonary diseases as well as other diseases, such as type 2 diabetes mellitus (T2DM) and neurodegenerative diseases. Occupational exposure to dust, fumes and diesel exhaust particulates can also cause adverse health outcomes and there are numerous occupations where workers are exposed to airborne particles that are similar to ambient air pollution. An individual's job title has normally been identified as a major determinant of workplace exposure in epidemiological studies. This has led to the development of Job-Exposure Matrices (JEMs) as a way of characterising specific workplace exposures. One JEM for airborne chemical exposures is the Airborne Chemical Exposure Job-Exposure Matrix (ACE JEM), developed specifically for the UK Biobank cohort. The objective of this paper is to evaluate the suitability of the ACE JEM in assessing occupational aerosol exposure of participants in the UK Biobank. We searched the scientific literature to identify exposure data linked to selected jobs in the ACE JEM and compared these data with the JEM assessments. Additionally, we carried out an independent expert-based assessment of exposure to compare with the JEM estimates. There is good published evidence to substantiate the high dust and biological dust assignments in the JEM and more limited evidence for diesel exhaust particulates. There is limited evidence in the published literature to substantiate moderate or low exposure assignments in the JEM. The independent expert-based assessment found good agreement at the two extremes of exposure in the JEM (high and no exposure), with uncertainty in all other classifications. The ACE JEM assignments are probably reliable for highly exposed jobs and for jobs assigned as unexposed. However, the assignments for medium and low exposures are less reliable. The ACE JEM is likely to be a good tool to examine associations between occupational exposures to particulates and chronic disease, although it should be used with caution. Further efforts should be made to improve the reliability of the ACE JEM.

Exposure to Environmental and Occupational Particulate Air Pollution as a Potential Contributor to Neurodegeneration and Diabetes: A Systematic Review of Epidemiological Research.

It has been hypothesised that environmental air pollution, especially airborne particles, is a risk factor for type 2 diabetes mellitus (T2DM) and neurodegenerative conditions. However, epidemiological evidence is inconsistent and has not been previously evaluated as part of a systematic review. Our objectives were to carry out a systematic review of the epidemiological evidence on the association between long-term exposure to ambient air pollution and T2DM and neurodegenerative diseases in adults and to identify if workplace exposures to particles are associated with an increased risk of T2DM and neurodegenerative diseases. Assessment of the quality of the evidence was carried out using the GRADE system, which considers the quality of the studies, consistency, directness, effect size, and publication bias. Available evidence indicates a consistent positive association between ambient air pollution and both T2DM and neurodegeneration risk, such as dementia and a general decline in cognition. However, corresponding evidence for workplace exposures are lacking. Further research is required to identify the link and mechanisms associated with particulate exposure and disease pathogenesis and to investigate the risks in occupational populations. Additional steps are needed to reduce air pollution levels and possibly also in the workplace environment to decrease the incidence of T2DM and cognitive decline.