Dataset Information

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

ABSTRACT: Human exposure to particulate air pollution (e.g., PM_2.5) 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 (PM_2.5) 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 PM_2.5 was associated with an odds ratio (OR) of 1.02 (95% CI 1.00 to 1.03) per unit exposure for developing T2DM, while PM_2.5 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.

SUBMITTER: Dimakakou E

PROVIDER: S-EPMC7767456 | biostudies-literature | 2020 Dec

REPOSITORIES: biostudies-literature

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

Dimakakou Eirini E Johnston Helinor J HJ Streftaris George G Cherrie John W JW

International journal of environmental research and public health 20201221 24

Human exposure to particulate air pollution (e.g., PM<sub>2.5</sub>) 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 ...[more]

PMID: 33371391

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Project description:BackgroundLong-term exposure to air pollution concentrations is known to be adversely associated with a broad range of single non-communicable diseases, but its role in multimorbidity has not been investigated in the UK. We aimed to assess associations between long-term air pollution exposure and multimorbidity status, severity, and patterns using the UK Biobank cohort.MethodsMultimorbidity status was calculated based on 41 physical and mental conditions. We assessed cross-sectional associations between annual modeled particulate matter (PM)2.5, PMcoarse, PM10, and nitrogen dioxide (NO2) concentrations (μg/m3-modeled to residential address) and multimorbidity status at the baseline assessment (2006-2010) in 364,144 people (mean age: 52.2 ± 8.1 years, 52.6% female). Air pollutants were categorized into quartiles to assess dose-response associations. Among those with multimorbidity (≥2 conditions; n = 156,395) we assessed associations between air pollutant exposure levels and multimorbidity severity and multimorbidity patterns, which were identified using exploratory factor analysis. Associations were explored using generalized linear models adjusted for sociodemographic, behavioral, and environmental indicators.ResultsHigher exposures to PM2.5, and NO2 were associated with multimorbidity status in a dose-dependent manner. These associations were strongest when we compared the highest air pollution quartile (quartile 4: Q4) with the lowest quartile (Q1) [PM2.5: adjusted odds ratio (adjOR) = 1.21 (95% CI = 1.18, 1.24); NO2: adjOR = 1.19 (95 % CI = 1.16, 1.23)]. We also observed dose-response associations between air pollutant exposures and multimorbidity severity scores. We identified 11 multimorbidity patterns. Air pollution was associated with several multimorbidity patterns with strongest associations (Q4 vs. Q1) observed for neurological (stroke, epilepsy, alcohol/substance dependency) [PM2.5: adjOR = 1.31 (95% CI = 1.14, 1.51); NO2: adjOR = 1.33 (95% CI = 1.11, 1.60)] and respiratory patterns (COPD, asthma) [PM2.5: adjOR = 1.24 (95% CI = 1.16, 1.33); NO2: adjOR = 1.26 (95% CI = 1.15, 1.38)].ConclusionsThis cross-sectional study provides evidence that exposure to air pollution might be associated with having multimorbid, multi-organ conditions. Longitudinal studies are needed to further explore these associations.

Project description:Chronic exposure to particulate air pollution may accelerate cognitive decline in older adults, although data on this association are limited. Our objective was to examine long-term exposure to particulate matter (PM) air pollution, both coarse ([PM 2.5-10 ?m in diameter [PM(2.5-10)]) and fine (PM <2.5 ?m in diameter [PM(2.5)]), in relation to cognitive decline.The study population comprised the Nurses' Health Study Cognitive Cohort, which included 19,409 US women aged 70 to 81 years. We used geographic information system-based spatiotemporal smoothing models to estimate recent (1 month) and long-term (7-14 years) exposures to PM(2.5-10), and PM(2.5) preceding baseline cognitive testing (1995-2001) of participants residing in the contiguous United States. We used generalized estimating equation regression to estimate differences in the rate of cognitive decline across levels of PM(2.5-10) and PM(2.5) exposures. The main outcome measure was cognition, via validated telephone assessments, administered 3 times at approximately 2-year intervals, including tests of general cognition, verbal memory, category fluency, working memory, and attention.Higher levels of long-term exposure to both PM(2.5-10) and PM(2.5) were associated with significantly faster cognitive decline. Two-year decline on a global score was 0.020 (95% CI, -0.032 to -0.008) standard units worse per 10 ?g/m(3) increment in PM(2.5-10) exposure and 0.018 (95% CI, -0.035 to -0.002) units worse per 10 ?g/m(3) increment in PM(2.5) exposure. These differences in cognitive trajectory were similar to those between women in our cohort who were approximately 2 years apart in age, indicating that the effect of a 10-?g/m(3) increment in long-term PM exposure is cognitively equivalent to aging by approximately 2 years.Long-term exposure to PM(2.5-10) and PM(2.5) at levels typically experienced by many individuals in the United States is associated with significantly worse cognitive decline in older women.

Project description:ObjectiveTo prospectively assess whether air pollution, including PM2.5, PM10, and NOx, is associated with the risk of all-cause dementia, Alzheimer's disease (AD), and vascular dementia, and to investigate the potential relationship between air pollution and genetic susceptibility in the development of AD.Methods and resultsOur study included 437,932 participants from the UK Biobank with a median follow-up period of over 10 years. Using a Cox proportional hazards model, we found that participants exposed to PM2.5 levels of ≥10 μg/m3 had a higher risk of developing all-cause dementia (HR = 1.1; 95% CI: 1.05-1.28; p < 0.05) compared to the group exposed to PM2.5 levels of <10 μg/m3. However, there was no significant association between PM10 levels of ≥15 μg/m3 and the risk of all-cause dementia, AD, or vascular dementia when compared to the group exposed to PM10 levels of <15 μg/m3. On the other hand, participants exposed to NOx levels of ≥50 μg/m3 had a significantly higher risk of all-cause dementia (HR = 1.14; 95% CI: 1.02-1.26; p < 0.05) and AD (HR = 1.26; 95% CI: 1.08-1.48; p < 0.05) compared to the group exposed to NOx levels of <50 μg/m3. Furthermore, we examined the combined effect of air pollution (PM2.5, PM10, and NOx) and Alzheimer's disease genetic risk score (AD-GRS) on the development of AD using a Cox proportional hazards model. Among participants with a high AD-GRS, those exposed to NOx levels of ≥50 μg/m3 had a significantly higher risk of AD compared to those in the group exposed to NOx levels of <50 μg/m3 (HR = 1.36; 95% CI: 1.03-1.18; p < 0.05). Regardless of air pollutant levels (PM2.5, PM10, or NOx), participants with a high AD-GRS had a significantly increased risk of developing AD. Similar results were obtained when assessing multiple variables using inverse probability of treatment weighting (IPTW).ConclusionOur findings indicate that individuals living in areas with PM2.5 levels of ≥10 μg/m3 or NOx levels of ≥50 μg/m3 are at a higher risk of developing all-cause dementia. Moreover, individuals with a high AD-GRS demonstrated an increased risk of developing AD, particularly in the presence of NOx ≥ 50 μg/m3.

Project description:Deprived communities in many cities are exposed to higher levels of outdoor air pollution, and there is increasing evidence of similar disparities for indoor air pollution exposure. There is a need to understand the drivers for this exposure disparity in order to develop effective interventions aimed at improving population health and reducing health inequities. With a focus on London, UK, this paper assembles evidence to examine why indoor exposure to PM2.5, NOx and CO may disproportionately impact low-income groups. In particular, five factors are explored, namely: housing location and ambient outdoor levels of pollution; housing characteristics, including ventilation properties and internal sources of pollution; occupant behaviours; time spent indoors; and underlying health conditions. Evidence is drawn from various sources, including building physics models, modelled outdoor air pollution levels, time-activity surveys, housing stock surveys, geographical data, and peer-reviewed research. A systems framework is then proposed to integrate these factors, highlighting how exposure to high levels of indoor air pollution in low-income homes is in large part due to factors beyond the control of occupants, and is therefore an area of systemic inequality.Policy relevanceThere is increasing public and political awareness of the impact of air pollution on public health. Strong scientific evidence links exposure to air pollution with morbidity and mortality. Deprived communities may be more affected, however, with limited evidence on how deprivation may influence their personal exposure to air pollution, both outdoors and indoors. This paper describes different factors that may lead to low-income households being exposed to higher levels of indoor air pollution than the general population, using available data and models for London (i.e. living in areas of higher outdoor air pollution, in poor-quality housing, undertaking more pollution-generating activities indoors and spending more time indoors). A systems approach is used to show how these factors lead to systemic exposure inequalities, with low-income households having limited opportunities to improve their indoor air quality. This paper can inform actions and public policies to reduce environmental health inequalities, considering both indoor and outdoor air.

Dataset Information

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

Publications

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

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