Dataset Information

Systemic inequalities in indoor air pollution exposure in London, UK.

ABSTRACT: 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 PM_2.5, NO_x 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 relevance

There 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.

SUBMITTER: Ferguson L

PROVIDER: S-EPMC7610964 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Because most people spend the majority of their time in microenvironments, indoor air pollution (IAP) has gained more attention than outdoor air pollution recently. It is indeed crucial to understand IAP sources and the factors that influence human exposure. We synthesized evidence on IAP levels and contributing factors in Ethiopia from available literature, utilizing findings from 19 studies to retrieve 66 relevant values. Particulate matters (PM2.5, PM4, PM10, and TSP), as well as gaseous pollutants such as carbon monoxide (CO), nitrogen dioxide (NO2), polyaromatic hydrocarbons (PAHs), and total volatile organic compounds (TVOCs), were analyzed. The calculated mean concentrations for PM2.5, PM10, NO2, TVOCs, and CO were 477.47 μg/m3, 228.38 μg/m3, 63.84 μg/m3, 1361.79 μg/m3, and 18.82 ppm, respectively, all of which exceeded the annual WHO exposure guidelines. Geographical location, stove type, and household activities showed a variation in pollutants concentration. The higher levels of pollutants were attributed to emissions from biomass fuel used for baking injera, wot preparation, and conducting a coffee ceremony, as well as poor ventilation, season, cooking time, and tobacco smoke. The health risk assessments for exposure to various domestic activities were found to be acceptable, except for PM10, with the highest correlation with an acute respiratory infection. Although improved cookstove technology has been proposed as a sustainable energy source, investigations in Ethiopia have revealed that there is still room for public health protection. There is a paucity of research on the relationship between indoor and outdoor air pollution. Future research should prioritize these issues, with a focus on the link between IAP exposure and health effects. In conclusion, there is a higher IAP concentration in Ethiopia so the community should be made aware of it as well as related health effects, and immediate mitigation measures are needed to achieve a reduction in exposure.

Project description:BackgroundAir pollution may cause inflammatory and oxidative stress damage to the brain, leading to neurodegenerative disease. The association between air pollution and dementia, and modification by apolipoprotein E genotype 4 (APOE-ε4) has yet to be fully investigated.ObjectivesTo examine associations of air pollution with three types of incident dementias (Alzheimer's disease (AD), frontotemporal dementia (FTD), and vascular dementia (VAD)), and their potential modification by APOE-ε4 genotype.MethodsThe UK Biobank enrolled >500,000 participants (2006-2010) with ongoing follow-up. We used annual averages of air pollution (PM2.5, PM10, PM2.5-10, PM2.5absorbance, NO2, NOX) for 2010 scaled to interquartile ranges (IQR). We included individuals aged ≥60 years, with no dementia diagnosis prior to January 1, 2010. Time to incident dementia and follow-up time were reported from baseline (January 01, 2010) to last censor event (death, last hospitalization, or loss to follow-up). Cox proportional hazard ratios (HR) and 95% confidence intervals (95% CI) were calculated to estimate the association of air pollutants and incident dementia, and modification of these associations by APOE-ε4.ResultsOur sample included 187,194 individuals (including N = 680 AD, N = 377 VAD, N = 63 FTD) with a mean follow-up of 7.04 years. We observed consistent associations of PM2.5 with greater risk of all-cause dementia (HR = 1.17, 95% CI: 1.10, 1.24) and AD (HR = 1.17, 95% CI: 1.06, 1.29). NO2 was also associated with greater risk of any incident dementia (HR = 1.18, 95% CI: 1.10, 1.25), AD (HR = 1.15, 95% CI: 1.04, 1.28) and VAD (HR = 1.18, 95% CI: 1.03, 1.35). APOE-ε4 did not modify the association between any air pollutants and dementia.DiscussionPM2.5 and NO2 levels were associated with several types of dementia, and these associations were not modified by APOE-ε4. Findings from the UK Biobank support and extend to other epidemiological evidence for the potential association of air pollutants with detrimental brain health during aging.

Project description:BACKGROUND: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people's noise exposure indoors in bedrooms. OBJECTIVES: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). METHODS: We evaluated 1,926 cohort participants at baseline (years 2003-2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. RESULTS: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 ?g/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (? = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (? = 1.23; 95% CI: 0.21, 2.25), and DBP (??= 0.56; 95% CI: -0.03, 1.14) per 10 ?g/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise-SBP association was stronger and statistically significant with a threshold at 30 dB(A). CONCLUSION: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity.

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Systemic inequalities in indoor air pollution exposure in London, UK.

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