The health burden of air pollution in the UK: a modelling study using updated exposure-risk associations.

BACKGROUND: Long-term exposure to ambient air pollution, in particular fine particles or PM2·5, is a leading global disease burden. PM2·5 in the UK, dominated by agricultural emissions of ammonia (NH3), has been estimated to be responsible for 29 000-34 000 adult early deaths a year. These estimates use models that relate exposure to health risk that predate cohort studies that have identified a supralinear relationship between exposure and risk at relatively low PM2·5 concentrations typical of the UK (5-12 mg m-3). Here we used this new knowledge to estimate adult premature mortality in the UK in 2019. METHODS: For this modelling study, we used the GEOS-Chem model nested over the UK to simulate ambient PM2·5 concentrations, UK Office for National Statistics (ONS) health data provided by the Global Burden of Disease (GBD), and a hybrid health-risk assessment model. The hybrid model fuses a well established linear relationship between PM2·5 and risk for PM2·5 exceeding 10 mg m-3 with a supralinear curve at lower concentrations that is constrained with cohort studies conducted in Canada and confirmed with similar relationships from cohort studies in the USA and Europe. FINDINGS: We estimated that adult premature mortality attributable to exposure to ambient PM2·5 in the UK totalled 48 625 deaths in 2019 (95% CI 45 118-52 595); 15 000-20 000 more deaths than those estimated using outdated health-risk assessment models. Older people (aged 65 years or older) account for most UK deaths (86%). All adult premature mortality (in people aged 25 years and older) in Greater London (4861, 95% CI 4549-5247) exceeded that in Scotland (3673, 3214-4073), Wales (2462, 2270-2660), and Northern Ireland (1052, 934-1156). INTERPRETATION: According to our findings, PM2·5 is more hazardous to UK adults than previously reported, but a supralinear exposure-response curve also suggests that there are substantial public health gains in targeting dominant source contributors to PM2·5, in particular the unregulated agricultural sector. FUNDING: Department for the Environment, Food and Rural Affairs (DEFRA).

Influence of Oil and Gas End-Use on Summertime Particulate Matter and Ozone Pollution in the Eastern US.

The influence of oil and gas end-use activities on ambient air quality is complex and understudied, particularly in regions where intensive end-use activities and large biogenic emissions of isoprene coincide. In these regions, vehicular emissions of nitrogen oxides (NOx≡NO + NO2) modulate the oxidative fate of isoprene, a biogenic precursor of the harmful air pollutants ozone, formaldehyde, and particulate matter (PM2.5). Here, we investigate the direct and indirect influence of the end-use emissions on ambient air quality. To do so, we use the GEOS-Chem model with focus on the eastern United States (US) in summer. Regional mean end-use NOx of 1.4 ppb suppresses isoprene secondary organic aerosol (OA) formation by just 0.02 µg m-3 and enhances abundance of the carcinogen formaldehyde by 0.3 ppb. Formation of other reactive oxygenated volatile organic compounds is also enhanced, contributing to end-use maximum daily mean 8-h ozone (MDA8 O3) of 8 ppb. End-use PM2.5 is mostly (67%) anthropogenic OA, followed by 20% secondary inorganic sulfate, nitrate and ammonium and 11% black carbon. These adverse effects on eastern US summertime air quality suggest potential for severe air quality degradation in regions like the tropics with year-round biogenic emissions, growing oil and gas end-use and limited environmental regulation.

Impact of Legislated and Best Available Emission Control Measures on UK Particulate Matter Pollution, Premature Mortality, and Nitrogen-Sensitive Habitats.

Past emission controls in the UK have substantially reduced precursor emissions of health-hazardous fine particles (PM2.5) and nitrogen pollution detrimental to ecosystems. Still, 79% of the UK exceeds the World Health Organization (WHO) guideline for annual mean PM2.5 of 5 µg m-3 and there is no enforcement of controls on agricultural sources of ammonia (NH3). NH3 is a phytotoxin and an increasingly large contributor to PM2.5 and nitrogen deposited to sensitive habitats. Here we use emissions projections, the GEOS-Chem model, high-resolution data sets, and contemporary exposure-risk relationships to assess potential human and ecosystem health co-benefits in 2030 relative to the present day of adopting legislated or best available emission control measures. We estimate that present-day annual adult premature mortality attributable to exposure to PM2.5 is 48,625 (95% confidence interval: 45,188-52,595), that harmful amounts of reactive nitrogen deposit to almost all (95%) sensitive habitat areas, and that 75% of ambient NH3 exceeds levels safe for bryophytes and lichens. Legal measures decrease the extent of the UK above the WHO guideline to 58% and avoid 6,800 premature deaths by 2030. This improves with best available measures to 36% of the UK and 13,300 avoided deaths. Both legal and best available measures are insufficient at reducing the extent of damage of nitrogen pollution to sensitive habitats. Far more ambitious reductions in nitrogen emissions (>80%) than is achievable with best available measures (34%) are required to halve the amount of excess nitrogen deposited to sensitive habitats.

Global Cancer Risk From Unregulated Polycyclic Aromatic Hydrocarbons.

In assessments of cancer risk from atmospheric polycyclic aromatic hydrocarbons (PAHs), scientists and regulators rarely consider the complex mixture of emitted compounds and degradation products, and they often represent the entire mixture using a single emitted compound-benzo[a]pyrene. Here, we show that benzo[a]pyrene is a poor indicator of PAH risk distribution and management: nearly 90% of cancer risk worldwide results from other PAHs, including unregulated degradation products of emitted PAHs. We develop and apply a global-scale atmospheric model and conduct health impact analyses to estimate human cancer risk from 16 PAHs and several of their N-PAH degradation products. We find that benzo[a]pyrene is a minor contributor to the total cancer risks of PAHs (11%); the remaining risk comes from other directly emitted PAHs (72%) and N-PAHs (17%). We show that assessment and policy-making that relies solely on benzo[a]pyrene exposure provides misleading estimates of risk distribution, the importance of chemical processes, and the prospects for risk mitigation. We conclude that researchers and decision-makers should consider additional PAHs as well as degradation products.