The World Health Organization (WHO) recently released new guidelines for outdoor fine particulate air pollution (PM 2.5 ) recommending an annual average concentration of 5 μg/m 3 . Yet, our understanding of the concentration-response relationship between outdoor PM 2.5 and mortality in this range of near-background concentrations remains incomplete. To address this uncertainty, we conducted a population-based cohort study of 7.1 million adults in one of the world’s lowest exposure environments. Our findings reveal a supralinear concentration-response relationship between outdoor PM 2.5 and mortality at very low (<5 μg/m 3 ) concentrations. Our updated global concentration-response function incorporating this new information suggests an additional 1.5 million deaths globally attributable to outdoor PM 2.5 annually compared to previous estimates. The global health benefits of meeting the new WHO guideline for outdoor PM 2.5 are greater than previously assumed and indicate a need for continued reductions in outdoor air pollution around the world.
The recent proliferation of cohort studies of long-term exposure to outdoor fine particulate air pollution and mortality has led to a significant increase in knowledge about this important global health risk factor. As scientific knowledge has grown, mortality relative risk estimators for fine particulate matter have evolved from simple risk models based on a single study to complex, computationally intensive, integration of multiple independent particulate sources based on nearly one hundred studies. Since its introduction nearly 10 years ago, the integrated exposure-response (IER) model has become the state-of-the art model for such estimates, now used by the Global Burden of Disease Study (GBD), the World Health Organization, the World Bank, the United States Environmental Protection Agency’s benefits assessment software, and scientists worldwide to estimate the burden of disease and examine strategies to improve air quality at global, national, and sub-national scales for outdoor fine particulate air pollution, secondhand smoke, and household pollution from heating and cooking. With each yearly update of the GBD, estimates of the IER continue to evolve, changing with the incorporation of new data and fitting methods. As the number of outdoor fine particulate air pollution cohort studies has grown, including recent estimates of high levels of fine particulate pollution in China, new estimators based solely on outdoor fine particulate air pollution evidence have been proposed which require fewer assumptions than the IER and yield larger relative risk estimates. This paper will discuss the scientific and technical issues analysts should consider regarding the use of these methods to estimate the burden of disease attributable to outdoor fine particulate pollution in their own settings.
In California, wildfire risk and severity have grown substantially in the last several decades. Research has characterized extensive adverse health impacts from exposure to wildfire-attributable fine particulate matter (PM 2.5 ), but few studies have quantified long-term outcomes, and none have used a wildfire-specific chronic dose-response mortality coefficient. Here, we quantified the mortality burden for PM 2.5 exposure from California fires from 2008 to 2018 using Community Multiscale Air Quality modeling system wildland fire PM 2.5 estimates. We used a concentration-response function for PM 2.5 , applying ZIP code–level mortality data and an estimated wildfire-specific dose-response coefficient accounting for the likely toxicity of wildfire smoke. We estimate a total of 52,480 to 55,710 premature deaths are attributable to wildland fire PM 2.5 over the 11-year period with respect to two exposure scenarios, equating to an economic impact of $432 to $456 billion. These findings extend evidence on climate-related health impacts, suggesting that wildfires account for a greater mortality and economic burden than indicated by earlier studies.
Ambient fine particulate matter (PM2.5) is associated with a wide range of acute and chronic health effects, including increased risk of respiratory infection. However, evidence specifically related to novel coronavirus disease (COVID-19) is limited. COVID-19 case counts for 111 Canadian health regions were obtained from the COVID-19 Canada Open Data portal. Annual PM2.5 data for 2000–2016 were estimated from a national exposure surface based on remote sensing, chemical transport modelling and ground observations, and minimum and maximum temperature data for 2000–2015 were based on a national interpolated surface derived from thin-plate smoothing splines. Population counts and sociodemographic data by health region were obtained from the 2016 census, and health data (self-rated health and prevalence of smoking, obesity, and selected chronic diseases) by health region, were obtained from the Canadian Community Health Survey. Data on total number of COVID-19 tests and changes in mobility comparing post-vs. pre-introduction of social distancing measures were available by province. Data were analyzed using negative binomial regression models. After controlling for province, temperature, demographic and health characteristics and days since peak incidence by health region, long-term PM2.5 exposure exhibited a positive association with COVID-19 incidence (incidence rate ratio 1.07, 95% confidence interval 0.97–1.18 per μg/m3). This association was larger in magnitude and statistically significant in analyses excluding provinces that reported cases only for aggregated health regions, excluding health regions with less than median population density, and restricted to the most highly affected provinces (Quebec and Ontario). We observed a positive association between COVID-19 incidence and long-term PM2.5 exposure in Canadian health regions. The association was larger in magnitude and statistically significant in more highly affected health regions and those with potentially less exposure measurement error. While our results generate hypotheses for further testing, they should be interpreted with caution and require further examination using study designs less prone to bias.
Estimating health benefits from improvements in ambient air quality requires the characterization of the magnitude and shape of the association between marginal changes in exposure and marginal changes in risk, and its uncertainty. Several attempts have been made to do this, each requiring different assumptions. These include the Log-Linear(LL), IntegratedExposure-Response(IER), and GlobalExposureMortalityModel(GEMM). In this paper we develop an improved relative risk model suitable for use in health benefits analysis that incorporates features of existing models while addressing limitations in each model. We model the derivative of the relative risk function within a meta-analytic framework; a quantity directly applicable to benefits analysis, incorporating a Fusion of algebraic functions used in previous models. We assume a constant derivative in concentration over low exposures, like the LL model, a declining derivative over moderate exposures observed in cohort studies, and a derivative declining as the inverse of concentration over high global exposures in a similar manner to the GEMM. The model properties are illustrated with examples of fitting it to data for the six specific causes of death previously examined by the GlobalBurdenofDisease program with ambient fine particulate matter (PM2.5). In a test case analysis assuming a 1% (benefits analysis) or 100% (burden analysis), reduction in country-specific fine particulate matter concentrations, corresponding estimated global attributable deaths using the Fusion model were found to lie between those of the IER and LL models, with the GEMM estimates similar to those based on the LL model.
Ambient air pollution has been associated with childhood cancer. However, little is known about the possible impact of ambient ultrafine particles (<0.1 μm) (UFPs) on childhood cancer incidence. This study aimed to evaluate the association between prenatal and childhood exposure to UFPs and development of childhood cancer. We conducted a population-based cohort study of within-city spatiotemporal variations in ambient UFPs across the City of Toronto, Canada using 653,702 singleton live births occurring between April 1, 1998 and March 31, 2017. Incident cases of 13 subtypes of paediatric cancers among children up to age 14 were ascertained using a cancer registry. Associations between ambient air pollutant concentrations and childhood cancer incidence were estimated using random-effects Cox proportional hazards models. We investigated both single- and multi-pollutant models accounting for co-exposures to PM2.5 and NO2. A total of 1,066 childhood cancers were identified. We found that first trimester exposure to UFPs (Hazard Ratio (HR) per 10,000/cm3 increase = 1.13, 95% CI: 1.03-1.22) was associated with overall cancer incidence diagnosed before 6 years of age after adjusting for PM2.5, NO2, and for personal and neighborhood-level covariates. Association between UFPs and overall cancer incidence exhibited a linear shape. No statistically significant associations were found for specific cancer subtypes. Ambient UFPs may represent a previously unrecognized risk factor in the aetiology of cancers in children. Our findings reinforce the importance of conducting further research on the effects of UFPs given their high prevalence of exposure in urban areas.