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Estimating Causal Effects of Local Air Pollution on Daily Deaths: Effect of Low Levels Estimating Causal Effects of Local Air Pollution on Daily Deaths: Effect of Low Levels The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Schwartz, Joel, Marie-Abele Bind, and Petros Koutrakis. 2016. “Estimating Causal Effects of Local Air Pollution on Daily Deaths: Effect of Low Levels.” Environmental Health Perspectives 125 (1): 23-29. doi:10.1289/EHP232. http://dx.doi.org/10.1289/EHP232. Published Version doi:10.1289/EHP232 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:30371186 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA A Section 508–conformant HTML version of this article is available at http://dx.doi.org/10.1289/EHP232. Research Estimating Causal Effects of Local Air Pollution on Daily Deaths: Effect of Low Levels Joel Schwartz, Marie-Abele Bind, and Petros Koutrakis Department of Environmental Health, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA et al. 2011; Bartoli et al. 2009; Brook et al. BACKGROUND: Although many time-series studies have established associations of daily pollution 2009; Hoffmann et al. 2012; Schwartz et al. variations with daily deaths, there are fewer at low concentrations, or focused on locally generated 2012; Wilker et al. 2010; Zanobetti et al. pollution, which is becoming more important as regulations reduce regional transport. Causal 2014), impair microvascular function (Brauner modeling approaches are also lacking. et al. 2008), increase coagulation and throm- OBJECTIVE: We used causal modeling to estimate the impact of local air pollution on mortality at bosis (Baccarelli et al. 2007, 2008; Bind et al. low concentrations. 2012; Bonzini et al. 2010; Carlsten et al. 2007; METHODS: Using an instrumental variable approach, we developed an instrument for variations Chuang et al. 2007; Gilmour et al. 2005; in local pollution concentrations that is unlikely to be correlated with other causes of death, and Nemmar et al. 2002), produce autonomic examined its association with daily deaths in the Boston, Massachusetts, area. We combined height changes (Adar et al. 2007b; Chahine et al. of the planetary boundary layer and wind speed, which affect concentrations of local emissions, to 2007; Chan et al. 2004; Ghelfi et al. 2008; develop the instrument for particulate matter ≤ 2.5 μm (PM2.5), black carbon (BC), or nitrogen Zhong et al. 2015), accelerate atherosclerosis dioxide (NO2) variations that were independent of year, month, and temperature. We also used Granger causality to assess whether omitted variable confounding existed. (Adar et al. 2010; Allen et al. 2009; Araujo et al. 2008; Bauer et al. 2010; Bhatnagar 2006; RESULTS: We estimated that an interquartile range increase in the instrument for local PM2.5 was associated with a 0.90% increase in daily deaths (95% CI: 0.25, 1.56). A similar result was found Hansen et al. 2007; Hoffmann et al. 2007; Sun et al. 2005, 2008; Suwa et al. 2002; Tzeng for BC, and a weaker association with NO2. The Granger test found no evidence of omitted variable confounding for the instrument. A separate test confirmed the instrument was not associated with et al. 2007), and destabilize atherosclerotic mortality independent of pollution. Furthermore, the association remained when all days with plaque (Suwa et al. 2002). 3 PM2.5 concentrations > 30 μg/m were excluded from the analysis (0.84% increase in daily deaths; There are fewer and less consistent studies 95% CI: 0.19, 1.50). assessing the effects of particle components. CONCLUSIONS: We conclude that there is a causal association of local air pollution with daily deaths For example, Krall et al. (2013) and Bell at concentrations below U.S. EPA standards. The estimated attributable risk in Boston exceeded et al. (2014) reported a greater toxicity for 1,800 deaths during the study period, indicating that important public health benefits can follow elemental (or black) carbon, a large fraction from further control efforts. of which is associated with local traffic and CITATION: Schwartz J, Bind MA, Koutrakis P. 2017. Estimating causal effects of local air domestic heating, whereas Franklin et al. pollution on daily deaths: effect of low levels. Environ Health Perspect 125:23–29; http://dx.doi. (2008), Beelen et al. (2015) and Dai et al. org/10.1289/EHP232 (2014) found greater effects for sulfur and not elemental carbon. There is biological support for a role of Introduction emissions of particulate and gaseous pollut- local traffic particles. Diesel particles have been Starting in the late 1980s, a large literature of ants will become a more important part of the shown to increase oxidative stress in endo- time series studies have reported associations pollution mix; thus it is important to enhance thelial cells (Furuyama et al. 2006; Hirano of daily air pollution concentrations with daily our understanding of their health impact. et al. 2003), inducing the production of deaths (Analitis et al. 2006; Bell et al. 2004, The observational epidemiology studies heme oxygenase-1, a rapid response part of 2013; Carbajal-Arroyo et al. 2011; Dominici cited above have been associational studies, Address correspondence to J. Schwartz, Department et al. 2005; Fischer et al. 2003; Krall et al. which do not assess causality. In general, when of Environmental Health, Harvard T.H. Chan 2013; Maynard et al. 2007; Peng et al. 2013; arguing for the causality of observed asso- School of Public Health, Landmark Center 404-M, Samoli et al. 2006; Schwartz 2004a, 2004b; ciations, authors have relied on Hill’s Criteria 401 Park Dr., Boston, MA 02215 USA. Telephone: Stölzel et al. 2007; Zanobetti and Schwartz (Hill 1965). For example, Brook et al. (2010) (617) 384-8752. E-mail: [email protected] 2008, 2009). The most consistent results have state “Many potential biological mechanisms This research was supported in part by National been that particle concentrations are associated exist whereby PM exposure could exacer- Institute of Environmental Health Sciences/National Institutes of Health grant ES-000002, and by U.S. with daily mortality. bate existing CVDs [cardiovascular diseases] Environmental Protection Agency (EPA) grant RD Fewer studies have examined the effects and trigger acute cardiovascular events (over 83479801 to J.S. and P.K. of source-specific particle contributions the short term) and instigate or accelerate The contents of this publication are solely the or individual particle species. Several large chronic CVDs (over the long run).” Besides responsibility of the grantee and do not necessarily multicity studies have reported stronger asso- biological plausibility, the PM2.5 (particulate represent the official views of the U.S. EPA. ciations for particle sulfate and nickel (Bell matter ≤ 2.5 μm) epidemiological studies The authors declare they have no actual or potential competing financial interests. et al. 2014; Dai et al. 2014; Franklin et al. were relatively consistent, and exposure Received: 18 June 2015; Revised: 7 September 2015; 2008). The U.S. Environmental Protection preceded effect. Accepted: 4 May 2016; Published: 20 May 2016. Agency’s (EPA’s) recent transport regula- The strength of the biological plausibility Note to readers with disabilities: EHP strives tion has already produced substantial reduc- argument has grown over time (Brook et al. to ensure that all journal content is accessible to all tions in sulfate particles, and is scheduled to 2004), and includes studies indicating that readers. However, some figures and Supplemental reduce remaining sulfur emissions further in particle exposure can induce lung and systemic Material published in EHP articles may not conform to 508 standards due to the complexity of the information the next few years (U.S. EPA 2016). As the inflammation (Adamkiewicz et al. 2004; being presented. If you need assistance accessing journal sulfate contribution to particle mass declines Adar et al. 2007a; Araujo 2010; Brook 2008; content, please contact [email protected]. and NOx (nitrogen oxides) controls affect Driscoll 2000; Dye et al. 2001; Folkmann Our staff will work with you to assess and meet your secondary organic particle formation, local et al. 2007), increase blood pressure (Baccarelli accessibility needs within 3 working days. Environmental Health Perspectives • VOLUME 125 | NUMBER 1 | January 2017 23 Schwartz et al. the body’s defense system against oxidative an instrumental variable. Figure 1 shows the is randomized with respect to confounders, stress (Choi and Alam 1996). The viability of directed acyclic graph (DAG) for this scenario. including unmeasured ones; and if that cell cultures of microvascular endothelial cells Consequently, At can be expressed as follows: fraction is associated with daily deaths, the was also impaired by diesel particles with an estimated effect should be causal. We discuss accompanying large increase in induction of At = Ztδ + ηt, [2] this further below. heme oxygenase-1 (Hirano et al. 2003). Planetary Boundary Layer and A key gap in the analysis of the acute where ηt represents the other sources of varia- effects of local air pollution sources has been tion in exposure, and particularly all of the Wind Speed as Instruments the lack of studies done in the framework exposure variations that are associated with The difficulty with instrumental variable of causal modeling, specifying potential other measured or unmeasured predictors of analyses is finding a valid instrument that is outcomes, and basing their analysis on esti- outcome. This follows because of the instru- associated only with outcome through the mating the difference or ratio of potential ment assumption, that Z is only related to Y exposure of interest. Mendelian randomiza- outcomes under different exposures. In this through A. Formally, E(ZtΦt) = 0 because of tion is an example of an instrumental variable paper, we use a causal modeling framework the instrument assumption.
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