Source location of air pollution and cardiac autonomic function: Trajectory cluster analysis for exposure assessment

Park, Sung Kyun; OʼNeill, Marie S.; Stunder, Barbara J. B.; Vokonas, Pantel; Sparrow, David; Koutrakis, Petros; Schwartz, Joel

doi:10.1038/sj.jes.7500552

Cited by 35 publications

(27 citation statements)

References 31 publications

(35 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In Boston, BC is a marker of traffic particles influenced by both local traffic, with a morning peak, and long-range transported traffic particles (Park et al 2007). NO 2 , a lower-airway irritant, is mainly a secondary pollutant, which in Boston mostly originates from traffic and regional sources including power plants and vehicular emissions (Rattigan et al 2010).…”

Section: Discussionmentioning

confidence: 99%

Epigenetic Influences on Associations between Air Pollutants and Lung Function in Elderly Men: The Normative Aging Study

Lepeule¹,

Bind²,

Baccarelli³

et al. 2014

Environ Health Perspect

Self Cite

106

View full text Add to dashboard Cite

Background: Few studies have been performed on pulmonary effects of air pollution in the elderly—a vulnerable population with low reserve capacity—and mechanisms and susceptibility factors for potential effects are unclear.Objectives: We evaluated the lag structure of air pollutant associations with lung function and potential effect modification by DNA methylation (< or ≥ median) at 26 individual CpG sites in nine candidate genes in a well-characterized cohort of elderly men.Methods: We measured forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and blood DNA methylation one to four times between 1999 and 2009 in 776 men from the Normative Aging Study. Air pollution was measured at fixed monitors 4 hr to 28 days before lung function tests. We used linear mixed-effects models to estimate the main effects of air pollutants and effect modification by DNA methylation.Results: An interquartile range (IQR) increase in subchronic exposure (3 to 28 days cumulated), but not in acute exposure (during the previous 4 hr, or the current or previous day), to black carbon, total and nontraffic particles with aerodynamic diameter ≤ 2.5 μm (PM2.5), carbon monoxide, and nitrogen dioxide was associated with a 1–5% decrease in FVC and FEV1 (p < 0.05). Slope estimates were greater for FVC than FEV1, and increased with cumulative exposure. The estimates slopes for air pollutants (28 days cumulated) were higher in participants with low (< median) methylation in TLR2 at position 2 and position 5 and high (≥ median) methylation in GCR.Conclusions: Subchronic exposure to traffic-related pollutants was associated with significantly reduced lung function in the elderly; nontraffic pollutants (particles, ozone) had weaker associations. Epigenetic mechanisms related to inflammation and immunity may influence these associations.Citation: Lepeule J, Bind MAC, Baccarelli AA, Koutrakis P, Tarantini L, Litonjua A, Sparrow D, Vokonas P, Schwartz JD. 2014. Epigenetic influences on associations between air pollutants and lung function in elderly men: the Normative Aging Study. Environ Health Perspect 122:566–572; http://dx.doi.org/10.1289/ehp.1206458

show abstract

Section: Discussionmentioning

confidence: 99%

Epigenetic Influences on Associations between Air Pollutants and Lung Function in Elderly Men: The Normative Aging Study

Lepeule¹,

Bind²,

Baccarelli³

et al. 2014

Environ Health Perspect

Self Cite

106

View full text Add to dashboard Cite

show abstract

“…We have shown that pollutant mixtures, as indexed by air masses with specific back trajectories, influence the health effects of particles (Park et al 2007). Specifically, the authors identified the paths that air masses traveled (‘back-trajectories’) before arriving in Boston, and they classified these trajectories into six clusters.…”

Section: Discussionmentioning

confidence: 99%

Health effects of multi-pollutant profiles

Zanobetti

Austin

Coull

et al. 2014

Environment International

Self Cite

View full text Add to dashboard Cite

Background The association between exposure to particle mass and mortality is well established; however, there are still uncertainties as to whether certain chemical components are more harmful than others. Moreover, understanding the health effects associated with exposure to pollutants mixtures may lead to new regulatory strategies. Objectives Recently we have introduced a new approach that uses cluster analysis to identify distinct air pollutant mixtures by classifying days into groups based on their pollutant concentration profiles. In Boston during the years 1999–2009, we examined whether the effect of PM2.5 on total mortality differed by distinct pollution mixtures. Methods We applied a time series analysis to examine the association of PM2.5 with daily deaths. Subsequently, we included an interaction term between PM2.5 and the pollution mixture clusters. Results We found a 1.1 % increase (95% CI: 0.0, 2.2) and 2.3% increase (95% CI: 0.9–3.7) in total mortality for a 10 µg/m3 increase in the same day and the two-day average of PM2.5 respectively. The association is larger in a cluster characterized by high concentrations of the elements related to primary traffic pollution and oil combustion emissions with a 3.7% increase (95% CI: 0.4, 7.1) in total mortality, per 10 µg/m3 increase in the same day average of PM2.5. Conclusions Our study shows a higher association of PM2.5 on total mortality during days with a strong contribution of traffic emissions, and fuel oil combustion. Our proposed method to create multi-pollutant profiles is robust, and provides a promising tool to identify multi-pollutant mixtures which can be linked to the health effects.

show abstract

“…One parameter used to assess this regulation is HRV; reduction in HRV is associated with increased risk of CV morbidity and mortality in both healthy individuals and patients following MI (Tsuji et al, 1996;Kleiger et al, 1987). Studies finding associations between BC and reduced HRV, often in older or chronically ill subjects, include Suh and Zanobetti (2010), Schwartz et al (2005a), Adar et al (2007), Wheeler et al (2006), and Park et al (2007. However, studies examining HRV in normal subjects, and even in an at-risk population with stable coronary heart disease, exposed to DEE showed no reproducible or consistent changes in HRV related to exposure (Peretz et al, 2008;Mills et al, 2011).…”

Section: Cardiovascular Morbidity-human Panel Studiesmentioning

confidence: 99%

“…It is surprising that poor exposure assessment did not cause BC associations to become insignificant in more studies than it did. Many of these studies commented that there was greater exposure misclassification for BC than for other pollutants (Chuang et al, 2008) and that poor subject exposure to BC should have attenuated BC associations or biased them toward the null, but did not (Bind et al, 2012;Baja et al, 2010;Baccarelli et al, 2009;O'Neill et al, 2007). Goldman et al (2010) estimated error in risk estimates due to spatial variability not accounted for when central monitor data were used as a proxy for subject exposure.…”

Section: Syntheses Of Findings From Studies In North America and Westmentioning

confidence: 99%

Public health and components of particulate matter: The changing assessment of black carbon

Grahame

Klemm

Schlesinger

2014

Journal of the Air & Waste Management Association

252

157

View full text Add to dashboard Cite

In 2012, the WHO classified diesel emissions as carcinogenic, and its European branch suggested creating a public health standard for airborne black carbon (BC). In 2011, EU researchers found that life expectancy could be extended four to nine times by reducing a unit of BC, vs reducing a unit of PM 2.5. Only recently could such determinations be made. Steady improvements in research methodologies now enable such judgments.In this Critical Review, we survey epidemiological and toxicological literature regarding carbonaceous combustion emissions, as research methodologies improved over time. Initially, we focus on studies of BC, diesel, and traffic emissions in the Western countries (where daily urban BC emissions are mainly from diesels). We examine effects of other carbonaceous emissions, e.g., residential burning of biomass and coal without controls, mainly in developing countries.Throughout the 1990s, air pollution epidemiology studies rarely included species not routinely monitored. As additional PM 2.5. chemical species, including carbonaceous species, became more widely available after 1999, they were gradually included in epidemiological studies. Pollutant species concentrations which more accurately reflected subject exposure also improved models.Natural "interventions" -reductions in emissions concurrent with fuel changes or increased combustion efficiency; introduction of ventilation in highway tunnels; implementation of electronic toll payment systems -demonstrated health benefits of reducing specific carbon emissions. Toxicology studies provided plausible biological mechanisms by which different PM species, e.g., carbonaceous species, may cause harm, aiding interpretation of epidemiological studies.Our review finds that BC from various sources appears to be causally involved in all-cause, lung cancer, and cardiovascular mortality, morbidity, and perhaps adverse birth and nervous system effects. We recommend that the U.S. EPA rubric for judging possible causality of PM 2.5. mass concentrations, be used to assess which PM 2.5. species are most harmful to public health. Implications: Black carbon (BC) and correlated co-emissions appear causally related with all-cause, cardiovascular, and lung cancer mortality, and perhaps with adverse birth outcomes and central nervous system effects. Such findings are recent, since widespread monitoring for BC is also recent. Helpful epidemiological advances (using many health relevant PM 2.5 species in models; using better measurements of subject exposure) have also occurred. "Natural intervention" studies also demonstrate harm from partly combusted carbonaceous emissions. Toxicology studies consistently find biological mechanisms explaining how such emissions can cause these adverse outcomes. A consistent mechanism for judging causality for different PM 2.5 species is suggested.A list of acronyms will be found at the end of the article. Aims of Critical ReviewThis critical review (CR) consists of three main sections. First, we review recent major regulatory and scien...

show abstract

Source location of air pollution and cardiac autonomic function: Trajectory cluster analysis for exposure assessment

Cited by 35 publications

References 31 publications

Epigenetic Influences on Associations between Air Pollutants and Lung Function in Elderly Men: The Normative Aging Study

Epigenetic Influences on Associations between Air Pollutants and Lung Function in Elderly Men: The Normative Aging Study

Health effects of multi-pollutant profiles

Public health and components of particulate matter: The changing assessment of black carbon

Contact Info

Product

Resources

About