Publications by authors named "Helen H Suh"

57 Publications

Preterm birth and PM in Puerto Rico: evidence from the PROTECT birth cohort.

Environ Health 2021 06 11;20(1):69. Epub 2021 Jun 11.

Department of Civil and Environmental Engineering, Tufts University, Anderson Hall, 200 College Avenue, Medford, MA, 02155, USA.

Background: Preterm birth (PTB, birth before 37 weeks of gestation) has been associated with adverse health outcomes across the lifespan. Evidence on the association between PTB and prenatal exposure to air pollutants is inconsistent, and is especially lacking for ethnic/racial minority populations.

Methods: We obtained data on maternal characteristics and behaviors and PTB and other birth outcomes for women participating in the Puerto Rico Testsite for Exploring Contamination Threats (PROTECT) cohort, who lived in municipalities located along the North Coast of Puerto Rico. We assessed pre-natal PM exposures for each infant based on the nearest US Environmental Protection Agency monitor. We estimated prenatal phthalate exposures as the geometric mean of urinary measurements obtained during pregnancy. We then examined the association between PM and PTB using modified Poisson regression and assessed modification of the association by phthalate exposure levels and sociodemographic factors such as maternal age and infant gender.

Results: Among 1092 singleton births, 9.1% of infants were born preterm and 92.9% of mothers had at least a high school education. Mothers had a mean (standard deviation) age of 26.9 (5.5) years and a median (range) of 2.0 (1.0-8.0) pregnancies. Nearly all women were Hispanic white, black, or mixed race. Median (range) prenatal PM concentrations were 6.0 (3.1-19.8) μ g/m. Median (interquartile range) prenatal phthalate levels were 14.9 (8.9-26.0) and 14.5 (8.4-26.0), respectively, for di-n-butyl phthalate (DBP) and di-isobutyl phthalate (DiBP). An interquartile range increase in PM was associated with a 1.2% (95% CI 0.4, 2.1%) higher risk of PTB. There was little difference in PTB risk in strata of infant sex, mother's age, family income, history of adverse birth outcome, parity, and pre-pregnancy body mass index. Pregnancy urinary phthalate metabolite levels did not modify the PM-PTB association.

Conclusion: Among ethnic minority women in Puerto Rico, prenatal PM exposure is associated with a small but significant increase in risk of PTB.
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http://dx.doi.org/10.1186/s12940-021-00748-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8196435PMC
June 2021

Non-nutritive suck and airborne metal exposures among Puerto Rican infants.

Sci Total Environ 2021 Oct 26;789:148008. Epub 2021 May 26.

Department of Civil and Environmental Engineering, Tufts University, 200 College Ave, Medford, MA 02155, USA. Electronic address:

Air pollution has been shown to impact multiple measures of neurodevelopment in young children. Its effects on particularly vulnerable populations, such as ethnic minorities, however, is less studied. To address this gap in the literature, we assess the associations between infant non-nutritive suck (NNS), an early indicator of central nervous system integrity, and air pollution exposures in Puerto Rico. Among infants aged 0-3 months enrolled in the Center for Research on Early Childhood Exposure and Development (CRECE) cohort from 2017 to 2019, we examined associations between exposure to fine particulate matter (PM) and its components on infant NNS in Puerto Rico. NNS was assessed using a pacifier attached to a pressure transducer, allowing for real-time visualization of NNS amplitude, frequency, duration, cycles/burst, cycles/min and bursts/min. These data were linked to 9-month average prenatal concentrations of PM and components, measured at three community monitoring sites. We used linear regression to examine the PM-NNS association in single pollutant models, controlling for infant sex, maternal age, gestational age, and season of birth in base and additionally for household smoke exposure, age at testing, and NNS duration in full models. Among 198 infants, the average NNS amplitude and burst duration was 17.1 cmHO and 6.1 s, respectively. Decreased NNS amplitude was consistently and significantly associated with 9-month average exposure to sulfur (-1.026 ± 0.507), zinc (-1.091 ± 0.503), copper (-1.096 ± 0.535) vanadium (-1.157 ± 0.537), and nickel (-1.530 ± 0.501). Decrements in NNS frequency were associated with sulfur exposure (0.036 ± 0.018), but not other examined PM components. Our findings provide new evidence that prenatal maternal exposure to specific PM components are associated with impaired neurodevelopment in Puerto Rican infants soon after birth.
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http://dx.doi.org/10.1016/j.scitotenv.2021.148008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8295239PMC
October 2021

Cohort profile: Center for Research on Early Childhood Exposure and Development in Puerto Rico.

BMJ Open 2020 07 19;10(7):e036389. Epub 2020 Jul 19.

Department of Civil and Environmental Engineering, Northeastern University, Boston, Massachusetts, USA.

Purpose: Puerto Rican children experience high rates of asthma and obesity. Further, infants born in Puerto Rico are more at risk for being born prematurely compared with infants on the mainland USA. Environmental exposures from multiple sources during critical periods of child development, potentially modified by psychosocial factors, may contribute to these adverse health outcomes. To date, most studies investigating the health effects of environmental factors on infant and child health have focused on single or individual exposures.

Participants: Infants currently in gestation whose mother is enrolled in Puerto Rico Testsite for Exploring Contamination Threats (PROTECT) cohort, and infants and children already born to mothers who participated in the PROTECT study.

Findings To Date: Data collection and processing remains ongoing. Demographic data have been collected on 437 mother-child pairs. Birth outcomes are available for 420 infants, neurodevelopmental outcomes have been collected on 319 children. Concentrations of parabens and phenols in maternal spot urine samples have been measured from 386 mothers. Center for Research on Early Childhood Exposure and Development mothers have significantly higher urinary concentrations of dichlorophenols, triclosan and triclocarban, but lower levels of several parabens compared with reference values from a similar population drawn from the National Health and Nutrition Examination Survey.

Future Plans: Data will continue to be collected through recruitment of new births with a target of 600 children. Seven scheduled follow-up visits with existing and new participants are planned. Further, our research team continues to work with healthcare providers, paediatricians and early intervention providers to support parent's ability to access early intervention services for participants.
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http://dx.doi.org/10.1136/bmjopen-2019-036389DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7371225PMC
July 2020

Low birth weight and PM in Puerto Rico.

Environ Epidemiol 2019 Aug;3(4)

Department of Civil and Environmental Engineering, Tufts University, Medford, MA.

Background: Low birth weight (LBW) has been associated with adverse health outcomes across the lifespan. Among ethnic/racial minority populations, few studies have examined the association between LBW (<2,500 or ≥2,500 g) and prenatal exposure to air pollution, a key modifiable environmental risk factor.

Methods: We examined the association between LBW and prenatal exposure to PM in a Hispanic and black population in Puerto Rico between 1999 and 2013, adjusting for individual and municipality-level confounders. We used modified Poisson regression to estimate the association and performed sensitivity analyses treating birth weight as continuous or polychotomous. In secondary analyses, we applied a 2-stage mixed effects model suitable for longitudinally measured exposures and binary outcomes.

Results: Among 332,129 total and 275,814 term births, 12.2% and 6.3% of infants had LBW, respectively. Eighty-eight percent of mothers were Hispanic. Mean (SD) PM concentrations declined from 9.9 (1.7) μg/m in 1999 to 6.1 (1.1) μg/m in 2013. Mean birth weights dropped to 3,044 g in 2010 and rose steadily afterward. Among term births, a SD increase in PM was associated with a 3.2% (95% CI = -1.0%, 6.3%) higher risk of LBW. First (risk ratio, 1.02; 95% CI = 1.00, 1.04) and second (1.02; 95% CI = 1.01, 1.05) trimester exposures were associated with increased LBW risk. In a 2-stage approach that longitudinally modeled monthly prenatal exposure levels, a standard deviation increase in average PM was associated with higher risk of LBW (odds ratio, 1.04; 95% CI = 1.01, 1.08).

Conclusions: In Puerto Rico, LBW is associated with prenatal PM exposure.
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http://dx.doi.org/10.1097/EE9.0000000000000058DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7039618PMC
August 2019

Long-term ozone exposures and cause-specific mortality in a US Medicare cohort.

J Expo Sci Environ Epidemiol 2020 07 16;30(4):650-658. Epub 2019 Apr 16.

Department of Civil and Environmental Engineering, Tufts University, Medford, MA, USA.

We examined the association of long-term, daily 1-h maximum O (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000-2008. We modeled the association between O and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM (particles with aerodynamic diameters <2.5 μm) and NO (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O into its temporal and spatio-temporal components and comparing estimated risk ratios. We also examined sensitivity of our results to alternate exposure measures based on warm-season 8-h daily maximum and 24-h average exposures. We found increased risks from long-term O exposures to be strongest and most consistent for mortality from respiratory disease (1.030, 95% CI: 1.027, 1.034) (including COPD (chronic obstructive pulmonary disease)), CHF (congestive heart failure), and lung cancer (1.015, 95% CI: 1.010, 1.020), with no evidence of confounding by PM, NO, and temperature and with results similar across O exposure measures. While significant, associations between long-term O exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O was used to assess exposures. In this large study, we provide strong evidence that O exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.
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http://dx.doi.org/10.1038/s41370-019-0135-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7197379PMC
July 2020

Close proximity to roadway and urbanicity associated with mental ill-health in older adults.

Sci Total Environ 2019 Mar 15;658:854-860. Epub 2018 Dec 15.

Department of Civil and Environmental Engineering, Tufts University, Medford, MA 02153, United States of America. Electronic address:

Evidence for the association between built environment and mental ill health, especially in older population where mental ill health is common, remains inconclusive. We examined the association of roadway distance and urbanicity, measured as percentage of urban land use within 1 km from participants' residence, with mental ill-health in a longitudinal study of community-dwelling older adults in the United States between 2005 and 2006 and 2011-2012. We evaluated perceived stress, depression and anxiety symptoms using the Cohen's Perceived Stress Scale, the Center for Epidemiological Studies - Depression, and the Hospital Anxiety and Depression Scale - anxiety subscale, respectively. Increment in roadway distance was significantly associated with -0.03 point (95% CI: -0.05, -0.01) change in depressive score, with loneliness and PM partially mediating the observed associations. Age, gender, race/ethnicity, and physical activity significantly modified the distance-depression association. Anxiety was inversely associated with roadway distance (-0.02; 95% CI: -0.03, 0.00), though the associations became insignificant upon adjusting for road traffic or noise. Urbanicity was significantly associated with 0.29 (95% CI: 0.10, 0.57) point increase in depressive symptoms in multivariable model; the association was partly mediated by loneliness, physical activity, social support and air pollution. No association was found between roadway distance and perceived stress, and between urbanicity, and anxiety and perceived stress. Built environment was associated with mental ill health, partially through pathways related to air pollution and certain individual characteristics (e.g. loneliness). Our study warrants further examination of the mediation and interaction of the built environment-mental health association.
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http://dx.doi.org/10.1016/j.scitotenv.2018.12.221DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004241PMC
March 2019

Association of neighborhood greenness with self-perceived stress, depression and anxiety symptoms in older U.S adults.

Environ Health 2018 04 16;17(1):39. Epub 2018 Apr 16.

Department of Civil and Environmental Engineering, Tufts University, Medford, MA, 02153, USA.

Background: Neighborhood environment, such as green vegetation, has been shown to play a role in coping with stress and mental ill health. Yet, epidemiological evidence of the association between greenness and mental health is inconsistent.

Methods: We examined whether living in green space is associated with self-perceived stress, depressive and anxiety symptoms in a nationally representative, longitudinal sample of community-dwelling older adults (N = 4118; aged 57-85 years) in the United States. We evaluated perceived stress, depression and anxiety symptoms using the Cohen's Perceived Stress Scale, the Center for Epidemiological Studies - Depression, and the Hospital Anxiety and Depression Scale - anxiety subscale, respectively. Greenness was assessed for each participant using the Normalized Difference Vegetation Index at 250-m resolution, as well as a buffer of 1000-m. We conducted longitudinal analyses to assess the associations between greenness and mental health upon adjusting for confounders (e.g., education), and to examine potential mediation and effect modification.

Results: An interquartile range (0.25 point) increase in contemporaneous greenness was significantly associated with 0.238 unit (95% CI: - 0.346, - 0.130) and 0.162 unit (95% CI: - 0.271, - 0.054) decrease in the perceived stress in base and multivariable models, respectively. The magnitude of the association was similar or even stronger when examining summer (- 0.161; 95% CI: - 0.295, - 0.027) and annual average of greenness (- 0.188; 95% CI: - 0.337, - 0.038), as well as greenness buffer of 1000-m. The greenness-stress association was partially mediated by physical activity (15.1% mediated), where increased greenness led to increased physical activity and less stress, and by history of respiratory diseases (- 3.8% mediated), where increased greenness led to increased respiratory disease and more stress. The association was also significantly modified by race, social support, physical function, socioeconomic status, and region. While greenness was not significantly associated with anxiety and depressive scores across all participants, significant inverse associations were found for Whites participants, and for individuals with higher socioeconomic status, who were physically active, as compared to their counterparts.

Conclusion: We found a direct association of greenness with perceived stress among older adults, and an indirect association mediated through physical activity and respiratory disease history. Our study findings warrant further examination of the mediation and modification of the greenness-mental health association.
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http://dx.doi.org/10.1186/s12940-018-0381-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5902952PMC
April 2018

Projected Changes in Temperature-related Morbidity and Mortality in Southern New England.

Epidemiology 2018 07;29(4):473-481

Department of Epidemiology, Brown University School of Public Health, Providence, RI.

Background: Climate change is expected to result in more heat-related, but potentially fewer cold-related, emergency department visits and deaths. The net effect of projected changes in temperature on morbidity and mortality remains incompletely understood. We estimated the change in temperature-related morbidity and mortality at two sites in southern New England, United States, through the end of the 21st century.

Methods: We used distributed lag Poisson regression models to estimate the present-day associations between daily mean temperature and all-cause emergency department visits and deaths in Rhode Island and in Boston, Massachusetts. We estimated the change in temperature-related visits and deaths in 2045-2054 and 2085-2094 (relative to 2001-2010) under two greenhouse gas emissions scenarios (RCP4.5 and RCP8.5) using downscaled projections from an ensemble of over 40 climate models, assuming all other factors remain constant.

Results: We observed U-shaped relationships between temperature and morbidity and mortality in Rhode Island, with minima at 10.9°C and 22.5°C, respectively. We estimated that, if this population were exposed to the future temperatures projected under RCP8.5 for 2085-2094, there would be 5,976 (95% eCI = 1,630, 11,379) more emergency department visits but 218 (95% eCI = -551, 43) fewer deaths annually. Results were similar in Boston and similar but less pronounced in the 2050s and under RCP4.5.

Conclusions: We estimated that in the absence of further adaptation, if the current southern New England population were exposed to the higher temperatures projected for future decades, temperature-related emergency department visits would increase but temperature-related deaths would not.
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http://dx.doi.org/10.1097/EDE.0000000000000825DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980746PMC
July 2018

Smoking and olfactory dysfunction: A systematic literature review and meta-analysis.

Laryngoscope 2017 08 31;127(8):1753-1761. Epub 2017 May 31.

Section of Otolaryngology-Head and Neck Surgery, Department of Surgery, University of Chicago, Chicago, Illinois, U.S.A.

Objectives/hypothesis: A systematic review and meta-analysis of the literature was undertaken, examining the association between tobacco smoking and olfactory function in humans, utilizing PubMed and Web of Science (1970-2015) as data sources.

Study Design: Systematic literature review and meta-analysis.

Methods: This database review of studies of smoking and olfaction, with a focus on identifying high-quality studies (based on modified versions of the Newcastle-Ottawa Scale), used validated olfactory tests among the generally healthy population.

Results: We identified 11 studies meeting inclusion criteria. Of 10 cross-sectional studies, two were excluded from meta-analysis because the cohorts they studied were included in another article in the review. In meta-analysis, current smokers had substantially higher odds of olfactory dysfunction compared to never smokers (odds ratio [OR] = 1.59, 95% confidence interval [CI] = 1.37-1.85). In contrast, former smokers were found to have no difference in risk of impaired olfaction compared to never smokers (OR = 1.05, 95% CI = 0.91-1.21). The single longitudinal study reviewed found a trend toward increased risk of olfactory decline over time in ever smokers; this trend was stronger in current as compared to former smokers.

Conclusions: Current smoking, but not former smoking, is associated with significantly increased risk of olfactory dysfunction, suggesting that the effects of smoking on olfaction may be reversible. Future studies that prospectively evaluate the impact of smoking cessation on improvement in olfactory function are warranted.

Level Of Evidence: N/A. Laryngoscope, 127:1753-1761, 2017.
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http://dx.doi.org/10.1002/lary.26558DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6731037PMC
August 2017

Long-Term PM2.5 Exposure and Respiratory, Cancer, and Cardiovascular Mortality in Older US Adults.

Am J Epidemiol 2017 Oct;186(8):961-969

The impact of chronic exposure to fine particulate matter (particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5)) on respiratory disease and lung cancer mortality is poorly understood. In a cohort of 18.9 million Medicare beneficiaries (4.2 million deaths) living across the conterminous United States between 2000 and 2008, we examined the association between chronic PM2.5 exposure and cause-specific mortality. We evaluated confounding through adjustment for neighborhood behavioral covariates and decomposition of PM2.5 into 2 spatiotemporal scales. We found significantly positive associations of 12-month moving average PM2.5 exposures (per 10-μg/m3 increase) with respiratory, chronic obstructive pulmonary disease, and pneumonia mortality, with risk ratios ranging from 1.10 to 1.24. We also found significant PM2.5-associated elevated risks for cardiovascular and lung cancer mortality. Risk ratios generally increased with longer moving averages; for example, an elevation in 60-month moving average PM2.5 exposures was linked to 1.33 times the lung cancer mortality risk (95% confidence interval: 1.24, 1.40), as compared with 1.13 (95% confidence interval: 1.11, 1.15) for 12-month moving average exposures. Observed associations were robust in multivariable models, although evidence of unmeasured confounding remained. In this large cohort of US elderly, we provide important new evidence that long-term PM2.5 exposure is significantly related to increased mortality from respiratory disease, lung cancer, and cardiovascular disease.
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http://dx.doi.org/10.1093/aje/kwx166DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6915823PMC
October 2017

Effects of Ambient Air Pollution Exposure on Olfaction: A Review.

Environ Health Perspect 2016 Nov 10;124(11):1683-1693. Epub 2016 Jun 10.

Pritzker School of Medicine, University of Chicago, Chicago, Illinois, USA.

Background: Olfactory dysfunction affects millions of people worldwide. This sensory impairment is associated with neurodegenerative disease and significantly decreased quality of life. Exposure to airborne pollutants has been implicated in olfactory decline, likely due to the anatomic susceptibility of the olfactory nerve to the environment. Historically, studies have focused on occupational exposures, but more recent studies have considered effects from exposure to ambient air pollutants.

Objectives: To examine all relevant human data evaluating a link between ambient pollution exposure and olfaction and to review supporting animal data in order to examine potential mechanisms for pollution-associated olfactory loss.

Methods: We identified and reviewed relevant articles from 1950 to 2015 using PubMed and Web of Science and focusing on human epidemiologic and pathophysiologic studies. Animal studies were included only to support pertinent data on humans. We reviewed findings from these studies evaluating a relationship between environmental pollutant exposure and olfactory function.

Results: We identified and reviewed 17 articles, with 1 additional article added from a bibliography search, for a total of 18 human studies. There is evidence in human epidemiologic and pathologic studies that increased exposure to ambient air pollutants is associated with olfactory dysfunction. However, most studies have used proxies for pollution exposure in small samples of convenience. Human pathologic studies, with supporting animal work, have also shown that air pollution can contact the olfactory epithelium, translocate to the olfactory bulb, and migrate to the olfactory cortex. Pollutants can deposit at each location, causing direct damage and disruption of tissue morphology or inducing local inflammation and cellular stress responses.

Conclusions: Ambient air pollution may impact human olfactory function. Additional studies are needed to examine air pollution-related olfactory impacts on the general population using measured pollution exposures and to link pollution exposure with olfactory dysfunction and related pathology. Citation: Ajmani GS, Suh HH, Pinto JM. 2016. Effects of ambient air pollution exposure on olfaction: a review. Environ Health Perspect 124:1683-1693; http://dx.doi.org/10.1289/EHP136.
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http://dx.doi.org/10.1289/EHP136DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5089874PMC
November 2016

Fine particulate matter exposure and olfactory dysfunction among urban-dwelling older US adults.

Environ Res 2016 Nov 29;151:797-803. Epub 2016 Sep 29.

Section of Otolaryngology-Head and Neck Surgery, The University of Chicago, Chicago, IL, USA. Electronic address:

Objectives: The olfactory nerve is anatomically susceptible to injury from pollution in inspired air, but there are no large-scale epidemiologic studies investigating this relationship.

Methods: Cross-sectional study using data from the National Social Life, Health, and Aging Project, a representative sample of home-dwelling US adults age 57-85 years. Olfactory function was tested using a validated 5-item odor identification test (Sniffin' Sticks). Exposure to fine particulate matter (PM) at each respondent's home was estimated as 1-12 month moving averages prior to olfactory assessment using validated spatio-temporal models.

Results: Olfactory dysfunction was significantly associated with PM exposures averaged over 3-12 months in urban-dwelling respondents. The strongest effect was for 6 month average exposure (per 1-IQR increase in PM: OR 1.28, 95% CI 1.05, 1.55) adjusting for age, gender, race/ethnicity, education, cognition, comorbidity, smoking, and the season. Interestingly, the most deleterious effects were observed among the youngest respondents, 57-64 years old, and those living in the northeast and south.

Conclusions: We show for the first time that air pollution exposure is associated with poor olfaction among urban-living, older US adults.
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http://dx.doi.org/10.1016/j.envres.2016.09.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554594PMC
November 2016

Nitrogen dioxide pollution exposure is associated with olfactory dysfunction in older U.S. adults.

Int Forum Allergy Rhinol 2016 12 13;6(12):1245-1252. Epub 2016 Sep 13.

Section of Otolaryngology-Head and Neck Surgery, The University of Chicago, Chicago, IL.

Background: Olfactory dysfunction has profound effects on quality of life, physical and social function, and mortality itself. Nitrogen dioxide (NO ) is a pervasive air pollutant that is associated with respiratory diseases. Given the olfactory nerve's anatomic exposure to airborne pollutants, we investigated the relationship between NO exposure and olfactory dysfunction.

Methods: The ability to identify odors was evaluated using a validated test in respondents from the National Social Life, Health, and Aging Project (NSHAP), a representative probability sample of home-dwelling, older U.S. adults age 57 to 85 years. Exposure to NO pollution was assessed using measurements obtained from the U.S. Environmental Protection Agency (EPA) Aerometric Information Retrieval System (AIRS) ambient monitoring site closest to each respondent's home. We tested the association between NO exposure and olfactory dysfunction using multivariate logistic regression.

Results: Among older adults in the United States, 22.6% had impaired olfactory function, defined as ≤3 correct (out of 5) on the odor identification test. Median NO exposure during the 365 days prior to the interview date was 14.7 ppb (interquartile range [IQR], 10.8 to 19.7 ppb). An IQR increase in NO exposure was associated with increased odds of olfactory dysfunction (OR, 1.35; 95% CI, 1.07 to 1.72), adjusting for age, gender, race/ethnicity, education, cognition, comorbidity, smoking, and season of the home interview (n = 1823).

Conclusion: We show for the first time that NO exposure is associated with olfactory dysfunction in older U.S. adults. These results suggest an important role for NO exposure on olfactory dysfunction, and, potentially, nasal disease more broadly.
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http://dx.doi.org/10.1002/alr.21829DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554588PMC
December 2016

Spatio-temporal modeling of particulate air pollution in the conterminous United States using geographic and meteorological predictors.

Environ Health 2014 Aug 5;13:63. Epub 2014 Aug 5.

Department of Public Health Sciences, The Pennsylvania State University College of Medicine, Hershey, PA, USA.

Background: Exposure to atmospheric particulate matter (PM) remains an important public health concern, although it remains difficult to quantify accurately across large geographic areas with sufficiently high spatial resolution. Recent epidemiologic analyses have demonstrated the importance of spatially- and temporally-resolved exposure estimates, which show larger PM-mediated health effects as compared to nearest monitor or county-specific ambient concentrations.

Methods: We developed generalized additive mixed models that describe regional and small-scale spatial and temporal gradients (and corresponding uncertainties) in monthly mass concentrations of fine (PM2.5), inhalable (PM10), and coarse mode particle mass (PM(2.5-10)) for the conterminous United States (U.S.). These models expand our previously developed models for the Northeastern and Midwestern U.S. by virtue of their larger spatial domain, their inclusion of an additional 5 years of PM data to develop predictions through 2007, and their use of refined geographic covariates for population density and point-source PM emissions. Covariate selection and model validation were performed using 10-fold cross-validation (CV).

Results: The PM2.5 models had high predictive accuracy (CV R2=0.77 for both 1988-1998 and 1999-2007). While model performance remained strong, the predictive ability of models for PM10 (CV R2=0.58 for both 1988-1998 and 1999-2007) and PM(2.5-10) (CV R2=0.46 and 0.52 for 1988-1998 and 1999-2007, respectively) was somewhat lower. Regional variation was found in the effects of geographic and meteorological covariates. Models generally performed well in both urban and rural areas and across seasons, though predictive performance varied somewhat by region (CV R2=0.81, 0.81, 0.83, 0.72, 0.69, 0.50, and 0.60 for the Northeast, Midwest, Southeast, Southcentral, Southwest, Northwest, and Central Plains regions, respectively, for PM2.5 from 1999-2007).

Conclusions: Our models provide estimates of monthly-average outdoor concentrations of PM2.5, PM10, and PM(2.5-10) with high spatial resolution and low bias. Thus, these models are suitable for estimating chronic exposures of populations living in the conterminous U.S. from 1988 to 2007.
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http://dx.doi.org/10.1186/1476-069X-13-63DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4137272PMC
August 2014

Proximity of US schools to major roadways: a nationwide assessment.

J Expo Sci Environ Epidemiol 2014 May-Jun;24(3):253-9. Epub 2014 Feb 5.

Department of Epidemiology, Brown University, Providence, Rhode Island, USA.

Long-term exposure to traffic pollution has been associated with adverse health outcomes in children and adolescents. A significant number of schools may be located near major roadways, potentially exposing millions of children to high levels of traffic pollution, but this hypothesis has not been evaluated nationally. We obtained data on the location and characteristics of 114,644 US public and private schools, grades prekindergarten through 12, and calculated their distance to the nearest major roadway. In 2005-2006, 3.2 million students (6.2%) attended 8,424 schools (7.3%) located within 100 m of a major roadway, and an additional 3.2 million (6.3%) students attended 8,555 (7.5%) schools located 100-250 m from a major roadway. Schools serving predominantly Black students were 18% (95% CI, 13-23%) more likely to be located within 250 m of a major roadway. Public schools eligible for Title I programs and those with a majority of students eligible for free/reduced price meals were also more likely to be near major roadways. In conclusion, 6.4 million US children attended schools within 250 m of a major roadway and were likely exposed to high levels of traffic pollution. Minority and underprivileged children were disproportionately affected, although some results varied regionally.
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http://dx.doi.org/10.1038/jes.2014.5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4179205PMC
December 2014

Short-term effects of air pollution on oxygen saturation in a cohort of senior adults in Steubenville, Ohio.

J Occup Environ Med 2014 Feb;56(2):149-54

From the Departments of Environmental Health (Drs Luttmann-Gibson, Sarnat, Suh, Schwartz, Zanobetti, and Gold) and Biostatistics (Dr Coull), Harvard School of Public Health, Boston, Mass; Department of Environmental and Occupational Health (Dr Sarnat), Emory University, Atlanta, Ga; Department of Health Sciences (Dr Suh), Northeastern University, Boston, Mass; and Channing Laboratory (Drs Schwartz and Gold), Harvard Medical School, Boston, Mass.

Objective: We examine whether ambient air pollution is associated with oxygen saturation in 32 elderly subjects in Steubenville, Ohio.

Methods: We used linear mixed models to examine the effects of fine particulate matter less than 2.5 μm (PM(2.5)), sulfate (SO(4)(-2)), elemental carbon, and gases on median oxygen saturation.

Results: An interquartile range increase of 13.4 μg/m in PM(2.5) on the previous day was associated with a decrease of -0.18% (95% confidence interval: -0.31 to -0.06) and a 5.1 μg/m(3) interquartile range increase in SO(4)(-2) on the previous day was associated with a decrease of -0.16% (95% confidence interval: -0.27 to -0.04) in oxygen saturation during the initial 5-minute rest period of the protocol.

Conclusions: Increased exposure to air pollution, including the nontraffic pollutant SO(4)(-2) from industrial sources, led to changes in oxygen saturation that may reflect particle-induced pulmonary inflammatory or vascular responses.
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http://dx.doi.org/10.1097/JOM.0000000000000089DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3987810PMC
February 2014

Structural equation modeling of parasympathetic and sympathetic response to traffic air pollution in a repeated measures study.

Environ Health 2013 Sep 23;12(1):81. Epub 2013 Sep 23.

Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.

Background: Traffic-related air pollution has been associated to a range of adverse health impacts, including decreased heart rate variability (HRV). The association between traffic-related pollution and HRV, however, has varied by traffic-related or HRV marker as well as by study, suggesting the need for a more comprehensive and integrative approach to examining air pollution-mediated biological impacts on these outcomes. In a Bayesian framework, we examined the effect of traffic pollution on HRV using structural equation models (SEMs) and looked at effect modification by participant characteristics.

Methods: We studied measurements of 5 HRV markers [high frequency (HF), low frequency (LF), 5-min standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive normal-to-normal intervals (rMSSD), and LF/HF ratio (LF/HF)] for 700 elderly men from the Normative Aging Study. Using SEMs, we fit a latent variable for traffic pollution that is reflected by levels of carbon monoxide, nitrogen monoxide, nitrogen dioxide, and black carbon (BC) to estimate its effect on latent variable for parasympathetic tone that included HF, SDNN and rMSSD, and the sympathetic tone marker, LF/HF. Exposure periods were assessed using 4-, 24-, 48-, 72-hour moving average pre-visit. We compared our main effect findings using SEMs with those obtained using linear mixed models.

Results: Traffic pollution was not associated with mean parasympathetic tone and LF/HF for all examined moving averages. In Bayesian linear mixed models, however, BC was related to increased LF/HF, an inter quartile range (IQR) increase in BC was associated with a 6.5% (95% posterior interval (PI): -0.7%, 14.2%) increase in mean LF/HF 24-hours later. The strongest association observed was for the 4-hour moving average (10.1%; 95% PI: 3.0%, 17.6%). The effect of traffic on parasympathetic tone was stronger among diabetic as compared to non-diabetic participants. Specifically, an IQR increase in traffic pollution in the 48-hr prior to the clinic visit was associated with a 44.3% (95% PI: -67.7%, -4.2%) lower mean parasympathetic tone among diabetics, and a 7.7% (95% PI: -18.0%, 41.4%) higher mean parasympathetic tone among non-diabetics.

Conclusions: BC was associated with adverse changes LF/HF in the elderly. Traffic pollution may decrease parasympathetic tone among diabetic elderly.
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http://dx.doi.org/10.1186/1476-069X-12-81DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3907044PMC
September 2013

The effect of primary organic particles on emergency hospital admissions among the elderly in 3 US cities.

Environ Health 2013 Aug 27;12(1):68. Epub 2013 Aug 27.

Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.

Background: Fine particle (PM2.5) pollution related to combustion sources has been linked to a variety of adverse health outcomes. Although poorly understood, it is possible that organic carbon (OC) species, particularly those from combustion-related sources, may be partially responsible for the observed toxicity of PM2.5. The toxicity of the OC species may be related to their chemical structures; however, few studies have examined the association of OC species with health impacts.

Methods: We categorized 58 primary organic compounds by their chemical properties into 5 groups: n-alkanes, hopanes, cyclohexanes, PAHs and isoalkanes. We examined their impacts on the rate of daily emergency hospital admissions among Medicare recipients in Atlanta, GA and Birmingham, AL (2006-2009), and Dallas, TX (2006-2007). We analyzed data in two stages; we applied a case-crossover analysis to simultaneously estimate effects of individual OC species on cause-specific hospital admissions. In the second stage we estimated the OC chemical group-specific effects, using a multivariate weighted regression.

Results: Exposures to cyclohexanes of six days and longer were significantly and consistently associated with increased rate of hospital admissions for CVD (3.40%, 95%CI = (0.64, 6.24%) for 7-d exposure). Similar increases were found for hospitalizations for ischemic heart disease and myocardial infarction. For respiratory related hospital admissions, associations with OC groups were less consistent, although exposure to iso-/anteiso-alkanes was associated with increased respiratory-related hospitalizations.

Conclusions: Results suggest that week-long exposures to traffic-related, primary organic species are associated with increased rate of total and cause-specific CVD emergency hospital admissions. Associations were significant for cyclohexanes, but not hopanes, suggesting that chemical properties likely play an important role in primary OC toxicity.
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http://dx.doi.org/10.1186/1476-069X-12-68DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765898PMC
August 2013

Structural equation modeling of the inflammatory response to traffic air pollution.

J Expo Sci Environ Epidemiol 2013 May-Jun;23(3):268-74. Epub 2012 Dec 12.

Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.

Several epidemiological studies have reported conflicting results on the effect of traffic-related pollutants on markers of inflammation. In a Bayesian framework, we examined the effect of traffic pollution on inflammation using structural equation models (SEMs). We studied measurements of C-reactive protein (CRP), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble intracellular adhesion molecule-1 (sICAM-1) for 749 elderly men from the Normative Aging Study. Using repeated measures SEMs, we fit a latent variable for traffic pollution that is reflected by levels of black carbon, carbon monoxide, nitrogen monoxide and nitrogen dioxide to estimate its effect on a latent variable for inflammation that included sICAM-1, sVCAM-1 and CRP. Exposure periods were assessed using 1-, 2-, 3-, 7-, 14- and 30-day moving averages previsit. We compared our findings using SEMs with those obtained using linear mixed models. Traffic pollution was related to increased inflammation for 3-, 7-, 14- and 30-day exposure periods. An inter-quartile range increase in traffic pollution was associated with a 2.3% (95% posterior interval (PI): 0.0-4.7%) increase in inflammation for the 3-day moving average, with the most significant association observed for the 30-day moving average (23.9%; 95% PI: 13.9-36.7%). Traffic pollution adversely impacts inflammation in the elderly. SEMs in a Bayesian framework can comprehensively incorporate multiple pollutants and health outcomes simultaneously in air pollution-cardiovascular epidemiological studies.
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http://dx.doi.org/10.1038/jes.2012.106DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4648554PMC
October 2013

Modeling the association between particle constituents of air pollution and health outcomes.

Am J Epidemiol 2012 Aug 31;176(4):317-26. Epub 2012 Jul 31.

Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.

There is increasing interest in evaluating the association between specific fine-particle (particles with aerodynamic diameters less than 2.5 µm; PM2.5) constituents and adverse health outcomes rather than focusing solely on the impact of total PM2.5. Because PM2.5 may be related to both constituent concentration and health outcomes, constituents that are more strongly correlated with PM2.5 may appear more closely related to adverse health outcomes than other constituents even if they are not inherently more toxic. Therefore, it is important to properly account for potential confounding by PM2.5 in these analyses. Usually, confounding is due to a factor that is distinct from the exposure and outcome. However, because constituents are a component of PM2.5, standard covariate adjustment is not appropriate. Similar considerations apply to source-apportioned concentrations and studies assessing either short-term or long-term impacts of constituents. Using data on 18 constituents and data from 1,060 patients admitted to a Boston medical center with ischemic stroke in 2003-2008, the authors illustrate several options for modeling the association between constituents and health outcomes that account for the impact of PM2.5. Although the different methods yield results with different interpretations, the relative rankings of the association between constituents and ischemic stroke were fairly consistent across models.
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http://dx.doi.org/10.1093/aje/kws018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3491968PMC
August 2012

Ambient air pollution and the risk of acute ischemic stroke.

Arch Intern Med 2012 Feb;172(3):229-34

Center for Environmental Health and Technology, Brown University, Providence, RI 02912, USA.

Background: The link between daily changes in level of ambient fine particulate matter (PM) air pollution (PM <2.5 μm in diameter [PM(2.5)]) and cardiovascular morbidity and mortality is well established. Whether PM(2.5) levels below current US National Ambient Air Quality Standards also increase the risk of ischemic stroke remains uncertain.

Methods: We reviewed the medical records of 1705 Boston area patients hospitalized with neurologist-confirmed ischemic stroke and abstracted data on the time of symptom onset and clinical characteristics. The PM(2.5) concentrations were measured at a central monitoring station. We used the time-stratified case-crossover study design to assess the association between the risk of ischemic stroke onset and PM(2.5) levels in the hours and days preceding each event. We examined whether the association with PM(2.5) levels differed by presumed ischemic stroke pathophysiologic mechanism and patient characteristics.

Results: The estimated odds ratio (OR) of ischemic stroke onset was 1.34 (95% CI, 1.13-1.58) (P < .001) following a 24-hour period classified as moderate (PM(2.5) 15-40 μg/m(3)) by the US Environmental Protection Agency's (EPA) Air Quality Index compared with a 24-hour period classified as good (≤15 μg/m(3)). Considering PM(2.5) levels as a continuous variable, we found the estimated odds ratio of ischemic stroke onset to be 1.11 (95% CI, 1.03-1.20) (P = .006) per interquartile range increase in PM(2.5) levels (6.4 μg/m(3)). The increase in risk was greatest within 12 to 14 hours of exposure to PM(2.5) and was most strongly associated with markers of traffic-related pollution.

Conclusion: These results suggest that exposure to PM(2.5) levels considered generally safe by the US EPA increase the risk of ischemic stroke onset within hours of exposure.
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http://dx.doi.org/10.1001/archinternmed.2011.732DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3639313PMC
February 2012

Ambient particulate matter and the response to orthostatic challenge in the elderly: the Maintenance of Balance, Independent Living, Intellect, and Zest in the Elderly (MOBILIZE) of Boston study.

Hypertension 2012 Mar 23;59(3):558-63. Epub 2012 Jan 23.

Department of Epidemiology, Center for Environmental Health and Technology, Brown University, Providence, RI 02912, USA.

Short-term elevations in ambient fine particulate matter (PM(2.5)) may increase resting systolic (SBP) and diastolic (DBP) blood pressures, but whether PM(2.5) alters hemodynamic responses to orthostatic challenge has not been studied in detail. We repeatedly measured SBP and DBP during supine rest and 1 and 3 minutes after standing among 747 elderly (aged 78.3±5.3 years, mean±SD) participants from a prospective cohort study. We used linear mixed models to assess the association between change in SBP (ΔSBP=standing SBP-supine SBP) and DBP (ΔDBP) on standing and mean PM(2.5) levels over the preceding 1 to 28 days, adjusting for meteorologic covariates, temporal trends, and medical history. We observed a 1.4-mm Hg (95% CI: 0.0-2.8 mm Hg; P=0.046) higher ΔSBP and a 0.7-mm Hg (95% CI: 0.0-1.4 mm Hg; P=0.053) higher ΔDBP at 1 minute of standing per interquartile range increase (3.8 μg/m(3)) in mean PM(2.5) levels in the past 7 days. ΔSBP and ΔDBP measured 3 minutes after standing were not associated with PM(2.5). Resting DBP (but not SBP or pulse pressure) was positively associated with PM(2.5) at longer averaging periods. Responses were more strongly associated with black carbon than sulfate levels. These associations did not differ significantly according to hypertension status, obesity, diabetes mellitus, or sex. These results suggest that ambient particles can increase resting DBP and exaggerate blood pressure responses to postural changes in elderly people. Increased vasoreactivity during posture change may be responsible, in part, for the adverse effect of ambient particles on cardiovascular health.
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http://dx.doi.org/10.1161/HYPERTENSIONAHA.111.180778DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3286019PMC
March 2012

Opposing effects of particle pollution, ozone, and ambient temperature on arterial blood pressure.

Environ Health Perspect 2012 Feb 21;120(2):241-6. Epub 2011 Oct 21.

Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts, USA.

Background: Diabetes increases the risk of hypertension and orthostatic hypotension and raises the risk of cardiovascular death during heat waves and high pollution episodes.

Objective: We examined whether short-term exposures to air pollution (fine particles, ozone) and heat resulted in perturbation of arterial blood pressure (BP) in persons with type 2 diabetes mellitus (T2DM).

Methods: We conducted a panel study in 70 subjects with T2DM, measuring BP by automated oscillometric sphygmomanometer and pulse wave analysis every 2 weeks on up to five occasions (355 repeated measures). Hourly central site measurements of fine particles, ozone, and meteorology were conducted. We applied linear mixed models with random participant intercepts to investigate the association of fine particles, ozone, and ambient temperature with systolic, diastolic, and mean arterial BP in a multipollutant model, controlling for season, meteorological variables, and subject characteristics.

Results: An interquartile increase in ambient fine particle mass [particulate matter (PM) with an aerodynamic diameter of ≤ 2.5 μm (PM2.5)] and in the traffic component black carbon in the previous 5 days (3.54 and 0.25 μg/m3, respectively) predicted increases of 1.4 mmHg [95% confidence interval (CI): 0.0, 2.9 mmHg] and 2.2 mmHg (95% CI: 0.4, 4.0 mmHg) in systolic BP (SBP) at the population geometric mean, respectively. In contrast, an interquartile increase in the 5-day mean of ozone (13.3 ppb) was associated with a 5.2 mmHg (95% CI: -8.6, -1.8 mmHg) decrease in SBP. Higher temperatures were associated with a marginal decrease in BP.

Conclusions: In subjects with T2DM, PM was associated with increased BP, and ozone was associated with decreased BP. These effects may be clinically important in patients with already compromised autoregulatory function.
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http://dx.doi.org/10.1289/ehp.1103647DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3279434PMC
February 2012

Particulate air pollution and socioeconomic position in rural and urban areas of the Northeastern United States.

Am J Public Health 2011 Dec 11;101 Suppl 1:S224-30. Epub 2011 Aug 11.

Exposure, Epidemiology and Risk Program, Department of Environmental Health, Harvard School of Public Health, Boston, MA 02465, USA.

Objectives: Although differential exposure by socioeconomic position (SEP) to hazardous waste and lead is well demonstrated, there is less evidence for particulate air pollution (PM), which is associated with risk of death and illness. This study determined the relationship of ambient PM and SEP across several spatial scales.

Methods: Geographic information system-based, spatio-temporal models were used to predict PM in the Northeastern United States. Predicted concentrations were related to census tract SEP and racial composition using generalized additive models.

Results: Lower SEP was associated with small, significant increases in PM. Annual PM(10) decreased between 0.09 and 0.93 micrograms per cubic meter and PM(2.5) between 0.02 and 0.94 micrograms per cubic meter for interquartile range increases in income. Decrements in PM with SEP increased with spatial scale, indicating that between-city spatial gradients were greater than within-city differences. The PM-SEP relation in urban tracts was not substantially modified by racial composition.

Conclusions: Lower compared with higher SEP populations were exposed to higher ambient PM in the Northeastern United States. Given the small percentage change in annual PM(2.5) and PM(10), SEP was not likely a major source of confounding in epidemiological studies of PM, especially those conducted within a single urban/metropolitan area.
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http://dx.doi.org/10.2105/AJPH.2011.300232DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3222475PMC
December 2011

Chemical properties of air pollutants and cause-specific hospital admissions among the elderly in Atlanta, Georgia.

Environ Health Perspect 2011 Oct 27;119(10):1421-8. Epub 2011 Jun 27.

Environmental Health Program, NORC at the University of Chicago, Newton, Massachusetts, USA.

Background: Health risks differ by fine particle (aerodynamic diameter ≤ 2.5 μm) component, although with substantial variability. Traditional methods to assess component-specific risks are limited, suggesting the need for alternative methods.

Objectives: We examined whether the odds of daily hospital admissions differ by pollutant chemical properties.

Methods: We categorized pollutants by chemical properties and examined their impacts on the odds of daily hospital admissions among Medicare recipients > 64 years of age in counties in Atlanta, Georgia, for 1998-2006. We analyzed data in two stages. In the first stage we applied a case-crossover analysis to simultaneously estimate effects of 65 pollutants measured in the Aerosol Research and Inhalation Epidemiology Study on cause-specific hospital admissions, controlling for temperature and ozone. In the second stage, we regressed pollutant-specific slopes from the first stage on pollutant properties. We calculated uncertainty estimates using a bootstrap procedure. We repeated the two-stage analyses using coefficients from first-stage models that included single pollutants plus ozone and meteorological variables only. We based our primary analyses on exposures on day of admission.

Results: We found that 24-hr transition metals and alkanes were associated with increased odds [0.26%; 95% confidence interval (CI), 0.02-0.48; and 0.37%; 95% CI, 0.04-0.72, respectively] of hospital admissions for cardiovascular disease (CVD). Transition metals were significantly associated with increased hospital admissions for ischemic heart disease, congestive heart failure, and atrial fibrillation. Increased respiratory-related hospital admissions were significantly associated with alkanes. Aromatics and microcrystalline oxides were significantly associated with decreased CVD- and respiratory-related hospital admissions.

Conclusions: The two-stage approach showed transition metals to be consistently associated with increased odds of CVD-related hospital admissions.
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http://dx.doi.org/10.1289/ehp.1002646DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3230427PMC
October 2011

Hourly measurements of fine particulate sulfate and carbon aerosols at the Harvard-U.S. Environmental Protection Agency Supersite in Boston.

J Air Waste Manag Assoc 2010 Nov;60(11):1327-34

Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA.

Hourly concentrations of ambient fine particle sulfate and carbonaceous aerosols (elemental carbon [EC], organic carbon [OC], and black carbon [BC]) were measured at the Harvard-U.S. Environmental Protection Agency Supersite in Boston, MA, between January 2007 and October 2008. These hourly concentrations were compared with those made using integrated filter-based measurements over 6-day or 24-hr periods. For sulfate, the two measurement methods showed good agreement. Semicontinuous measurements of EC and OC also agreed (but not as well as for sulfate) with those obtained using 24-hr integrated filter-based and optical BC reference methods. During the study period, 24-hr PM2.5 (particulate matter [PM] < or = 2.5 microm in aerodynamic diameter) concentrations ranged from 1.4 to 37.6 microg/m3, with an average of 9.3 microg/m3. Sulfate as the equivalent of ammonium sulfate accounted for 39.1% of the PM2.5 mass, whereas EC and OC accounted for 4.2 and 35.2%, respectively. Hourly sulfate concentrations showed no distinct diurnal pattern, whereas hourly EC and BC concentrations peaked during the morning rush hour between 7:00 and 9:00 a.m. OC concentrations also exhibited nonpronounced, small peaks during the day, most likely related to traffic, secondary organic aerosol, and local sources, respectively.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3700403PMC
http://dx.doi.org/10.3155/1047-3289.60.11.1327DOI Listing
November 2010

Exposure error masks the relationship between traffic-related air pollution and heart rate variability.

J Occup Environ Med 2010 Jul;52(7):685-92

Department of Environmental Health, Harvard School of Public Health, Boston, MA 02215, USA.

Objective: We examined whether more precise exposure measures would better detect associations between traffic-related pollution, elemental carbon (EC), nitrogen dioxide (NO2), and heart rate variability (HRV).

Methods: Repeated 24-hour personal and ambient PM2.5, EC, and NO2 were measured for 30 people living in Atlanta, GA. The association between HRV and either ambient concentrations or personal exposures was examined using linear mixed effects models.

Results: Ambient PM2.5, EC, NO2, and personal PM2.5 were not associated with HRV. Personal EC and NO2 measured 24 hours before HRV were associated with decreased RMSSD, PNN50, and HF and with increased LF/HF. RMSSD decreased by 10.97% (95% confidence interval: -18.00 to -3.34) for an inter-quartile range change in personal EC (0.81 microg/m3).

Conclusions: Results indicate decreased vagal tone in response to traffic pollutants, which can best be detected with precise personal exposure measures.
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http://dx.doi.org/10.1097/JOM.0b013e3181e8071fDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2911027PMC
July 2010

Systemic inflammation, heart rate variability and air pollution in a cohort of senior adults.

Occup Environ Med 2010 Sep 2;67(9):625-30. Epub 2010 Jun 2.

Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02215, USA.

Objectives: Short-term elevation of ambient particulate air pollution has been associated with autonomic dysfunction and increased systemic inflammation, but the interconnections between these pathways are not well understood. We examined the association between inflammation and autonomic dysfunction and effect modification of inflammation on the association between air pollution and heart rate variability (HRV) in elderly subjects.

Methods: 25 elderly subjects in Steubenville, Ohio, were followed up to 24 times with repeated 30-min ECG Holter monitoring (545 observations). C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), soluble inter-cellular adhesion molecule 1 (sICAM-1), and white blood cell and platelet counts were measured in peripheral blood samples collected in the first month of the study. Increased systemic inflammation was defined for subjects within the upper 20% of the distribution for each marker. A central ambient monitoring station provided daily fine particle (PM(2.5)) and sulphate (SO(4)(2-)) data. Linear mixed models were used to identify associations between inflammatory markers and HRV and to assess effect modification of the association between air pollution and HRV due to inflammatory status.

Results: A 5.8 mg/l elevation in CRP was associated with decreases of between -8% and -33% for time and frequency domain HRV outcomes. A 5.1 microg/m(3) increase in SO(4)(2-) on the day before the health assessment was associated with a decrease of -6.7% in the SD of normal RR intervals (SDNN) (95% CI -11.8% to -1.3%) in subjects with elevated CRP, but not in subjects with lower CRP (p value interaction=0.04), with similar findings for PM(2.5).

Conclusions: Increased systemic inflammation is associated with autonomic dysfunction in the elderly. Air pollution effects on reduced SDNN are stronger in subjects with elevated systemic inflammation.
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http://dx.doi.org/10.1136/oem.2009.050625DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4472481PMC
September 2010

Traffic-related air pollution and QT interval: modification by diabetes, obesity, and oxidative stress gene polymorphisms in the normative aging study.

Environ Health Perspect 2010 Jun 1;118(6):840-6. Epub 2010 Mar 1.

Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115 , USA.

Background: Acute exposure to ambient air pollution has been associated with acute changes in cardiac outcomes, often within hours of exposure.

Objectives: We examined the effects of air pollutants on heart-rate-corrected QT interval (QTc), an electrocardiographic marker of ventricular repolarization, and whether these associations were modified by participant characteristics and genetic polymorphisms related to oxidative stress.

Methods: We studied repeated measurements of QTc on 580 men from the Veterans Affairs Normative Aging Study (NAS) using mixed-effects models with random intercepts. We fitted a quadratic constrained distributed lag model to estimate the cumulative effect on QTc of ambient air pollutants including fine particulate matter
Results: Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in BC cumulative during the 10 hr before the visit was associated with increased QTc [1.89 msec change; 95% confidence interval (CI), -0.16 to 3.93]. We found a similar association with QTc for an IQR change in 1-hr BC that occurred 4 hr before the visit (2.54 msec change; 95% CI, 0.28-4.80). We found increased QTc for IQR changes in NO2 and CO, but the change was statistically insignificant. In contrast, we found no association between QTc and PM2.5, SO2, and O3. The association between QTc and BC was stronger among participants who were obese, who had diabetes, who were nonsmokers, or who had higher GSSs.

Conclusions: Traffic-related pollutants may increase QTc among persons with diabetes, persons who are obese, and nonsmoking elderly individuals; the number of genetic variants related to oxidative stress increases this effect.
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http://dx.doi.org/10.1289/ehp.0901396DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898862PMC
June 2010

Air pollution and homocysteine: more evidence that oxidative stress-related genes modify effects of particulate air pollution.

Epidemiology 2010 Mar;21(2):198-206

Exposure, Epidemiology, and Risk Program, Harvard School of Public Health, Boston, MA 02215, USA.

Background: Ambient particles are associated with cardiovascular events and recently with total plasma homocysteine. High total plasma homocysteine is a risk for human health. However, the biologic mechanisms are not fully understood. One of the putative pathways is through oxidative stress. We aimed to examine whether associations of PM2.5 and black carbon with homocysteine were modified by genotypes including HFE H63D, C282Y, CAT (rs480575, rs1001179, rs2284367, and rs2300181), NQO1 (rs1800566), GSTP1 I105V, GSTM1, GSTT1 (deletion vs. nondeletion), and HMOX-1 (any short vs. both long). We attempted to replicate identified genes in an analysis of heart rate variability and in other outcomes reported in the literature.

Methods: Study subjects were 1000 white non-Hispanic men in the Boston area, participating in a cohort study of aging. PM2.5, black carbon, total plasma homocysteine, and other covariates were measured at several points in time between 1995 and 2006. We fit mixed models to examine effect modification of genes on associations of pollution with total plasma homocysteine.

Results: Interquartile range increases in PM2.5 and black carbon (7-day moving averages) were associated with 1.5% (95% confidence interval = 0.2% to 2.8%) and 2.2% (0.6% to 3.9%) increases in total plasma homocysteine, respectively. GSTT1 and HFE C282Y modified effects of black carbon on total plasma homocysteine, and HFE C282Y and CAT (rs2300181) modified effects of PM2.5 on homocysteine. Several genotypes marginally modified effects of PM2.5 and black carbon on various endpoints. All genes with significant interactions with particulate air pollution had modest main effects on total plasma homocysteine.

Conclusions: : Effects of PM2.5 and black carbon on various endpoints appeared to be mediated by genes related to oxidative stress pathways.
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http://dx.doi.org/10.1097/EDE.0b013e3181cc8bfcDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3939788PMC
March 2010
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