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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. 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. 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. 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. 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.

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.

We examined the association of long-term, daily 1-h maximum O3 (ozone) exposures on cause-specific mortality for 22.2 million US Medicare beneficiaries between 2000–2008. We modeled the association between O3 and mortality using age-gender-race stratified log-linear regression models, adjusted for state of residence. We examined confounding by (1) adjusting for PM2.5 (particles with aerodynamic diameters <2.5 μm) and NO2 (nitrogen dioxide) exposures, temperature, and neighborhood-level characteristics and behaviors, and (2) decomposing O3 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 O3 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 PM2.5, NO2, and temperature and with results similar across O3 exposure measures. While significant, associations between long-term O3 exposures and CVD (cardiovascular)-related mortality (1.005, 95% CI: 1.003, 1.007) were confounded by PM2.5 and varied with the exposure measure, with associations no longer significantly positive when warm-season 8-h maximum or 24-h average O3 was used to assess exposures. In this large study, we provide strong evidence that O3 exposure is associated with mortality from respiratory-related causes and for the first-time, lung cancer, but raise questions regarding O3-related impacts on CVD mortality. Our findings demonstrate the need to further identify potential confounders.

Exposure to particulate air pollution has been related to increased hospitalization and death, particularly from cardiovascular disease. Lower blood DNA methylation content is found in processes related to cardiovascular outcomes, such as oxidative stress, aging, and atherosclerosis. We evaluated whether particulate pollution modifies DNA methylation in heavily methylated sequences with high representation throughout the human genome. We measured DNA methylation of long interspersed nucleotide element (LINE)-1 and Alu repetitive elements by quantitative polymerase chain reaction-pyrosequencing of 1,097 blood samples from 718 elderly participants in the Boston area Normative Aging Study. We used covariate-adjusted mixed models to account for within-subject correlation in repeated measures. We estimated the effects on DNA methylation of ambient particulate pollutants (black carbon, particulate matter with aerodynamic diameter < or = 2.5 microm [PM2.5], or sulfate) in multiple time windows (4 h to 7 d) before the examination. We estimated standardized regression coefficients (beta) expressing the fraction of a standard deviation change in DNA methylation associated with a standard deviation increase in exposure. Repetitive element DNA methylation varied in association with time-related variables, such as day of the week and season. LINE-1 methylation decreased after recent exposure to higher black carbon (beta = -0.11; 95% confidence interval [CI], -0.18 to -0.04; P = 0.002) and PM2.5 (beta = -0.13; 95% CI, -0.19 to -0.06; P < 0.001 for the 7-d moving average). In two-pollutant models, only black carbon, a tracer of traffic particles, was significantly associated with LINE-1 methylation (beta = -0.09; 95% CI, -0.17 to -0.01; P = 0.03). No association was found with Alu methylation (P > 0.12). We found decreased repeated-element methylation after exposure to traffic particles. Whether decreased methylation mediates exposure-related health effects remains to be determined.

Background Risk factors contributing to sepsis-related mortality include clinical conditions such as cardiovascular disease, chronic lung disease, and diabetes, all of which have also been shown to be associated with air pollution exposure. However, the impact of chronic exposure to air pollution on sepsis-related mortality has been little studied.  Methods In a cohort of 53 million Medicare beneficiaries (228,439 sepsis-related deaths) living across the conterminous United States between 2000 and 2008, we examined the association of long-term PM 2.5 exposure and sepsis-related mortality. For each Medicare beneficiary (ages 65–120), we estimated the 12-month moving average PM 2.5 concentration for the 12 month before death, for their ZIP code of residence using well validated GIS-based spatio-temporal models. Deaths were categorized as sepsis-related if they have ICD-10 codes for bacterial or other sepsis. We used Cox proportional hazard models to assess the association of long-term PM 2.5 exposure on sepsis-related mortality. Models included strata for age, sex, race, and ZIP code and controlled for neighborhood socio-economic status (SES). We also evaluated confounding through adjustment of neighborhood behavioral covariates. Results A 10 μg/m 3 increase in 12-month moving average PM 2.5 was associated with a 9.1% increased risk of sepsis mortality (95% CI: 3.6–14.9) in models adjusted for age, sex, race, ZIP code, and SES. HRs for PM 2.5 were higher and statistically significant for older (> 75), Black, and urban beneficiaries. In stratified analyses, null associations were found for younger beneficiaries (65–75), beneficiaries who lived in non-urban ZIP codes, and those residing in low-SES urban ZIP codes. Conclusions Long-term PM 2.5 exposure is associated with elevated risks of sepsis-related mortality.

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 [paniculate 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.

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 3 personal EC (0.81μg/m³ ). Conclusions: Results indicate decreased vagal tone in response to traffic pollutants, which can best be detected with precise personal exposure measures.

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 2.5 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 2.5 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 2.5 concentrations were 6.0 (3.1–19.8) μ g/m 3 . 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 2.5 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 2.5 -PTB association. Conclusion Among ethnic minority women in Puerto Rico, prenatal PM 2.5 exposure is associated with a small but significant increase in risk of PTB.

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 partículate matter < 2.5 urn in aerodynamic diameter (PM₂.₄), ozone (CO₃), black carbon nitrogen dioxide (NO₂), carbon monoxide (CO), and sulfur dioxide (SO₂) concentrations during the 10 hr before the visit. We genotyped polymorphisms related to oxidative stress and analyzed pollution-susceptibility score interactions using the genetic susceptibility score (GSS) method. RESULTS: Ambient traffic pollutant concentrations were related to longer QTc. An interquartile range (IQR) change in 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 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, SO₃, and O₃. The association between QTc and 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.

PurposePuerto 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.ParticipantsInfants 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 dateData 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 plansData 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.