Air pollution exposure is associated with rhinitis in older US adults via specific immune mechanisms.

BACKGROUND: Pathophysiology of rhinitis in older adults is largely unknown. We tested whether air pollution is associated with this condition and how immune mechanisms may play a role in this relationship. METHODS: We analyzed cross-sectional data from the National Social Life, Health, and Aging Project, a nationally representative study of older adults born between 1920 and 1947. Particulate matter ≤2.5 µm (PM2.5 ) air pollution exposure estimates were generated using validated spatiotemporal models. Presence of rhinitis was defined based on medication use (≥1: intranasal medications: steroids, antihistamines, lubricants, and/or decongestants, and/or oral medications: antihistamines and/or decongestants). K-means cluster analysis (Jaccard method) was used to group 13 peripheral blood cytokines into 3 clusters to facilitate functional determination. We fitted multivariate logistic regressions to correlate PM2.5 exposure with presence of rhinitis, controlling for confounders, and then determined the role of cytokines in this relationship. RESULTS: Long- (but not short-) term exposure to PM2.5 was associated with presence of rhinitis: 3-year exposure window, odds ratio (OR) = 1.32, 95% confidence interval (CI): 0.98, 1.80, per 1 standard deviation (SD) PM2.5 increase. Inclusion of cytokine cluster in the model led to a modestly stronger effect of PM2.5 exposure on rhinitis (OR = 1.37; 95% CI: 1.00, 1.87; 3-year exposure window). The particular immune profile responsible for this result was composed of elevated IL-3, IL-12, and IFN-γ (OR = 4.86, 95% CI: 1.10, 21.58, immune profile-PM2.5 exposure interaction term). CONCLUSION: We show for the first time that IL-3, IL-12, and IFN-γ explain in part the relationship between PM2.5 exposure and rhinitis in older US adults. If confirmed, these immune pathways may be used as therapeutic targets.

Long-term PM2.5 exposure and sepsis mortality in a US medicare cohort.

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 PM2.5 exposure and sepsis-related mortality. For each Medicare beneficiary (ages 65-120), we estimated the 12-month moving average PM2.5 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 PM2.5 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/m3 increase in 12-month moving average PM2.5 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 PM2.5 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 PM2.5 exposure is associated with elevated risks of sepsis-related mortality.

The impact of Long-Term PM2.5 constituents and their sources on specific causes of death in a US Medicare cohort.

BACKGROUND: Our understanding of the impact of long-term exposures to PM2.5 constituents and sources on mortality is limited. OBJECTIVES: To examine associations between long-term exposures to PM2.5 constituents and sources and cause-specific mortality in US older adults. METHODS: We obtained demographic and mortality data for 15.4 million Medicare beneficiaries living within the conterminous United States (US) between 2000 and 2008. We assessed PM2.5 constituents exposures for each beneficiary and used factor analysis and residual-based methods to characterize PM2.5 sources and mixtures, respectively. In age-, sex-, race- and site- stratified Cox proportional hazard models adjusted for neighborhood socio-economic status (SES), we assessed associations of individual PM2.5 constituents, sources, and mixtures and cause-specific mortality and examined modification of these associations by participant demographics and location of residence. We assessed the robustness of our findings to additional adjustment for behavioral risk factors and to alternate exposure definitions and exposure windows. RESULTS: Hazard ratios (HR) were highest for all causes of death, except COPD, for PM2.5 constituents and the coal combustion-related PM2.5 components, with no evidence of confounding by behavioral covariates. We further found Pb and metal-related PM2.5 components to be significantly associated with increased HR of all causes of death, except COPD and lung cancer mortality, and nitrate (NO3-) and silicon (Si) and associated source-related PM2.5 components (traffic and soil, respectively) to be significantly associated with increased all-cause, CVD, respiratory and all cancer-related mortality HR. Associations for other examined constituents and mortality were inconsistent or largely null. Our analyses of mixtures were generally consistent with these findings. Mortality HRs were greatest for minority, especially Black, low-income urban, younger, and male beneficiaries. DISCUSSION: PM2.5 components related to coal combustion, traffic, and to a lesser extent, soil were strongly associated with mortality from CVD, respiratory disease, and cancer.

Non-pharmaceutical interventions and COVID-19 cases in US summer camps: results from an American Camp Association survey.

BACKGROUND: Most camps remained closed during Summer 2020, due to concerns regarding child transmission of SARS-CoV-2 and limited information about the effectiveness of non-pharmaceutical interventions (NPIs) within child congregate settings. METHODS: We surveyed US camps about on-site operations, camper and staff demographics, COVID-19 cases among campers and staff, and NPI usage as related to pre-camp quarantine, facial coverings, physical distancing, cleaning and facility modifications. For all NPIs, save quarantine, responses were provided on a 5-point Likert scale format. RESULTS: Within 486 on-site camps, a range of NPIs were instituted, most often related to reduced camper interactions, staff face coverings, cleaning and hand hygiene. Camper facial coverings were less common, with campers always wearing masks at ~34% of the camps. Approximately 15% of camps reported 1+ confirmed COVID-19 case in either campers or staff, with three camps reporting a COVID-19 outbreak. In both single and multi-NPI analyses, the risk of COVID-19 cases was lowest when campers always wore facial coverings. Constant use of staff facial coverings and targeted physical distancing measures, but not pre-camp quarantine, also reduced COVID-19 risks. CONCLUSIONS: We found constant facial coverings, especially for campers, and targeted physical distancing measures to reduce risks of SARS-CoV-2 transmission within summer camps. Our findings provide valuable insights for future operations of summer camps and other child congregate settings regarding the use of NPIs to reduce the risk of SARS-CoV-2 infection.

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

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 (PM2.5) 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 PM2.5 and components, measured at three community monitoring sites. We used linear regression to examine the PM2.5-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 cmH2O 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.

Preterm birth and PM2.5 in Puerto Rico: evidence from the PROTECT birth cohort.

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 PM2.5 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 PM2.5 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 PM2.5 concentrations were 6.0 (3.1-19.8) µ g/m3. 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 PM2.5 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 PM2.5-PTB association. CONCLUSION: Among ethnic minority women in Puerto Rico, prenatal PM2.5 exposure is associated with a small but significant increase in risk of PTB.

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

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.

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

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.

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

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 PM2.5 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.

Low birth weight and PM2.5 in Puerto Rico.

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 PM2.5 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) PM2.5 concentrations declined from 9.9 (1.7) µg/m3 in 1999 to 6.1 (1.1) µg/m3 in 2013. Mean birth weights dropped to 3,044 g in 2010 and rose steadily afterward. Among term births, a SD increase in PM2.5 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 PM2.5 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 PM2.5 exposure.

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

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.

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

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.

Impact of long-term temporal trends in fine particulate matter (PM2.5) on associations of annual PM2.5 exposure and mortality: An analysis of over 20 million Medicare beneficiaries.

Decreasing ambient fine particulate matter (PM2.5) concentrations over time together with increasing life expectancy raise concerns about temporal confounding of associations between PM2.5 and mortality. To address this issue, we examined PM2.5-associated mortality risk ratios (MRRs) estimated for approximately 20,000,000 US Medicare beneficiaries, who lived within six miles of an Environmental Protection Agency air quality monitoring site, between December 2000 and December 2012. We assessed temporal confounding by examining whether PM2.5-associated MRRs vary by study period length. We then evaluated three approaches to control for temporal confounding: (1) assessing exposures using the residual of PM2.5 regressed on time; (2) adding a penalized spline term for time to the health model; and (3) including a term that describes temporal variability in PM2.5 into the health model, with this term estimated using decomposition approaches. We found a 10 µg/m3 increase in PM2.5 exposure to be associated with a 1.20 times (95% confidence interval [CI] = 1.20, 1.21) higher risk of mortality across the 13-year study period, with the magnitude of the association decreasing with shorter study periods. MRRs remained statistically significant but were attenuated when models adjusted for long-term time trends in PM2.5. The residual-based, time-adjusted MRR equaled 1.12 (95% CI = 1.11, 1.12) per 10 µg/m3 for the 13-year study period and did not change when shorter study periods were examined. Spline- and decomposition-based approaches produced similar but less-stable MRRs. Our findings suggest that epidemiological studies of long-term PM2.5 can be confounded by long-term time trends, and this confounding can be controlled using the residuals of PM2.5 regressed on time.

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

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.

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

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.

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

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 (PM2.5) 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 PM2.5 exposures averaged over 3-12 months in urban-dwelling respondents. The strongest effect was for 6 month average exposure (per 1-IQR increase in PM2.5: 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.

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

BACKGROUND: Olfactory dysfunction has profound effects on quality of life, physical and social function, and mortality itself. Nitrogen dioxide (NO2 ) 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 NO2 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 NO2 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 NO2 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 NO2 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 NO2 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 NO2 exposure is associated with olfactory dysfunction in older U.S. adults. These results suggest an important role for NO2 exposure on olfactory dysfunction, and, potentially, nasal disease more broadly.

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

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.

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

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.