Long-term nitrogen dioxide exposure and cause-specific mortality in the U.S. Medicare population.

BACKGROUND: Since 1971, the annual National Ambient Air Quality Standard (NAAQS) for nitrogen dioxide (NO2) has remained at 53 ppb, the impact of long-term NO2 exposure on mortality is poorly understood. OBJECTIVES: We examined associations between long-term NO2 exposure (12-month moving average of NO2) below the annual NAAQS and cause-specific mortality among the older adults in the U.S. METHODS: Cox proportional-hazard models were used to estimate Hazard Ratio (HR) for cause-specific mortality associated with long-term NO2 exposures among about 50 million Medicare beneficiaries living within the conterminous U.S. from 2001 to 2008. RESULTS: A 10 ppb increase in NO2 was associated with increased mortality from all-cause (HR: 1.06; 95% CI: 1.05-1.06), cardiovascular (HR: 1.10; 95% CI: 1.10-1.11), respiratory disease (HR: 1.09; 95% CI: 1.08-1.11), and cancer (HR: 1.01; 95% CI: 1.00-1.02) adjusting for age, sex, race, ZIP code as strata ZIP code- and state-level socio-economic status (SES) as covariates, and PM2.5 exposure using a 2-stage approach. NO2 was also associated with elevated mortality from ischemic heart disease, cerebrovascular disease, congestive heart failure, chronic obstructive pulmonary disease, pneumonia, and lung cancer. We found no evidence of a threshold, with positive and significant HRs across the range of NO2 exposures for all causes of death examined. Exposure-response curves were linear for all-cause, supra-linear for cardiovascular-, and sub-linear for respiratory-related mortality. HRs were highest consistently among Black beneficiaries. CONCLUSIONS: Long-term NO2 exposure is associated with elevated risks of death by multiple causes, without evidence of a threshold response. Our findings raise concerns about the sufficiency of the annual NAAQS for NO2.

Respirable Particulate Constituents and Risk of Cause-Specific Mortality in the Hong Kong Population.

Emerging studies examined the associations of particulate matter constituents with nonaccidental and cardiorespiratory diseases, but few have investigated more specific causes of cardiorespiratory diseases or other system diseases, especially in Asia. We estimated the association between respirable particulate matter (PM10) constituents and a spectrum of deaths using a quasi-Poisson time-series model in Hong Kong. Positive associations were identified between cause-specific deaths and elemental carbon, organic carbon (OC), nitrate, and potassium ion (K+), but only the associations for OC and K+ were robust in the two-constituent models adjusting for other constituents. The estimated effects of OC were strongest on mortality from the respiratory system with cumulative percent excess risk (ER%) of 3.82% (95% CI: 0.96%, 6.92%) per interquartile range (6.7 µg/m3) increase over 7 days prior to death (lag0-7), especially for pneumonia (ER%: 4.32%; 95% CI: 0.70%, 8.26%). The digestive system was most sensitive to K+ with cumulative ER% of 6.74% (95% CI: 0.37%, 14.01%) per interquartile range (0.6 µg/m3) increase. This study indicates that PM10 constituents from biomass burning (OC and K+) were more toxic than other constituents for deaths in Hong Kong, especially for mortalities from respiratory and digestive systems. These findings should have potential biological and pollution control implications.

Associations of long-term fine particulate matter exposure with prevalent hypertension and increased blood pressure in older Americans.

BACKGROUND: Hypertension is a highly prevalent cardiovascular risk factor. It is possible that air pollution, also an established cardiovascular risk factor, may contribute to cardiovascular disease through increasing blood pressure. Previous studies evaluating associations between air pollution and blood pressure have had mixed results. METHODS: We examined the association between long-term (one-year moving average) air pollutant exposures, prevalent hypertension and blood pressure in 4121 older Americans (57+ years) enrolled in the National Social Life, Health, and Aging Project. We estimated exposures to PM2.5 using spatio-temporal models and used logistic regression accounting for repeated measures to evaluate the association between long-term average PM2.5 and prevalence odds of hypertension. We additionally used linear regression to evaluate the associations between air pollutants and systolic, diastolic, mean arterial, and pulse pressures. Health effect models were adjusted for a number of demographic, health and socioeconomic covariates. RESULTS: An inter-quartile range (3.91 µg/m3) increase in the one-year moving average of PM2.5 was associated with increased: Odds of prevalent hypertension (POR 1.24, 95% CI: 1.11, 1.38), systolic blood pressure (0.93 mm Hg, 95% CI: 0.05, 1.80) and pulse pressure (0.89 mm Hg, 95% CI: 0.21, 1.58). Dose-response relationships were also observed. CONCLUSIONS: PM2.5 was associated with increased odds of prevalent hypertension, and increased systolic pressure and pulse pressure in a cohort of older Americans. These findings add to the growing evidence that air pollution may be an important risk factor for hypertension and perturbations in blood pressure.

Personal exposure to fine particles (PM2.5) and respiratory inflammation of common residents in Hong Kong.

BACKGROUND: Given the lack of research on the personal exposure to fine particles (PM2.5) in Hong Kong, we examined the association between short-term personal exposure to PM2.5 and their constituents and inflammation in exhaled breath in a sample of healthy adult residents. METHOD: Forty-six participants underwent personal PM2.5 monitoring for averagely 6 days to obtain 276 samples. Fractional exhaled nitric oxide (FeNO), a biomarker of inflammation in exhaled breath, was measured at the end of each 24-h personal monitoring. PM2.5 chemical constituents, including organic carbon, elemental carbon, 16 polycyclic aromatic hydrocarbons (PAHs), and 6 phthalate esters, were speciated from the personal samples collected. A mixed-effects model was used to estimate the association of PM2.5 and their constituents with FeNO. The comparison was also made with parallel analyses using ambient concentrations. RESULTS: Personal exposures to PM2.5 (28.1 ±â€¯23.3 µg/m3) were higher than the ambient levels (13.3 ±â€¯6.4 µg/m3) monitored by stations. The composition profile and personal-to-ambient concentration ratio varied among subjects with different occupations. An interquartile range (IQR) change in personal exposure to PM2.5 was positively associated with 12.8% increase in FeNO (95% confidence interval, CI: 5.5-20.7%), while nil association was found for ambient PM2.5. Among the constituents measured, only the carcinogenic PAHs were significantly associated with 12% increase in FeNO responses (95% CI, 0.0-25.6%). CONCLUSION: In conclusion, our study provides the first understanding about personal exposure to PM2.5 and possible sources in Hong Kong. The results also showed that personal exposure to PM2.5 and c-PAHs were linked to increased FeNO levels among healthy adults.

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.

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.

Erectile dysfunction and exposure to ambient Air pollution in a nationally representative cohort of older Men.

BACKGROUND: Little is known about the association between air pollution and erectile dysfunction (ED), a disorder occurring in 64% of men over the age of 70, and to date, no studies have been published. To address this significant knowledge gap, we explored the relationship between ED and air pollution in a group of older men who were part of the National Social Life, Health, and Aging Project (NSHAP), a nationally representative cohort study of older Americans. METHODS: We obtained incident ED status and participant data for 412 men (age 57-85). Fine particulate matter (PM2.5) exposures were estimated using spatio-temporal models based on participants' geocoded addresses, while nitrogen dioxide (NO2) and ozone (O3) concentrations were estimated using nearest measurements from the Environmental Protection Agency's Air Quality System. The association between air pollution and incident ED (newly developed in Wave 2) was examined and logistic regression models were run with adjusted models controlling for race, education, season, smoking, obesity, diabetes, depression, and median household income of census tract. RESULTS: We found positive, although statistically insignificant, associations between PM2.5, NO2, and O3 exposures and odds of incident ED for each of our examined exposure windows, including 1 to 7 year moving averages. Odds ratios (OR) for 1 and 7 year moving averages equaled 1.16 (95% CI: 0.87, 1.55) and 1.16 (95% CI: 0.92, 1.46), respectively, for an IQR increase in PM2.5 exposures. Observed associations were robust to model specifications and were not significantly modified by any of the examined risk factors for ED. CONCLUSIONS: We found associations between PM2.5, NO2, and O3 exposures and odds of developing ED that did not reach nominal statistical significance, although exposures to each pollutant were consistently associated with higher odds of developing ED. While more research is needed, our findings suggest a relationship between air pollutant exposure and incident cases of ED, a common condition in older men.

Differential distributed lag patterns of source-specific particulate matter on respiratory emergency hospitalizations.

While different emission sources and formation processes generate mixtures of particulate matter (PM) with different physicochemical compositions that may differentially affect PM toxicity, evidence of associations between PM sources and respiratory events is scarce. We estimated PM10 sources contributed from 19 chemical constituents by positive matrix factorization, and examined association of short-term sources exposure with emergency respiratory hospitalizations using generalized additive models for single- and distributed lag periods. PM10 contributions from eight sources were identified. Respiratory risks over a consecutive 6-day exposure period were the highest for vehicle exhaust [2.01%; 95% confidence interval (CI): 1.04, 2.99], followed by secondary sulfate (1.59%; 95% CI: 0.82, 2.37). Vehicle exhaust, regional combustion, and secondary nitrate were significantly associated with 0.93%-2.04% increase in respiratory hospitalizations at cumulative lag2-5; significant associations of aged sea salt (1.2%; 95% CI: 0.63, 1.78) and soil/road dust (0.42%; 95% CI: 0.03, 0.82) were at lag0-1. Some effect estimates were no longer significant in two-pollutant models adjusting for PM10; however, a similar temporal pattern of associations remains. Differential lag associations of respiratory hospitalizations with PM10 sources were indicated, which may reflect the different particle size fractions that sources tend to emit. Findings may have potential biological and policy implications.

Ambient carbon monoxide and the risk of hospitalization due to chronic obstructive pulmonary disease.

Data from recent experimental and clinical studies have indicated that lower concentrations of inhaled carbon monoxide might have beneficial antiinflammatory effects. Inhaled carbon monoxide has the potential to be a therapeutic agent for chronic obstructive pulmonary diseases (COPD). However, population-based epidemiologic studies of environmentally relevant carbon monoxide exposure have generated mixed findings. We conducted a time-series study in Hong Kong to estimate the association of short-term exposure to ambient carbon monoxide with emergency hospitalizations for COPD. We collected daily emergency hospital admission data and air pollution data from January 2001 to December 2007. We used log-linear Poisson models to estimate the associations between daily hospital admissions for COPD and the average daily concentrations of carbon monoxide while controlling for the traffic-related co-pollutants nitrogen dioxide and particulate matter with an aerodynamic diameter less than 2.5 µm. Results showed that ambient carbon monoxide was negatively associated with the risk of hospitalizations for COPD. After adjustment for levels nitrogen dioxide or particulate matter with an aerodynamic diameter less than 2.5 µm, the negative associations of carbon monoxide with COPD hospitalizations became stronger. The risk estimates were similar for female and male subjects. In conclusion, short-term exposure to ambient carbon monoxide was associated with a decreased risk of hospitalization for COPD, which suggests that carbon monoxide exposure provides some acute protection of against exacerbation of COPD.

Coarse particulate matter associated with increased risk of emergency hospital admissions for pneumonia in Hong Kong.

BACKGROUND: Epidemiological research on the effects of coarse particles (PMc, particulate matter between 2.5 and 10 µm in aerodynamic diameter) on respiratory morbidity is sparse and inconclusive. Pneumonia is an inflammatory condition of lung caused by infections, which may be triggered and exacerbated by PMc exposure. AIM: To estimate the effect of PMc on emergency hospital admissions for pneumonia after controlling for PM(2.5) and gaseous pollutants. METHOD: PMc concentrations were estimated by subtracting PM(2.5) from PM(10) measurements in each of the 10 air monitoring stations from January 2011 to December 2012 in Hong Kong and then citywide daily average concentrations of PMc were computed from the 10 stations. Generalised additive Poisson models were used to examine the relationship between PMc and daily emergency hospital admissions for pneumonia, adjusting for PM(2.5) and gaseous pollutants (NO(2), SO(2) and O(3)). Subgroup analyses by gender and age were also performed to identify the most susceptible subpopulations. RESULTS: PMc and PM(2.5) were significantly associated with emergency pneumonia hospitalisations. Every 10 µg/m(3) increment of PMc in the past 4 days (lag0-lag3) was associated with a 3.33% (95% CI 1.54% to 5.15%) increase in emergency hospitalisations for pneumonia. The effect estimates of PMc were robust to the adjustment of PM(2.5), NO(2) or SO(2), but attenuated on the inclusion of O(3) in the model. Women, children and older people might be more vulnerable to PMc exposure. CONCLUSIONS: Short-term PMc exposure is associated with emergency hospitalisations for pneumonia in Hong Kong. Air quality regulation specifically for PMc might be considered.

Ambient carbon monoxide associated with reduced risk of hospital admissions for respiratory tract infections.

RATIONALE: Recent experimental and clinical studies suggest that exogenous carbon monoxide (CO) at lower concentrations may have beneficial effects under certain circumstances, whereas population-based epidemiologic studies of environmentally relevant CO exposure generated mixed findings. OBJECTIVES: To examine the acute effects of ambient CO on respiratory tract infection (RTI) hospitalizations. METHODS: A time series study was conducted. Daily emergency hospital admission and air pollution data in Hong Kong were collected from January 2001 to December 2007. Log-linear Poisson models were used to estimate the associations between daily hospital admissions for RTI and daily average concentrations of CO across three background air monitoring stations and three roadside stations, respectively, controlling for other traffic-related copollutants. MEASUREMENTS AND MAIN RESULTS: CO concentrations were low during the study period with a daily average of 0.6 ppm in background stations and 1.0 ppm in roadside stations. Negative associations were found between ambient CO concentrations and daily hospital admissions for RTI. One ppm increase in background CO at lag 0-2 days was associated with -5.7% (95% confidence interval, -9.2 to -2.1) change in RTI admissions from the whole population according to single-pollutant model; the negative association became stronger when nitrogen dioxide or particulate matter with aerodynamic diameter less than 10 µm was adjusted for in two-pollutant models. The negative association seemed to be stronger in the adults than in the children and elderly. CONCLUSIONS: Short-term exposure to ambient CO was associated with decreased risk of hospital admissions for RTI, suggesting some acute protective effects of low ambient CO exposure on respiratory infection.

Ambient and household air pollution on early-life determinants of stunting-a systematic review and meta-analysis.

Stunting is an important risk factor for early growth and health implications throughout the life course, yet until recently, studies have rarely focused on populations exposed to high levels of particulate matter pollution or on developing countries most vulnerable to stunting and its associated health and developmental impacts. We systematically searched for epidemiologic studies published up to 15 August 2020 that examined the association between ambient and household particulate exposure and postnatal stunting (height-for-age z-score) and prenatal determinants (small for gestational age or SGA, or equivalent) of stunting. We conducted the literature search in PUBMED, MEDLINE, EMBASE, and Web of Science databases in August 2020, using keywords including, but not limited to, "particulate matter," "indoor/household air pollution," and "adverse birth outcomes," to identify relevant articles. Forty-five studies conducted in 29 countries met our inclusion criteria for meta-analysis. We found significant positive associations between SGA and a 10 µg/m3 increase in fine particulate matter (PM2.5) exposure over the entire pregnancy [OR = 1.08; 95% confidence interval (CI): 1.03-1.13], with similar SGA impact during the second and third trimesters, and from high exposure quartile of PM2.5 exposure during the entire pregnancy. A 19% increased risk of postnatal stunting (95% CI: 1.10, 1.29) was also associated with postnatal exposure to household air pollution. Our analysis shows consistent, significant, and noteworthy evidence of elevated risk of stunting-related health outcomes with ambient PM2.5 and household air pollution exposure. This evidence reinforces the importance of promoting clean air as part of an integrated approach to preventing stunting.

Smoking status and cessation counseling practices among physicians, Guangxi, China, 2007.

INTRODUCTION: We examined Chinese physicians' smoking behavior, knowledge of smoking's health effects, and compliance with accepted cessation counseling practices. METHODS: We used a structured questionnaire adapted from the Global Health Professionals Survey of the World Health Organization to survey Chinese physicians based at 5 hospitals in Nanning, Guangxi Province, China. RESULTS: The response rate was 85% for a total of 673 completed questionnaires. Of the 673 respondents, 73% were men, 42% were aged 30 years or younger, and 26% were smokers (men, 35%; women, 3%). Only 28% of the smokers were ready to quit immediately. A substantial proportion of physicians did not have adequate knowledge of smoking-related health hazards or favorable attitudes toward smoking cessation counseling. Asking patients whether they smoked and recording smoking status in the medical record were significantly associated with being female and being very well or somewhat prepared to counsel patients about smoking cessation. Advising patients to quit smoking was significantly associated with being female, being a nonsmoker, being very well or somewhat prepared to counsel patients about smoking cessation, and having read any smoking cessation guidelines. CONCLUSION: Our findings suggest that smoking is common among male Chinese physicians and that Chinese physicians have inadequate knowledge of smoking's health hazards and of how to help smokers quit. Physicians in China and their patients who smoke would benefit from widely accessible Chinese clinical practice guidelines on smoking cessation, better medical school education about the health risks of smoking, and government funding of cessation medications.

Blood pressure and pulmonary health effects of ozone and black carbon exposure in young adult runners.

Physical activity has been shown to promote health and well-being, however, exercising in environments with high level of air pollution might increase the risk of cardio-respiratory impairments. In this crossover study, we constructed linear mixed models to investigate the impact of short-term exposure to black carbon (BC) and ozone on blood pressure and pulmonary functions among 30 healthy adult runners after 30-minute run on a clean and polluted route on separate days in August 2015 in Hong Kong. Runners were on average 20.6 years old, with mean body mass index of 20.3 kg/m2. Air pollution concentrations were higher in the polluted route than in the clean route, with the highest difference in BC (5.4 µg/m3 versus 1.3 µg/m3). In single-pollutant models, no significant association was found between air pollution and changes in blood pressures, forced vital capacity, forced expiratory volume in 1 s, peak expiratory flow and fractional exhaled nitric oxide, after adjusting for gender, type of route, temperature and relative humidity. When further adjusting for both BC and ozone simultaneously, increment in BC became statistically significantly associated with increase in systolic blood pressure (relative risk = 3.18; 95% CI: 0.24, 6.13) after running exercise. Stratified analysis further shows that the significant adverse association between systolic blood pressure and BC was only observed in the polluted route (e.g., relative risk = 4.51, 95% CI: 0.75, 8.27 in two-pollutant). Our finding of BC is consistent with existing literature, while further studies with greater sample size and longer exposure time are needed to investigate the effects of ozone to cardio-respiratory functions in runners. Given that exercise has clear health benefits, one should consider ways to minimize the air pollution exposure.

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.

Short-term effects of fine and coarse particles on deaths in Hong Kong elderly population: An analysis of mortality displacement.

BACKGROUND: While numerous studies worldwide have evaluated the short-term associations of fine and coarse particulate matter (PM) air pollution with mortality and morbidity, these studies may be susceptible to short-term harvesting effect. We aimed to investigate the short-term association between mortality and PM with aerodynamic diameter less than 2.5 µm (PM2.5) and those between 2.5 and 10 µm (PMc) within a month prior to death, and assess the mortality displacement by PM2.5 and PMc among elderly population in Hong Kong. METHODS: We obtained air pollution data from January 2011 to December 2015 from Environmental Protection Department, and daily cause-specific mortality data from Census and Statistical Department of Hong Kong. We performed generalized additive distributed lag model to examine the acute, delayed and long-lasting effects of PM2.5 and PMc within one month on mortality. RESULTS: We observed a statistically significant association of PM2.5 and PMc exposure over lags 0-6 days with all natural mortality and cardio-respiratory mortality. The overall cumulative effect of PM2.5 over 0-30 lag days was 3.44% (95% CI: 0.30-6.67%) increase in all natural mortality and 6.90% (95% CI: 0.58-13.61%) increase of circulatory mortality, which suggested the absence of mortality displacement by PM2.5. On the other hand, no significant cumulative association with mortality was found for PMc over 0-30 lag exposure window, and thus mortality displacement by PMc cannot be ruled out. Findings remained robust in various sensitivity analyses. CONCLUSIONS: We found adverse effect of both PM2.5 and PMc exposure within one week prior to death. While there was no evidence of mortality displacement in the association of PM2.5 exposure over one month prior with all natural and circulatory mortality, mortality displacement by PMc cannot be ruled out. PM2.5 may contribute more to the longer term effect of particulate matter than PMc.

Association of Ambient Air Pollution with Depressive and Anxiety Symptoms in Older Adults: Results from the NSHAP Study.

BACKGROUND: Ambient fine particulate matter (PM2.5) is among the most prevalent sources of environmentally induced inflammation and oxidative stress, both of which are implicated in the pathogenesis of most mental disorders. Evidence, however, concerning the impact of PM2.5 on mental health is just emerging. OBJECTIVE: We examined the association between PM2.5 and current level of depressive and anxiety symptoms using a nationally representative probability sample (n = 4,008) of older, community-dwelling individuals living across the United States (the National Social Life, Health and Aging project). METHODS: Mental health was evaluated using validated, standardized questionnaires and clinically relevant cases were identified using well-established cutoffs; daily PM2.5 estimates were obtained using spatiotemporal models. We used generalized linear mixed models, adjusting for potential confounders, and explored effect modification. RESULTS: An increase in PM2.5 was significantly associated with anxiety symptoms, with the largest increase for 180-days moving average (OR = 1.61; 95% CI: 1.35, 1.92) after adjusting for socioeconomic measures (SES); PM2.5 was positively associated with depressive symptoms, and significantly for 30-day moving average (OR = 1.16; 95% CI: 1.05, 1.29) upon SES adjustment. The observed associations were enhanced among individuals who had low SES and history of comorbidity. When considering mental health as chronic conditions, PM2.5 was significantly associated with incident depressive symptoms for all exposure windows examined, but with incident anxiety symptoms only for shorter exposure windows, which may be due to a drop in power resulting from the decreased between-subject variability in chronic PM2.5 exposure. CONCLUSION: PM2.5 was associated with depressive and anxiety symptoms, with associations the strongest among individuals with lower SES or among those with certain health-related characteristics. Citation: Pun VC, Manjourides J, Suh H. 2017. Association of ambient air pollution with depressive and anxiety symptoms in older adults: results from the NSHAP study. Environ Health Perspect 125:342-348; http://dx.doi.org/10.1289/EHP494.

Associations between long-term exposure to air pollution, glycosylated hemoglobin and diabetes.

BACKGROUND: Air pollution exposures have been shown to adversely impact health through a number of biological pathways associated with glucose metabolism. However, few studies have evaluated the associations between air pollution and glycosylated hemoglobin (HbA1c) levels. Further, no studies have evaluated these associations in US populations or investigated whether associations differ in diabetic as compared to non-diabetic populations. To address this knowledge gap, we investigated the associations between airborne fine particulate matter (PM2.5) and nitrogen dioxide (NO2) and HbA1c levels in both diabetic and non-diabetic older Americans. We also examined the impact of PM2.5 and NO2 on prevalent diabetes mellitus (DM) in this cohort. METHODS: We used multilevel logistic and linear regression models to evaluate the association between long-term average air pollutant levels and prevalence of DM and HbA1c levels, respectively, among 4121 older (57+ years) Americans enrolled in the National Social Life, Health, and Aging Project between 2005 and 2011. All models adjusted for age, sex, body mass index, smoking status, race, household income, education level, neighborhood socioeconomic status, geographic region, urbanicity and diabetic medication use. We estimated participant-specific exposures to PM2.5 on a six-kilometer grid covering the conterminous U.S. using spatio-temporal models, and to NO2 using nearest measurements from the Environmental Protection Agency's Air Quality System. HbA1c levels were measured for participants in each of two data collection waves from dried blood spots and log-transformed prior to analysis. Participants were considered diabetic if they had HbA1c values≥6.5% or reported taking diabetic medication. RESULTS: The prevalence of diabetes at study entry was 22.2% (n=916) and the mean HbA1c was 6.0±1.1%. Mean one-year moving average PM2.5 and NO2 exposures were 10.4±3.0µg/m3 and 13.1±7.0 ppb, respectively. An inter-quartile range (IQR, 3.9µg/m3) increase in one-year moving average PM2.5 was positively associated with increased diabetes prevalence (prevalence odds ratio, POR 1.35, 95% CI: 1.19, 1.53). Similarly, an IQR (8.6 ppb) increase in NO2 was also significantly associated with diabetes prevalence (POR 1.27, 95% CI: 1.10, 1.48). PM2.5 (1.8%±0.6%, p<0.01) and NO2 (2.0%±0.7%, p<0.01) exposures were associated with higher HbA1c levels in diabetic participants, while only NO2 was significantly associated with HbA1c in non-diabetic participants (0.8%±0.2%, p<0.01). Significant dose response relationships were identified for both pollutants in diabetic participants and for NO2 in non-diabetic participants. CONCLUSIONS/INTERPRETATIONS: In a cohort of older men and women in the United States, PM2.5 and NO2 exposures were significantly associated with prevalence of DM and increased HbA1c levels among both non-diabetic and diabetic participants. These associations suggest that air pollution could be a key risk factor for abnormal glucose metabolism and diabetes in the elderly.

Anemia prevalence and hemoglobin levels are associated with long-term exposure to air pollution in an older population.

BACKGROUND: Anemia, a highly prevalent disorder in elderly populations, is associated with numerous adverse health outcomes, including increased mortality, impaired functional status and cognitive disorders. Approximately two-thirds of anemia in American elderly is caused by chronic inflammation or is unexplained. A potential contributing factor may include air pollution exposures, which have been shown to increase systemic inflammation and affect erythropoiesis. Few studies, however, have investigated the associations of air pollution on hemoglobin levels and anemia. METHODS: We used linear regression models and modified Poisson regression with robust error variance to examine the associations of particulate matter (PM2.5) and nitrogen dioxide (NO2) on hemoglobin concentrations and prevalence of anemia, respectively, among 4121 older Americans enrolled in the National Social Life, Health, and Aging Project. We estimated participant-specific exposures to PM2.5 using spatio-temporal models, and to NO2 using nearest measurements from Environmental Protection Agency's Air Quality System. Hemoglobin levels were measured for participants in each of two data collection waves from dried blood spots. Anemia was defined using World Health Organization hemoglobin-based criteria of <13 and <12g/dL for men and women, respectively. Models were adjusted for age, sex, smoking status, race, income, education, neighborhood socioeconomic status, region, urbanicity and medication use. Mediation by C-reactive protein (CRP), a marker of systemic inflammation, was also investigated. RESULTS: An inter-quartile range (IQR, 3.9µg/m3) increase in the one-year moving average PM2.5 was positively associated with anemia prevalence (prevalence ratio, or PR 1.33, 95% CI: 1.23, 1.45) and decreases in average hemoglobin of 0.81g/dL (p<0.001). Similarly, an IQR (9.6ppb) increase in NO2 was associated with anemia prevalence (PR 1.43, 95% CI: 1.25, 1.63) and a decrease in average hemoglobin of 0.81g/dL (p<0.001). Strong dose-response relationships were identified for both pollutants. Mediation of the effect of PM2.5 by CRP was also identified (p=0.007). CONCLUSIONS/INTERPRETATIONS: Air pollution exposures were significantly associated with increased prevalence of anemia and decreased hemoglobin levels in a cohort of older Americans. If causal, these associations could indicate that chronic air pollution exposure is an important risk factor for anemia in older adults.

Cognitive impacts of ambient air pollution in the National Social Health and Aging Project (NSHAP) cohort.

BACKGROUND: Pathways through which air pollution may impact cognitive function are poorly understood, particularly with regard to whether and how air pollution interacts with social and emotional factors to influence cognitive health. OBJECTIVE: To examine the association between air pollutant exposures and cognitive outcomes among older adults participating in the National Social Life, Health, and Aging Project (NSHAP) cohort study. METHODS: Measures of cognitive function, social connectedness, and physical and mental health were obtained for each NSHAP participant starting with Wave 1 of the study in 2005. Cognitive function was assessed using the Chicago Cognitive Function Measure (CCFM) for 3377 participants. Exposures to fine particles (PM2.5) were estimated for each participant using GIS-based spatio-temporal models, and exposures to nitrogen dioxide (NO2) were obtained from the nearest EPA monitors. RESULTS: In adjusted linear regression models, IQR increases in 1 to 7year PM2.5 exposures were associated with a 0.22 (95% CI: -0.44, -0.01) to a 0.25 (95% CI: -0.43, -0.06) point decrease in CCFM scores, equivalent to aging 1.6years, while exposures to NO2 were equivalent to aging 1.9years. The impacts of PM2.5 on cognition were modified by stroke, anxiety, and stress, and were mediated by depression. The impacts of NO2 were mediated by stress and effect modification by impaired activities of daily living for NO2 was found. CONCLUSIONS: Exposures to long-term PM2.5 and NO2 were associated with decreased cognitive function in our cohort of older Americans, and individuals who experienced a stroke or elevated anxiety were more susceptible to the effects of PM2.5 on cognition. Additionally, mediation results suggest that PM2.5 may impact cognition through pathways related to mood disorders.