Background: Ambient fine particulate matter (PM 2.5 ) 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 PM 2.5 on mental health is just emerging. oBjective: We examined the association between PM 2.5 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 PM 2.5 estimates were obtained using spatio temporal models. We used generalized linear mixed models, adjusting for potential confounders, and explored effect modification. results: An increase in PM 2.5 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 socio economic measures (SES); PM 2.5 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, PM 2.5 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 PM 2.5 exposure.

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.

BackgroundNeighborhood 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.MethodsWe 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.ResultsAn 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.ConclusionWe 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.Electronic supplementary materialThe online version of this article (10.1186/s12940-018-0381-2) contains supplementary material, which is available to authorized users.

Background Epidemiological research on the effects of coarse particles (PM c , 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 PM c exposure. Aim To estimate the effect of PM c on emergency hospital admissions for pneumonia after controlling for PM 2.5 and gaseous pollutants. Method PM c 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 PM c were computed from the 10 stations. Generalised additive Poisson models were used to examine the relationship between PM c 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 PM c and PM 2.5 were significantly associated with emergency pneumonia hospitalisations. Every 10 μg/m 3 increment of PM c in the past 4 days (lag 0 -lag 3 ) was associated with a 3.33% (95% CI 1.54% to 5.15%) increase in emergency hospitalisations for pneumonia. The effect estimates of PM c 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 PM c exposure. Conclusions Short-term PM c exposure is associated with emergency hospitalisations for pneumonia in Hong Kong. Air quality regulation specifically for PM c might be considered.

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 4,121 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 ± 3.0 μg/m3 and 13.1 ± 7.0 ppb, respectively. An inter-quartile range (IQR, 3.9 μg/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 elde...

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.

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 4,121 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 <12 g/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, 3.9 μg/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 0.81 g/dL (p<0.001). Similarly, an IQR (9.6 ppb) increase in NO2 was associated with anemia prevalence (PR 1.43, 95% CI: 1.25, 1.63) and a decrease in average hemoglobin of 0.81 g/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.

The results of this review suggest that while smoking habits of Chinese physicians vary among studies and across physicians in different specialties; prevalence rates tend to be higher than in physicians in the developed countries. Quitting rates were low among Chinese physicians, and the delivery of advice on quitting smoking was not common across the studies. Strategies to improve Chinese physicians' engagement in smoking cessation should address multiple factors including tobacco use and quitting practices among the physicians, their training needs and awareness of their professional responsibility with a healthcare system change approach.