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Under long-standing threat of seasonal influenza outbreaks, it remains imperative to understand the drivers of influenza dynamics which can guide mitigation measures. While the role of absolute humidity and temperature is extensively studied, the possibility of ambient ozone (O3) as an environmental driver of influenza has received scant attention. Here, using state-level data in the USA during 2010–2015, we examined such research hypothesis. For rigorous causal inference by evidence triangulation, we applied 3 distinct methods for data analysis: Convergent Cross Mapping from state-space reconstruction theory, Peter-Clark-momentary-conditional-independence plus as graphical modeling algorithms, and regression-based Generalised Linear Model. The negative impact of ambient O3 on influenza activity at 1-week lag is consistently demonstrated by those 3 methods. With O3 commonly known as air pollutant, the novel findings here on the inhibition effect of O3 on influenza activity warrant further investigations to inform environmental management and public health protection. Temperature and absolute humidity are associated with influenza activity, and recent data from Hong Kong have suggested ozone as an additional environmental driver. Here, the authors investigate the relationship between ozone and influenza transmission using surveillance data from the USA and find evidence for an inhibitory effect. [ABSTRACT FROM AUTHOR]

Numerous studies have indicated that ambient particulate matter is closely associated with increased risk of cardiovascular disease, yet the evidence for its association with renal disease remains underrecognized. We aimed to estimate the association between long-term exposure to fine particulate matter, defined as particulate matter with an aerodynamic diameter less than or equal to 2.5 μm (PM2.5), and mortality from renal failure (RF) among participants in the Elderly Health Service Cohort in Hong Kong, China, from 1998 to 2010. PM2.5 concentration at the residential address of each participant was estimated based on a satellite-based spatiotemporal model. We used Cox proportional hazards regression to estimate risks of overall RF and cause-specific mortality associated with PM2.5. After excluding 5,373 subjects without information on residential address or relevant covariates, we included 61,447 participants in data analyses. We identified 443 RF deaths during the 10 years of follow-up. For an interquartile-range increase in PM2.5 concentration (3.22 μg/m3), hazard ratios for RF mortality were 1.23 (95% confidence interval: 1.06, 1.43) among all cohort participants and 1.42 (95% confidence interval: 1.16, 1.74) among patients with chronic kidney disease. Long-term exposure to atmospheric PM2.5 might be an important risk factor for RF mortality in the elderly, especially among persons with existing renal diseases. [ABSTRACT FROM AUTHOR]

Recent studies suggested that long-term exposure to fine particulate matter (PM 2.5) was related to a higher risk of dementia incidence or hospitalizations in western populations, but the evidence is limited in Asian cities. Here we explored the link between long-term PM 2.5 exposure and dementia incidence in the Hong Kong population and whether it varied by population sub-group. We utilized a Hong Kong Chinese cohort of 66,820 people aged ≥65 years who were voluntarily enrolled during 1998–2001 and were followed up to 2011. Prevalent dementia cases were excluded based on the face-to-face interview at baseline. We ascertained the first occurrence of hospitalization for all-cause dementia and major subtypes during the follow-up period. We assessed PM 2.5 concentrations using a satellite data-based model with a 1 × 1 km2 resolution on the residential address. Cox proportional hazards models were adopted to estimate associations of annual mean PM 2.5 exposure with dementia incidence, adjusting for potential confounders. We identified 1183 incident cases of all-cause dementia during the follow-up period, of which 655 (55.4%) were cases of Alzheimer's disease, and 334 (28.2%) were those of vascular dementia. We found a positive association between annual mean PM 2.5 exposure and all-cause dementia incidence in the fully adjusted model. The estimated hazard ratio was 1.06 (95% confidence interval (CI): 1.00, 1.13) per every 3.8 μg/m3 increase in annual mean PM 2.5 exposure. And the estimated HRs for Alzheimer's disease and vascular dementia were 1.03 (95% CI: 0.94, 1.12) and 1.09 (95% CI: 0.98, 1.22), respectively. We did not find effect modifications by age, sex, BMI, hypertension, diabetes, or heart disease on the associations. Results suggest that long-term exposure to PM 2.5 is associated with a higher risk of dementia incidence in the Asian population. Image 1 • Evidence of long-term PM 2.5 effects on dementia in Asian cities is limited. • PM 2.5 exposure was positively associated with dementia in Hong Kong aged population. • The association of vascular dementia was stronger than that of Alzheimer's disease. • Effect modifications by age, sex, BMI, co-existing diseases were not evident. Long-term exposure to PM 2.5 was positively associated with the increased risk of all-cause dementia incidence in the Hong Kong aged population. Potential positive associations with the incidence of Alzheimer's disease and vascular dementia were also observed but not of statistical significance. The association of vascular dementia seemed to be stronger than that of Alzheimer's disease. Effect modifications by age, sex, BMI, and co-existing diseases were not evident in the associations. [ABSTRACT FROM AUTHOR]

Emerging epidemiologic studies suggested that particulate matter (PM) was a risk factor for the incidence of chronic kidney disease (CKD). However, few studies were conducted to examine whether PM was associated with cause-specific deaths in the CKD progression. This study aimed to estimate the association between fine particulate matter (PM 2.5) and a spectrum of deaths among CKD patients. We took leverage of the Elderly Health Service cohort (n = 66,820), a large Hong Kong elderly cohort followed up till 2010. A total of 902 CKD incident patients in the cohort were identified during the follow-up period. We estimated yearly PM 2.5 at the residential address for each CKD patient based on a satellite-based spatiotemporal model. We used Cox proportional hazards models with attained age as the underlying timescale to assess the association between long-term exposure to PM 2.5 and cause-specific mortality among CKD patients. A total of 496 patients died during the follow-up, where 147 died from cardiovascular disease, 61 from respiratory disease and 154 from renal failure. The mortality hazard ratio (HR) per interquartile-range increase in PM 2.5 (4.0 μg/m3) was 1.97 (95% confidence interval (CI): 1.34 to 2.91) for ischemic heart disease (IHD) among CKD patients, and was 1.42 (95%CI: 1.05 to 1.93) for CKD among those patients concomitantly with hypertension. Associations were not of statistical significance between PM 2.5 and mortality hazard ratios of all-cause, stroke, and pneumonia among CKD patients. Our findings suggest that long-term exposure to PM 2.5 may contribute to the CKD progression into ischemic heart diseases. • Evidence is limited on cause-specific mortality HRs with PM 2.5 among CKD patients. • Long-term exposure to PM 2.5 may increase the mortality HR of IHD among CKD patients. • PM 2.5 was associated with renal failure mortality among patients with hypertension. • Associations with all-cause, stroke and pneumonia mortality were not significant. [ABSTRACT FROM AUTHOR]