Hilda Tsang

Satellite-Based Estimates of Long-Term Exposure to Fine Particles and Association with Mortality in Elderly Hong Kong Residents

Background A limited number of studies on long-term effects of particulate matter with aerodynamic diameter < 2.5 μm (PM2.5) on health suggest it can be an important cause of morbidity and mortality. In Asia where air quality is poor and deteriorating, local data on long-term effects of PM2.5 to support policy on air quality management are scarce. Objectives We assessed long-term effects of PM2.5 on the mortality in a single Asian city. Methods For 10–13 years, we followed up a cohort of 66,820 participants ≥ 65 years of age who were enrolled and interviewed in all 18 Elderly Health Centres of the Department of Health, Hong Kong, in 1998–2001. Their residential addresses were geocoded into x- and y-coordinates, and their proxy exposures to PM2.5 at their addresses in 1 × 1 km grids were estimated from the U.S. National Aeronautics and Space Administration (NASA) satellite data. We used Cox regression models to calculate hazard ratios (HRs) of mortality associated with PM2.5. Results Mortality HRs per 10-μg/m3 increase in PM2.5 were 1.14 (95% CI: 1.07, 1.22) for all natural causes, 1.22 (95% CI: 1.08, 1.39) for cardiovascular causes, 1.42 (95% CI: 1.16, 1.73) for ischemic heart disease, 1.24 (95% CI: 1.00, 1.53) for cerebrovascular disease, and 1.05 (95% CI: 0.90, 1.22) for respiratory causes. Conclusions Our methods in using NASA satellite data provide a readily accessible and affordable approach to estimation of a sufficient range of individual PM2.5 exposures in a single city. This approach can expand the capacity to conduct environmental accountability studies in areas with few measurements of fine particles. Citation Wong CM, Lai HK, Tsang H, Thach TQ, Thomas GN, Lam KB, Chan KP, Yang L, Lau AK, Ayres JG, Lee SY, Chan WM, Hedley AJ, Lam TH. 2015. Satellite-based estimates of long-term exposure to fine particles and association with mortality in elderly Hong Kong residents. Environ Health Perspect 123:1167–1172; http://dx.doi.org/10.1289/ehp.1408264

Cancer Mortality Risks from Long-term Exposure to Ambient Fine Particle

Background: Few studies have assessed long-term effects of particulate matter (PM) with aerodynamic diameter < 2.5 μm (PM2.5) on mortality for causes of cancer other than the lung; we assessed the effects on multiple causes. In Hong Kong, most people live and work in urban or suburban areas with high-rise buildings. This facilitates the estimation of PM2.5 exposure of individuals, taking into account the height of residence above ground level for assessment of the long-term health effects with sufficient statistical power. Methods: We recruited 66,820 persons who were ≥65 in 1998 to 2001 and followed up for mortality outcomes until 2011. Annual concentrations of PM at their residential addresses were estimated using PM2.5 concentrations measured at fixed-site monitors, horizontal–vertical locations, and satellite data. We used Cox regression model to assess the HR of mortality for cancer per 10 μg/m3 increase of PM2.5. Results: PM2.5 was associated with increased risk of mortality for all causes of cancer [HR, 1.22 (95% CI, 1.11–1.34)] and for specific cause of cancer in upper digestive tract [1.42 (1.06–1.89)], digestive accessory organs [1.35 (1.06–1.71)] in all subjects; breast [1.80 (1.26–2.55)] in females; and lung [1.36 (1.05–1.77)] in males. Conclusions: Long-term exposures to PM2.5 are associated with elevated risks of cancer in various organs. Impact: This study is particularly timely in China, where compelling evidence is needed to support the pollution control policy to ameliorate the health damages associated with economic growth. Cancer Epidemiol Biomarkers Prev; 25(5); 839–45. ©2016 AACR.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses spheroids attachment on endometrial epithelial cells through the down-regulation of the Wnt-signaling pathway.

The environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects embryo development, implantation and fertility in humans. The underlying molecular mechanism by which TCDD suppresses implantation remains largely unknown. We used the trophoblastic spheroids (embryo surrogate)-endometrial cells co-culture assay to study the attachment of trophoblastic spheroids (BeWo and Jeg-3) onto the endometrial epithelial (RL95-2 and Ishikawa) cells. TCDD dose-dependently induced cytochrome P450 1A1 (Cyp1A1) expression in trophoblastic and endometrial epithelial cells. Moreover, TCDD at 1 and 10 nM suppressed β-catenin (a Wnt-signaling molecule) and E-cadherin expression, as well as spheroids attachment onto endometrial cells. Interestingly, activation of the canonical Wnt-signaling pathway via Wnt3a or lithium chloride reverted the suppressive effect of TCDD on β-catenin and E-cadherin expressions in the BeWo and RL95-2 cells, and restored the spheroids attachment rate to be comparable to the untreated controls. Taken together, TCDD induces Cyp1A1 expression, modulates the Wnt-signaling pathway and suppresses spheroids attachment onto endometrial cells.

Temperature as a modifier of the effects of fine particulate matter on acute mortality in Hong Kong.

Interactions between particulate matter with aerodynamic diameter less than or equal to 2.5 μm (PM2.5) and temperature on mortality have not been well studied, and results are difficult to synthesize. We aimed to assess modification of temperature on the association between PM2.5 and cause-specific mortality by stratifying temperature into low, medium, and high stratum in Hong Kong, using data from 1999 to 2011. The mortality effects of PM2.5 were stronger in low temperature stratum than those in high. The excess risk (%) per 10 μg/m(3) increase in PM2.5 at lag 0-1 in low temperature stratum were 0.94% (95% confidence interval: 0.65, 1.24) for all natural, 0.88% (0.38, 1.37) for cardiovascular, and 1.15% (0.51, 1.79) for respiratory mortality. We found statistically significant interaction of PM2.5 and temperature between low and high temperature stratum for all natural mortality. Our results suggested that temperature might modify mortality effects of PM2.5 in Hong Kong.

Health impact assessment of exposure to fine particulate matter based on satellite and meteorological information

Air pollution in China, especially in the Pearl River Delta (PRD) region, has drastically increased in recent years. We modelled annual mean ground-level PM2.5 concentrations based on worldwide satellite information and meteorological data from 40 cities outside the PRD. The model of PM2.5 concentration (R = 0.845) was best explained by aerosol optical thickness (43.8%). We validated the spatial-temporal dimensions of the model and estimated that the annual mean PM2.5 concentration in PRD ranged between 22 and 65 μg m(-3). Then we used meta-analysis to obtain the pooled excess risks of mortality in China and assessed the health impacts. We found an inverse association between short-term excess risks of mortality and annual mean PM2.5 concentrations. Based on the above models and analyses, the associated excess deaths for all-cause and cardiopulmonary diseases were 3386 and 2639 respectively. The corresponding risk-standardized excess death rates were 2006 and 1069 per million people.

Perfluorooctanoate suppresses spheroid attachment on endometrial epithelial cells through peroxisome proliferator- activated receptor alpha and down-regulation of Wnt signaling

Exposure of animals to perfluorooctanoic acid (PFOA), a surfactant used in emulsion polymerization processes causes early pregnancy loss, delayed growth and development of fetuses. The mechanisms of action are largely unknown. We studied the effect of PFOA on implantation using an in vitro spheroid-endometrial cell co-culture model. PFOA (10-100μM) significantly reduced Jeg-3 spheroid attachment on RL95-2 endometrial cells. PFOA also suppressed β-catenin expression in Jeg-3 cells. The Wnt agonist Wnt3a stimulated β-catenin expression in Jeg-3 cells and reversed the PFOA suppression of the spheroid attachment. The putative PFOA receptors (PPARα, β, γ) present in both cell lines were not affected by PFOA (0.01-100μM). The PPARα antagonist MK886 restored the β-catenin and E-cadherin expression levels in Jeg-3 cells and reversed the suppression of the spheroid attachment caused by PFOA. Taken together, PFOA suppresses spheroid attachment through PPARα and Wnt signaling pathways via down-regulation of β-catenin and E-cadherin expression.

Fine particulate matter exposure and incidence of stroke: A cohort study in Hong Kong

Objective: We aimed to assess the association of long-term residential exposure to fine particulate matter (PM) with aerodynamic diameter less than 2.5 μm (PM2.5) with the incidence of stroke and its major subtypes. Methods: We ascertained the first occurrence of emergency hospital admission for stroke in a Hong Kong Chinese cohort of 66,820 older people (65+ years) who enrolled during 1998–2001 (baseline) and were followed up to December 31, 2010. High-resolution (1 × 1 km) yearly mean concentrations of PM2.5 were predicted from local monitoring data and US National Aeronautics and Space Administration satellite data using linear regression. Baseline residential PM2.5 exposure was used as a proxy for long-term exposure. We used Cox proportional hazards to evaluate the risk of incident stroke associated with PM2.5 exposure adjusted for potential confounders, including individual and neighborhood factors. Results: Over a mean follow-up of 9.4 years, we ascertained 6,733 cases of incident stroke, of which 3,526 (52.4%) were ischemic and 1,175 (17.5%) were hemorrhagic. The hazard ratio for every 10 μg/m3 higher PM2.5 concentration was statistically significant at 1.21 (95% confidence interval [CI] 1.04–1.41) for ischemic and non-statistically significant at 0.90 (95% CI 0.70–1.17) for hemorrhagic stroke in fully adjusted model 3. The estimates for ischemic stroke were higher in older participants (>70 years), less educated participants, and in men for current smokers. Conclusion: Long-term PM2.5 exposure was associated with higher risk of incident ischemic stroke, but the association with incident hemorrhagic stroke was less clear.

The influence of pre-existing health conditions on short-term mortality risks of temperature: Evidence from a prospective Chinese elderly cohort in Hong Kong.

BACKGROUND Both cold and hot temperatures are associated with adverse health outcomes. Less is known about the role of pre-existing medical conditions to confer individuals susceptibility to temperature extremes. METHODS We studied 66,820 subjects aged ≥65 who were enrolled and interviewed in all the 18 Elderly Health Centers of Department of Health, Hong Kong from 1998 to 2001, and followed up for 10-13 years. The distributed lag nonlinear model (DLNM) combined with a nested case-control study design was applied to estimate the nonlinear and delayed effects of cold or hot temperature on all natural mortality among subjects with different pre-existing diseases. RESULTS The relative risk of all natural mortality associated with a decrease of temperature from 25th percentile (19.5°C) to 1st percentile (11.3°C) over 0-21 lag days for participants who reported to have an active disease at the baseline was 2.21 (95% confidence interval (CI): 1.19, 4.10) for diabetes mellitus (DM), 1.59 (1.12, 2.26) for circulatory system diseases (CSD), and 1.23 (0.53, 2.84) for chronic obstructive pulmonary disease (COPD), whereas 1.04 (0.59, 1.85) for non-disease group (NDG). Compared with NDG, elders with COPD had excess risk of mortality associated with thermal stress attributable to hot temperature, while elders with DM and CSD were vulnerable to both hot and cold temperatures. CONCLUSIONS Elders with pre-existing health conditions were more vulnerable to excess mortality risk to hot and/or cold temperature. Preventative measures should target on elders with chronic health problems.

Global estimates of mortality associated with long-term exposure to outdoor fine particulate matter

Significance Exposure to outdoor concentrations of fine particulate matter is considered a leading global health concern, largely based on estimates of excess deaths using information integrating exposure and risk from several particle sources (outdoor and indoor air pollution and passive/active smoking). Such integration requires strong assumptions about equal toxicity per total inhaled dose. We relax these assumptions to build risk models examining exposure and risk information restricted to cohort studies of outdoor air pollution, now covering much of the global concentration range. Our estimates are severalfold larger than previous calculations, suggesting that outdoor particulate air pollution is an even more important population health risk factor than previously thought. Exposure to ambient fine particulate matter (PM2.5) is a major global health concern. Quantitative estimates of attributable mortality are based on disease-specific hazard ratio models that incorporate risk information from multiple PM2.5 sources (outdoor and indoor air pollution from use of solid fuels and secondhand and active smoking), requiring assumptions about equivalent exposure and toxicity. We relax these contentious assumptions by constructing a PM2.5-mortality hazard ratio function based only on cohort studies of outdoor air pollution that covers the global exposure range. We modeled the shape of the association between PM2.5 and nonaccidental mortality using data from 41 cohorts from 16 countries—the Global Exposure Mortality Model (GEMM). We then constructed GEMMs for five specific causes of death examined by the global burden of disease (GBD). The GEMM predicts 8.9 million [95% confidence interval (CI): 7.5–10.3] deaths in 2015, a figure 30% larger than that predicted by the sum of deaths among the five specific causes (6.9; 95% CI: 4.9–8.5) and 120% larger than the risk function used in the GBD (4.0; 95% CI: 3.3–4.8). Differences between the GEMM and GBD risk functions are larger for a 20% reduction in concentrations, with the GEMM predicting 220% higher excess deaths. These results suggest that PM2.5 exposure may be related to additional causes of death than the five considered by the GBD and that incorporation of risk information from other, nonoutdoor, particle sources leads to underestimation of disease burden, especially at higher concentrations.

STROBE-Long-Term Exposure to Ambient Fine Particulate Air Pollution and Hospitalization Due to Peptic Ulcers.

AbstractLittle is known about the effect of air pollution on the gastrointestinal (GI) system. We investigated the association between long-term exposures to outdoor fine particles (PM2.5) and hospitalization for peptic ulcer diseases (PUDs) in a large cohort of Hong Kong Chinese elderly.A total of 66,820 subjects aged ≥65 years who were enrolled in all 18 Government Elderly Health Service centers of Hong Kong participated in the study voluntarily between 1998 and 2001. They were prospectively followed up for more than 10 years. Annual mean exposures to PM2.5 at residence of individuals were estimated by satellite data through linkage with address details including floor level. All hospital admission records of the subjects up to December 31, 2010 were retrieved from the central database of Hospital Authority. We used Cox regression to estimate the hazard ratio (HR) for PUD hospitalization associated with PM2.5 exposure after adjustment for individual and ecological covariates.A total of 60,273 subjects had completed baseline information including medical, socio-demographic, lifestyle, and anthropometric data at recruitment. During the follow-up period, 1991 (3.3%) subjects had been hospitalized for PUD. The adjusted HR for PUD hospitalization per 10 &mgr;g/m3 of PM2.5 was 1.18 (95% confidence interval: 1.02–1.36, P = 0.02). Further analysis showed that the associations with PM2.5 were significant for gastric ulcers (HR 1.29; 1.09–1.53, P = 0.003) but not for duodenal ulcers (HR 0.98; 0.78 to 1.22, P = 0.81).Long-term exposures to PM2.5 were associated with PUD hospitalization in elder population. The mechanism underlying the PM2.5 in the development of gastric ulcers warrants further research.