Temperature enhanced effects of ozone on cardiovascular mortality in 95 large US communities, 1987-2000 - assessment using the NMMAPS data

A few studies examined interactive effects between air pollution and temperature on health outcomes. This study is to examine if temperature modified effects of ozone and cardiovascular mortality in 95 large US cities. A nonparametric and a parametric regression models were separately used to explore interactive effects of temperature and ozone on cardiovascular mortality during May and October, 1987-2000. A Bayesian meta-analysis was used to pool estimates. Both models illustrate that temperature enhanced the ozone effects on mortality in the northern region, but obviously in the southern region. A 10-ppb increment in ozone was associated with 0.41 % (95% posterior interval (PI): -0.19 %, 0.93 %), 0.27 % (95% PI: -0.44 %, 0.87 %) and 1.68 % (95% PI: 0.07 %, 3.26 %) increases in daily cardiovascular mortality corresponding to low, moderate and high levels of temperature, respectively. We concluded that temperature modified effects of ozone, particularly in the northern region

Does Particulate Matter Modify the Association between Temperature and Cardiorespiratory Diseases?

BACKGROUND: A number of studies have shown that both temperature and air pollution are associated with health outcomes. In assessing air pollution effects, temperature is usually considered a confounder. However, only a few recent studies considered air pollution as confounders while assessing temperature effects. Few studies are available on whether or not air pollution modifies the temperature–disease relationship. METHODS: In this study, we used three parallel Poisson generalized additive models to examine whether particulate matter < 10 μm in aerodynamic diameter (PM(10)) modified the effects of minimum temperature on cardiorespiratory morbidity and mortality in Brisbane, Australia. RESULTS: Results show that PM(10) statistically significantly modified the effects of temperature on respiratory and cardiovascular hospital admissions, all nonexternal-cause mortality, and cardiovascular mortality at different lags. The enhanced adverse temperature effects were found at higher levels of PM(10), but no clear evidence emerged for interactive effects on respiratory and cardiovascular emergency visits. Three parallel models produced similar results, which strengthened the validity of findings. CONCLUSION: We conclude that it is important to evaluate the modification role of air pollution in the assessment of temperature-related health impacts

The Effects of Indoor Environmental Exposures on Pediatric Asthma: A Discrete Event Simulation Model

Background: In the United States, asthma is the most common chronic disease of childhood across all socioeconomic classes and is the most frequent cause of hospitalization among children. Asthma exacerbations have been associated with exposure to residential indoor environmental stressors such as allergens and air pollutants as well as numerous additional factors. Simulation modeling is a valuable tool that can be used to evaluate interventions for complex multifactorial diseases such as asthma but in spite of its flexibility and applicability, modeling applications in either environmental exposures or asthma have been limited to date. Methods: We designed a discrete event simulation model to study the effect of environmental factors on asthma exacerbations in school-age children living in low-income multi-family housing. Model outcomes include asthma symptoms, medication use, hospitalizations, and emergency room visits. Environmental factors were linked to percent predicted forced expiratory volume in 1 second (FEV1%), which in turn was linked to risk equations for each outcome. Exposures affecting FEV1% included indoor and outdoor sources of $NO_2$ and $PM_{2.5}$, cockroach allergen, and dampness as a proxy for mold. Results: Model design parameters and equations are described in detail. We evaluated the model by simulating 50,000 children over 10 years and showed that pollutant concentrations and health outcome rates are comparable to values reported in the literature. In an application example, we simulated what would happen if the kitchen and bathroom exhaust fans were improved for the entire cohort, and showed reductions in pollutant concentrations and healthcare utilization rates. Conclusions: We describe the design and evaluation of a discrete event simulation model of pediatric asthma for children living in low-income multi-family housing. Our model simulates the effect of environmental factors (combustion pollutants and allergens), medication compliance, seasonality, and medical history on asthma outcomes (symptom-days, medication use, hospitalizations, and emergency room visits). The model can be used to evaluate building interventions and green building construction practices on pollutant concentrations, energy savings, and asthma healthcare utilization costs, and demonstrates the value of a simulation approach for studying complex diseases such as asthma

Modifiers of short-term effects of ozone on mortality in eastern Massachusetts - A case-crossover analysis at individual level

<p>Abstract</p> <p>Background</p> <p>Substantial epidemiological studies demonstrate associations between exposure to ambient ozone and mortality. A few studies simply examine the modification of this ozone effect by individual characteristics and socioeconomic status, but socioeconomic status was usually coded at the city level.</p> <p>Methods</p> <p>This study used a case-crossover design to examine whether impacts of ozone on mortality were modified by socioeconomic status coded at the tract or characteristics at an individual level in eastern Massachusetts, US for a period May-September, 1995-2002, with a total of 157,197 non-accident deaths aging 35 years or older. We used moving averages of maximal 8-hour concentrations of ozone monitored at 8 stationary stations as personal exposure.</p> <p>Results</p> <p>A 10 ppb increase in the four-day moving average of maximal 8-hour ozone was associated with 1.68% (95% confidence interval (CI): 0.51%, 2.87%), 1.96% (95% CI: -1.83%, 5.90%), 8.28% (95% CI: 0.66%, 16.48%), 0.44% (95% CI: -1.45%, 2.37%), -0.83% (95% CI: -2.94%, 1.32%), -1.09% (95% CI: -4.27%, 2.19%) and 6.5% (95% CI: 1.74%, 11.49%) changes in all natural deaths, respiratory disorders, diabetes, cardiovascular diseases, heart diseases, acute myocardial infarction and stroke, respectively. We did not find any evidence that the associations were significantly modified by socioeconomic status or individual characteristics although small differences of estimates across subpopulations were demonstrated.</p> <p>Conclusions</p> <p>Exposure to ozone was associated with specific cause mortality in Eastern Massachusetts during May-September, 1995-2002. There was no evidence that effects of ozone on mortality were significantly modified by socioeconomic status and individual characteristics.</p

Effect modification of air pollution on Urinary 8-Hydroxy-2'-Deoxyguanosine by genotypes: an application of the multiple testing procedure to identify significant SNP interactions

<p>Abstract</p> <p>Background</p> <p>Air pollution is associated with adverse human health, but mechanisms through which pollution exerts effects remain to be clarified. One suggested pathway is that pollution causes oxidative stress. If so, oxidative stress-related genotypes may modify the oxidative response defenses to pollution exposure.</p> <p>Methods</p> <p>We explored the potential pathway by examining whether an array of oxidative stress-related genes (twenty single nucleotide polymorphisms, SNPs in nine genes) modified associations of pollutants (organic carbon (OC), ozone and sulfate) with urinary 8-hydroxy-2-deoxygunosine (8-OHdG), a biomarker of oxidative stress among the 320 aging men. We used a Multiple Testing Procedure in R modified by our team to identify the significance of the candidate genes adjusting for <it>a priori </it>covariates.</p> <p>Results</p> <p>We found that glutathione S-tranferase P1 (GSTP1, rs1799811), M1 and catalase (rs2284367) and group-specific component (GC, rs2282679, rs1155563) significantly or marginally significantly modified effects of OC and/or sulfate with larger effects among those carrying the wild type of GSTP1<it/>, catalase, non-wild type of <it>GC </it>and the non-null of GSTM1.</p> <p>Conclusions</p> <p>Polymorphisms of oxidative stress-related genes modified effects of OC and/or sulfate on 8-OHdG, suggesting that effects of OC or sulfate on 8-OHdG and other endpoints may be through the oxidative stress pathway.</p

The population approach to falls injury prevention in older people: findings of a two community trial

<p>Abstract</p> <p>Background</p> <p>There is a sound rationale for the population-based approach to falls injury prevention but there is currently insufficient evidence to advise governments and communities on how they can use population-based strategies to achieve desired reductions in the burden of falls-related injury. The aim of the study was to quantify the effectiveness of a streamlined (and thus potentially sustainable and cost-effective), population-based, multi-factorial falls injury prevention program for people over 60 years of age.</p> <p>Methods</p> <p>Population-based falls-prevention interventions were conducted at two geographically-defined and separate Australian sites: Wide Bay, Queensland, and Northern Rivers, NSW. Changes in the prevalence of key risk factors and changes in rates of injury outcomes within each community were compared before and after program implementation and changes in rates of injury outcomes in each community were also compared with the rates in their respective States.</p> <p>Results</p> <p>The interventions in neither community substantially decreased the rate of falls-related injury among people aged 60 years or older, although there was some evidence of reductions in occurrence of multiple falls reported by women. In addition, there was some indication of improvements in fall-related risk factors, but the magnitudes were generally modest.</p> <p>Conclusions</p> <p>The evidence suggests that low intensity population-based falls prevention programs may not be as effective as those that are intensively implemented.</p

Health effects of ambient air pollution – recent research development and contemporary methodological challenges

Exposure to high levels of air pollution can cause a variety of adverse health outcomes. Air quality in developed countries has been generally improved over the last three decades. However, many recent epidemiological studies have consistently shown positive associations between low-level exposure to air pollution and health outcomes. Thus, adverse health effects of air pollution, even at relatively low levels, remain a public concern. This paper aims to provide an overview of recent research development and contemporary methodological challenges in this field and to identify future research directions for air pollution epidemiological studies

Evaluation of interactive effects between temperature and air pollution on health outcomes

A large number of studies have shown that both temperature and air pollution (eg, particulate matter and ozone) are associated with health outcomes. So far, it has received limited attention whether air pollution and temperature interact to affect health outcomes. A few studies have examined interactive effects between temperature and air pollution, but produced conflicting results. This thesis aimed to examine whether air pollution (including ozone and particulate matter) and temperature interacted to affect health outcomes in Brisbane, Australia and 95 large US communities. In order to examine the consistency across different cities and different countries, we used two datasets to examine interactive effects of temperature and air pollution. One dataset was collected in Brisbane City, Australia, during 1996-2000. The dataset included air pollution (PM10, ozone and nitrogen dioxide), weather conditions (minimum temperature, maximum temperature, relative humidity and rainfall) and different health outcomes. Another dataset was collected from the 95 large US communities, which included air pollution (ozone was used in the thesis), weather conditions (maximum temperature and dew point temperature) and mortality (all non-external cause mortality and cardiorespiratory mortality). Firstly, we used three parallel time-series models to examine whether maximum temperature modified PM10 effects on cardiovascular hospital admissions (CHA), respiratory hospital admissions (RHA), cardiovascular emergency visits (CEV), respiratory emergency visits (REV), cardiovascular mortality (CM) and non-external cause mortality (NECM), at lags of 0-2 days in Brisbane. We used a Poisson generalized additive model (GAM) to fit a bivariate model to explore joint response surfaces of both maximum temperature and particulate matter less than 10 μm in diameter (PM10) on individual health outcomes at each lag. Results show that temperature and PM10 interacted to affect different health outcomes at various lags. Then, we separately fitted non-stratification and stratification GAM models to quantify the interactive effects. In the non-stratification model, we examined the interactive effects by including a pointwise product for both temperature and the pollutant. In the stratification model, we categorized temperature into two levels using different cut-offs and then included an interactive term for both pollutant and temperature. Results show that maximum temperature significantly and positively modified the associations of PM10 with RHA, CEV, REV, CM and NECM at various lags, but not for CHA. Then, we used the above Poisson regression models to examine whether PM10 modified the associations of minimum temperature with CHA, RHA, CEV, REV, CM and NECM at lags of 0-2 days. In this part, we categorized PM10 into two levels using the mean as cut-off to fit the stratification model. The results show that PM10 significantly modified the effects of temperature on CHA, RHA, CM and NECM at various lags. The enhanced adverse temperature effects were found at higher levels of PM10, but there was no clear evidence for synergistic effects on CEV and REV at various lags. Three parallel models produced similar results, which strengthened the validity of these findings. Thirdly, we examined whether there were the interactive effects between maximum temperature and ozone on NECM in individual communities between April and October, 1987-2000, using the data of 60 eastern US communities from the National Morbidity, Mortality, and Air Pollution Study (NMMAPS). We divided these communities into two regions (northeast and southeast) according to the NMMAPS study. We first used the bivariate model to examine the joint effects between temperature and ozone on NECM in each community, and then fit a stratification model in each community by categorizing temperature into three levels. After that, we used Bayesian meta-analysis to estimate overall effects across regions and temperature levels from the stratification model. The bivariate model shows that temperature obviously modified ozone effects in most of the northeast communities, but the trend was not obviously in the southeast region. Bayesian meta-analysis shows that in the northeast region, a 10-ppb increment in ozone was associated with 2.2% (95% posterior interval [PI]: 1.2%, 3.1 %), 3.1% (95% PI: 2.2%, 3.8 %) and 6.2 % (95% PI: 4.8%, 7.6 %) increase in mortality for low, moderate and high temperature levels, respectively, while in the southeast region, a 10-ppb increment in ozone was associated with 1.1% (95% PI: -1.1%, 3.2 %), 1.5% (95% PI: 0.2%, 2.8%) and 1.3% (95% PI: -0.3%, 3.0 %) increase in mortality. In addition, we examined whether temperature modified ozone effects on cardiovascular mortality in 95 large US communities between May and October, 1987-2000 using the same models as the above. We divided the communities into 7 regions according to the NMMAPS study (Northeast, Industrial Midwest, Upper Midwest, Northwest, Southeast, Southwest and Southern California). The bivariate model shows that temperature modified ozone effects in most of the communities in the northern regions (Northeast, Industrial Midwest, Upper Midwest, Northwest), but such modification was not obvious in the southern regions (Southeast, Southwest and Southern California). Bayesian meta-analysis shows that temperature significantly modified ozone effects in the Northeast, Industrial Midwest and Northwest regions, but not significant in Upper Midwest, Southeast, Southwest and Southern California. Nationally, temperature marginally positively modified ozone effects on cardiovascular mortality. A 10-ppb increment in ozone was associated with 0.4% (95% posterior interval [PI]: -0.2, 0.9 %), 0.3% (95% PI: -0.3%, 1.0%) and 1.6% (95% PI: 4.8%, 7.6%) increase in mortality for low, moderate and high temperature levels, respectively. The difference of overall effects between high and low temperature levels was 1.3% (95% PI: - 0.4%, 2.9%) in the 95 communities. Finally, we examined whether ozone modified the association between maximum temperature and cardiovascular mortality in 60 large eastern US communities during the warmer days, 1987-2000. The communities were divided into the northeast and southeast regions. We restricted the analyses to the warmer days when temperature was equal to or higher than the median in each community throughout the study period. We fitted a bivariate model to explore the joint effects between temperature and ozone on cardiovascular mortality in individual communities and results show that in general, ozone positively modified the association between temperature and mortality in the northeast region, but such modification was not obvious in the southeast region. Because temperature effects on mortality might partly intermediate by ozone, we divided the dataset into four equal subsets using quartiles as cut-offs. Then, we fitted a parametric model to examine the associations between temperature and mortality across different levels of ozone using the subsets. Results show that the higher the ozone concentrations, the stronger the temperature-mortality associations in the northeast region. However, such a trend was not obvious in the southeast region. Overall, this study found strong evidence that temperature and air pollution interacted to affect health outcomes. PM10 and temperature interacted to affect different health outcomes at various lags in Brisbane, Australia. Temperature and ozone also interacted to affect NECM and CM in US communities and such modification varied considerably across different regions. The symmetric modification between temperature and air pollution was observed in the study. This implies that it is considerably important to evaluate the interactive effect while estimating temperature or air pollution effects and further investigate reasons behind the regional variability