Association of HTR2A T102C and A-1438G polymorphisms with susceptibility to major depressive disorder: a meta-analysis.

Serotonin 2A receptor (HTR2A) gene was implicated to be associated with major depressive disorder (MDD) susceptibility due to its role of key neurotransmitter in many physiologic processes. A great number of related studies reported in different populations have emerged. The results of these studies, however, have been inconsistent and thereby definite conclusions are difficult to establish. With the cumulative data in recent years, it was necessary to carry out a comprehensive analysis of previous findings. Electronic databases were systematically searched for studies published before May 2013. Pooled odds ratios (OR) and 95 % confidence interval (CI) were estimated under three different genetic models. Subgroup and sensitivity analyses were also performed. A total of 21 studies, 3,299 patients and 4,092 controls, met the selection criteria. 15 studies included HTR2A T102C polymorphism (with a total of 2,409 patients and 3,130 controls), and 9 studies included HTR2A A-1438G polymorphism (with a total of 1,510 patients and 2,281 controls). Our results showed that no significant association of MDD susceptibility with T102C polymorphism was found in allelic analysis and genotypic analysis (For T vs. C: OR = 1.06, 95 % CI = 0.95-1.18, P = 0.307; For TT + TC vs. CC: OR = 1.07, 95 % CI = 0.90-1.28, P = 0.451; For TT vs. TC + CC: OR = 1.08, 95 % CI = 0.95-1.22, P = 0.235). With respect to A-1438G polymorphism, however, carriers with A allele tend to suffer from MDD (AA + AG vs. GG: OR = 1.20, 95 % CI = 1.02-1.43, P = 0.030). When stratified by race for T102C polymorphism and A-1438G polymorphism of the HTR2A, we found no significant association. In conclusions, our study suggests that the A allele of A-1438G polymorphism might play a role in susceptibility to MDD. On the contrary, T102C polymorphism does not seem to be capable of modifying MDD risk.

Short form 36-Item Health Survey test result on the empty nest elderly in China: a meta-analysis.

The aim of this study was to evaluate the quality of life of the empty nest elderly in China using meta-analytic techniques. Electronic databases were searched for studies concerning the quality of life of the empty nest elderly published before December 2011. Pooled weighted mean difference (WMD) and 95% confidence interval (95% CI) were estimated with fixed and random effect models. Subgroup analyses, sensitivity analyses and publication bias were also performed. Ten studies (6948 empty nesters and 4560 non-empty nesters) were included in this meta-analysis. Vitality (WMD -1.946; 95% CI -3.183 to -0.708), role emotional (WMD -6.084; 95% CI -8.545 to -3.623) and mental health (WMD -2.606; 95% CI -3.964 to -1.249) were statistically significantly low in the empty nest elderly whereas physical functioning, role physical, bodily pain, general health, and social functioning showed no statistical significance. Subgroup analyses showed a statistical significance with WMD of role emotional and mental health in urban area, that of role physical, bodily pain, vitality, role emotional and mental health in rural area, and that of vitality, social functioning, role emotional and mental health in mix area. This meta-analysis indicated that among eight dimensions of the Short Form 36-Item Health Survey (SF-36), only vitality, role emotional and mental health (mental components) were statistically significantly low in the empty nest elderly. More studies are needed to confirm this finding.

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 NO2 and PM2.5, 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.

Interleukin 1 beta -511 C/T gene polymorphism and susceptibility to febrile seizures: a meta-analysis.

One previous meta-analysis found no evidence that interleukin 1 beta (IL-1ß) -511 gene polymorphism was associated with febrile seizures (FS) by pooling a limited number of studies. However, it is necessary for the meta-analysis to reevaluate the relationship with more recent findings. Electronic databases were systematically searched for studies published before June 2011. Pooled odds ratios (OR) and 95% confidence interval (CI) were estimated by means of a genetic model free approach. Subgroup and sensitivity analyses were also performed. All statistical analyses were conducted using Stata 9.0. A total of eight studies, 728 FS cases and 1,223 controls, met the selection criteria. The results show a significant association between IL-1ß -511 C/T gene polymorphism and FS (recessive genetic model TT vs. CC + CT: OR = 1.361, 95% CI: 1.065-1.738, P = 0.014). Subgroup analyses show a significant association in Asia (OR = 1.394, 95% CI: 1.005-1.935, P = 0.047), but not in Europe (OR = 1.387, 95% CI: 0.750-2.565, P = 0.298). IL-1ß -511 C/T gene polymorphism may play a role in susceptibility to FS, especially in Asia. Geographic differences may be a critical factor in the risk of FS.

Ambient temperature, air pollution, and heart rate variability in an aging population.

Studies show that ambient temperature and air pollution are associated with cardiovascular disease and that they may interact to affect cardiovascular events. However, few epidemiologic studies have examined mechanisms through which ambient temperature may influence cardiovascular function. The authors examined whether temperature was associated with heart rate variability (HRV) in a Boston, Massachusetts, study population and whether such associations were modified by ambient air pollution concentrations. The population was a cohort of 694 older men examined between 2000 and 2008. The authors fitted a mixed model to examine associations between temperature and air pollution and their interactions with repeated HRV measurements, adjusting for covariates selected a priori on the basis of their previous studies. Results showed that higher ambient temperature was associated with decreases in HRV measures (standard deviation of normal-to-normal intervals, low-frequency power, and high-frequency power) during the warm season but not during the cold season. These warm-season associations were significantly greater when ambient ozone levels were higher (>22.3 ppb) but did not differ according to levels of ambient fine (≤2.5 µm) particulate matter. The authors conclude that temperature and ozone, exposures to both of which are expected to increase with climate change, might act together to worsen cardiovascular health and/or precipitate cardiovascular events via autonomic nervous system dysfunction.

Urinary 8-hydroxy-2'-deoxyguanosine as a biomarker of oxidative DNA damage induced by ambient pollution in the Normative Aging Study.

BACKGROUND: Studies show that exposure to air pollution damages human health, but the mechanisms are not fully understood. One suggested pathway is via oxidative stress. OBJECTIVES: This study examines associations between exposure to air pollution and oxidative DNA damage, as indicated by urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) concentrations in ageing participants during 2006-2008. METHODS: We fit linear regression models to examine associations between air pollutants and 8-OHdG adjusting for potential confounders. RESULTS: 8-OHdG was significantly associated with ambient particulate matter ≤2.5 µm in aerodynamic diameter (PM(2.5)), nitrogen dioxide (NO(2)), maximal 1 h ozone (O(3)), sulphate (SO(4)(2-)) and organic carbon (OC), but not with black carbon (BC), carbon monoxide (CO), the number of particles (PN) or elemental carbon (EC). Effects were more apparent with multi-week averages of exposures. Per IQR increases in 21-day averages of PM(2.5), PN, BC, EC, OC, CO, SO(4)(2-), NO(2) and maximal 1 h O(3) were associated with 30.8% (95% CI 9.3% to 52.2%), -13.1% (95% CI -41.7% to 15.5%), 3.0% (95% CI -19.8% to 25.8%), 5.3% (95% CI -23.6% to 34.2%), 24.4% (95% CI 1.8% to 47.1%), -2.0% (95% CI -12.4% to 8.3%), 29.8% (95% CI 6.3% to 53.3%), 32.2% (95% CI 7.4% to 56.9%) and 47.7% (95% CI 3.6% to 91.7%) changes in 8-OHdG, respectively. CONCLUSIONS: This study suggests that ageing participants experienced an increased risk of developing oxidative DNA injury after exposure to secondary, but not primary, ambient pollutants.

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.

BACKGROUND: 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. METHODS: 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 a priori covariates. RESULTS: 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, catalase, non-wild type of GC and the non-null of GSTM1. CONCLUSIONS: 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.

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: The evidence suggests that low intensity population-based falls prevention programs may not be as effective as those that are intensively implemented.

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

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Air pollution and homocysteine: more evidence that oxidative stress-related genes modify effects of particulate air pollution.

BACKGROUND: Ambient particles are associated with cardiovascular events and recently with total plasma homocysteine. High total plasma homocysteine is a risk for human health. However, the biologic mechanisms are not fully understood. One of the putative pathways is through oxidative stress. We aimed to examine whether associations of PM2.5 and black carbon with homocysteine were modified by genotypes including HFE H63D, C282Y, CAT (rs480575, rs1001179, rs2284367, and rs2300181), NQO1 (rs1800566), GSTP1 I105V, GSTM1, GSTT1 (deletion vs. nondeletion), and HMOX-1 (any short vs. both long). We attempted to replicate identified genes in an analysis of heart rate variability and in other outcomes reported in the literature. METHODS: Study subjects were 1000 white non-Hispanic men in the Boston area, participating in a cohort study of aging. PM2.5, black carbon, total plasma homocysteine, and other covariates were measured at several points in time between 1995 and 2006. We fit mixed models to examine effect modification of genes on associations of pollution with total plasma homocysteine. RESULTS: Interquartile range increases in PM2.5 and black carbon (7-day moving averages) were associated with 1.5% (95% confidence interval = 0.2% to 2.8%) and 2.2% (0.6% to 3.9%) increases in total plasma homocysteine, respectively. GSTT1 and HFE C282Y modified effects of black carbon on total plasma homocysteine, and HFE C282Y and CAT (rs2300181) modified effects of PM2.5 on homocysteine. Several genotypes marginally modified effects of PM2.5 and black carbon on various endpoints. All genes with significant interactions with particulate air pollution had modest main effects on total plasma homocysteine. CONCLUSIONS: : Effects of PM2.5 and black carbon on various endpoints appeared to be mediated by genes related to oxidative stress pathways.

Excess deaths during the 2004 heatwave in Brisbane, Australia.

The paper examines whether there was an excess of deaths and the relative role of temperature and ozone in a heatwave during 7-26 February 2004 in Brisbane, Australia, a subtropical city accustomed to warm weather. The data on daily counts of deaths from cardiovascular disease and non-external causes, meteorological conditions, and air pollution in Brisbane from 1 January 2001 to 31 October 2004 were supplied by the Australian Bureau of Statistics, Australian Bureau of Meteorology, and Queensland Environmental Protection Agency, respectively. The relationship between temperature and mortality was analysed using a Poisson time series regression model with smoothing splines to control for nonlinear effects of confounding factors. The highest temperature recorded in the 2004 heatwave was 42 degrees C compared with the highest recorded temperature of 34 degrees C during the same periods of 2001-2003. There was a significant relationship between exposure to heat and excess deaths in the 2004 heatwave [estimated increase in non-external deaths: 75 ([95% confidence interval, CI: 11-138; cardiovascular deaths: 41 (95% CI: -2 to 84)]. There was no apparent evidence of substantial short-term mortality displacement. The excess deaths were mainly attributed to temperature but exposure to ozone also contributed to these deaths.

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. In this study, the authors aimed to examine whether temperature modified effects of ozone on cardiovascular mortality in 95 large US cities. The authors separately used a nonparametric regression model and a parametric regression model to explore interactive effects of temperature and ozone on cardiovascular mortality between May and October of the years from 1987 to 2000. The authors used a Bayesian meta-analysis to pool estimates. The nonparametric and parametric regression models both showed that temperature enhanced effects of ozone on mortality, but the effect modification varied across regions. A 10-ppb increment in average ozone concentration at 3 previous days 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 in all 95 US cities, respectively. The authors concluded that temperature modified effects of ozone, particularly in the northern regions.

Repeated hospital encounters for asthma in children and exposure to traffic-related air pollution near the home.

BACKGROUND: Aggregate hospital encounters for asthma (admissions or emergency department visits) have been associated with daily regional air pollution. There are fewer data on relationships between repeated hospital encounters and traffic-related air pollution near the home. OBJECTIVE: To estimate the association of local traffic-generated air pollution with repeated hospital encounters for asthma in children. METHODS: Hospital records for 2,768 children aged 0 to 18 years (697 of whom had > or = 2 encounters) were obtained for a catchment area of 2 hospitals in northern Orange County, California. Residential addresses were geocoded. A line source dispersion model was used to estimate individual seasonal exposures to local traffic-generated pollutants (nitrogen oxides and carbon monoxide) longitudinally beginning with the first hospital encounter. Recurrent proportional hazards analysis was used to estimate risk of exposure to air pollution adjusting for sex, age, health insurance, census-derived poverty, race/ethnicity, residence distance to hospital, and season. The adjustment variables and census-derived median household income were tested for effect modification. RESULTS: Adjusted hazard ratios for interquartile range increases in nitrogen oxides (4.00 ppb) and carbon monoxide (0.056 ppm) were 1.10 (95% confidence interval, 1.03-1.16) and 1.07 (1.01-1.14), respectively. Associations were strongest for girls and infants but were not significantly different from other groups. Stronger associations in children from higher-income block groups (P < .09 for trend) may have been due to more accurate data. CONCLUSIONS: Associations for repeated hospital encounters suggest that locally generated air pollution near the home affects asthma severity in children. Risk may begin during infancy and continue in later childhood, when asthma diagnoses are clearer.

Association between local traffic-generated air pollution and preeclampsia and preterm delivery in the south coast air basin of California.

BACKGROUND: Preeclampsia is a major complication of pregnancy that can lead to substantial maternal and perinatal morbidity, mortality, and preterm birth. Increasing evidence suggests that air pollution adversely affects pregnancy outcomes. Yet few studies have examined how local traffic-generated emissions affect preeclampsia in addition to preterm birth. OBJECTIVES: We examined effects of residential exposure to local traffic-generated air pollution on preeclampsia and preterm delivery (PTD). METHODS: We identified 81,186 singleton birth records from four hospitals (1997-2006) in Los Angeles and Orange Counties, California (USA). We used a line-source dispersion model (CALINE4) to estimate individual exposure to local traffic-generated nitrogen oxides (NO(x)) and particulate matter < 2.5 mum in aerodynamic diameter (PM(2.5)) across the entire pregnancy. We used logistic regression to estimate effects of air pollution exposures on preeclampsia, PTD (gestational age < 37 weeks), moderate PTD (MPTD; gestational age < 35 weeks), and very PTD (VPTD; gestational age < 30 weeks). RESULTS: We observed elevated risks for preeclampsia and preterm birth from maternal exposure to local traffic-generated NO(x) and PM(2.5). The risk of preeclampsia increased 33% [odds ratio (OR) = 1.33; 95% confidence interval (CI), 1.18-1.49] and 42% (OR = 1.42; 95% CI, 1.26-1.59) for the highest NO(x) and PM(2.5) exposure quartiles, respectively. The risk of VPTD increased 128% (OR = 2.28; 95% CI, 2.15-2.42) and 81% (OR = 1.81; 95% CI, 1.71-1.92) for women in the highest NO(x) and PM(2.5) exposure quartiles, respectively. CONCLUSION: Exposure to local traffic-generated air pollution during pregnancy increases the risk of preeclampsia and preterm birth in Southern California women. These results provide further evidence that air pollution is associated with adverse reproductive outcomes.

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.

Does temperature modify short-term effects of ozone on total mortality in 60 large eastern US communities? An assessment using the NMMAPS data.

Many studies have indicated that ozone is associated with morbidity and mortality. A few studies have reported that the association is heterogeneous across seasons and geographic regions. However, little information is available on whether both temperature and geographic factors simultaneously modify the ozone effect. This study used a Poisson regression model to explore whether temperature modifies the effect of ozone on mortality in the 60 large eastern US communities during April to October, 1987-2000. Results show that temperature modified ozone-mortality associations and that such modification varied across geographic regions. In the northeast region, a 10-ppb increment in ozone was associated with an increase of 2.22% (95% posterior interval [PI]: 1.19%, 3.13%), 3.06% (95% PI: 2.21%, 3.76%) and 6.22% (95% PI: 4.77%, 7.56%) in mortality at low, moderate and high temperature level, respectively, while in the southeast region a 10-ppb increment in ozone was associated with an increase of 1.13% (95% PI:-1.12%, 3.18%), 1.50% (95% PI: 0.22%, 2.81%) and 1.29% (95% PI:-0.33%, 2.96%) in mortality, respectively. We concluded that temperature synergistically modified the ozone-mortality association in the northeast region, but such a pattern was not apparent in the southeast region. Thus, both temperature and geographic factors should be considered in the assessment of ozone effects.

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 mum in aerodynamic diameter (PM10) modified the effects of minimum temperature on cardiorespiratory morbidity and mortality in Brisbane, Australia. RESULTS: Results show that PM10 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 PM10, 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.

Temperature modifies the health effects of particulate matter in Brisbane, Australia.

A few epidemiological studies have examined whether there was an interactive effect between temperature and ambient particulate matter on cardiorespiratory morbidity and mortality, but the results were inconsistent. The present study used three time-series approaches to explore whether maximum temperature modified the impact of ambient particulate matter less than 10 microm in diameter (PM(10)) on daily respiratory hospital admissions, cardiovascular hospital admissions, respiratory emergency visits, cardiovascular emergency visits, non-external cause mortality and cardiovascular mortality in Brisbane between 1996 and 2001. The analytical approaches included a bivariate response surface model, a non-stratification parametric model and a stratification parametric model. Results show that there existed a statistically significant interaction between PM(10) and temperature on most health outcomes at various lags. PM(10) exhibited more adverse health effects on warm days than cold days. The choice of the degree of freedom for smoothers to adjust for confounders and the selection of arbitrary cut-offs for temperature affected the interaction estimates to a certain extent, but did not change the overall conclusion. The results imply that it is important to control and reduce the emission of air particles in Brisbane, particularly when temperature increases.