Although interests in assessing the relationship between temperature and mortality have arisen due to climate change, relatively few data are available on lag structure of temperature–mortality relationship, particularly in the Southern Hemisphere. This study identified the lag effects of mean temperature on mortality among age groups and death categories using polynomial distributed lag models in Brisbane, Australia, a subtropical city, 1996–2004. For a 1 °C increase above the threshold, the highest percent increase in mortality on the current day occurred among people over 85 years (7.2% (95% CI: 4.3%, 10.2%)). The effect estimates among cardiovascular deaths were higher than those among all-cause mortality. For a 1 °C decrease below the threshold, the percent increases in mortality at 21 lag days were 3.9% (95% CI: 1.9%, 6.0%) and 3.4% (95% CI: 0.9%, 6.0%) for people aged over 85 years and with cardiovascular diseases, respectively. These findings may have implications for developing intervention strategies to reduce and prevent temperature-related mortality.

Type 2 Diabetes (T2D) and particulate air pollution are associated with inflammatory dysregulation. We assessed the modifying effects of diabetes medications on the association of C-reactive protein (CRP), a marker of inflammation, and traffic exposure in adults with T2D (n = 379). CRP concentrations were significantly positively associated with residence ≤100 m of a roadway, >100 m and ≤200 m of a roadway and increased traffic density for individuals using insulin. For individuals using oral hypoglycemic medications (OHAs), CRP was significantly negatively associated with residence >100 m – ≤200 m of a roadway and multiple roadway exposure in an interaction model. Among people with diabetes, individuals on insulin appear to be most vulnerable to the effects of traffic exposure. Disease severity among insulin users may promote the pro-inflammatory response to traffic exposure, though diabetes medications may also modify the response. Possible anti-inflammatory effects of OHAs with traffic exposure merit further evaluation.

Human hair and indoor dust from urban, e-waste, and rural areas in south China were collected and analyzed for brominated flame retardants (BFRs). BFRs concentrations in hair from occupational e-waste recycling workers were higher than those from non-occupational exposed residents in other sampling areas. Polybrominated diphenyl ethers (PBDEs) and decabromodiphenyl ethane (DBDPE) are two major BFRs in hair samples. The PBDE congener profiles in hair from the e-waste area are different from those from urban and rural areas with relatively higher contribution of lower brominated congeners. DBDPE, instead of BDE209, has become the major BFR in non-e-waste recycling areas. Significant correlations were found between hair level and dust level for DBDPE and BTBPE but not for PBDEs. The different PBDE congener profiles between dust and hair may suggest that exogenous exposure to the PBDE adsorbed on dust is not a major source of hair PBDEs.

Purpose Recent evidence indicates that exposure to persistent organic pollutants (POPs) is emerging as an important risk factor for atherosclerosis-related diseases, including stroke. Hypertension (HTN) is a major risk factor for stroke, and some studies suggest that exposure to POPs is also a risk factor for HTN. We hypothesized that POPs increase the environmental burden of stroke with comorbid HTN. Methods A population-based study of hospitalization rates for stroke with comorbid HTN in populations presumably exposed to POPs, based on the zip code of residence, was conducted. Data on hospitalizations for stroke with comorbid HTN were obtained from the New York Statewide Planning and Research Cooperative System for 1993-2004. Relative risks, with 95% confidence intervals (RR, 95% CI), of hospitalization were estimated by multiple Poisson regression analysis. Results RR of hospitalization for stroke with comorbid HTN was 13.4% higher in populations residing in zip codes containing or abutting environmental sources of POPs (RR = 1.134; 95% CI, 1.036-1.241; p = 0.006). Also, hospitalization rates were significantly higher in males than in females (RR = 1.397; 95% CI, 1.357-1.437; p < 0.001), in African Americans than in Caucasians (RR = 3.902; 95% CI, 3.617-4.208; p < 0.001), and in older age groups (p for trend < 0.001). These statistically significant findings of the effect of demographic factors are highly consistent with the current knowledge of stroke and serve as indirect quality indicators for our model. Conclusions Results of our study support the hypothesis that exposure to POPs increases the environmental burden of both stroke and HTN.