Solar reflective cool roofs and walls can be used to mitigate the urban heat island effect. While many past studies have investigated the climate impacts of adopting cool surfaces, few studies have investigated their effects on air pollution, especially on particulate matter (PM). This research for the first time investigates the influence of widespread deployment of cool walls on urban air pollutant concentrations, and systematically compares cool wall to cool roof effects. Simulations using a coupled meteorology-chemistry model (WRF-Chem) for a representative summertime period show that cool walls and roofs can reduce urban air temperatures, wind speeds, and planetary boundary heights in the Los Angeles Basin. Consequently, increasing wall (roof) albedo by 0.80, an upper bound scenario, leads to maximum daily 8-h average ozone concentration reductions of 0.35 (0.83) ppbv in Los Angeles County. However, cool walls (roofs) increase daily average PM_2.5 concentrations by 0.62 (0.85) μg m^-3. We investigate the competing processes driving changes in concentrations of speciated PM_2.5. Increases in primary PM (elemental carbon and primary organic aerosols) concentrations can be attributed to reductions in ventilation of the Los Angeles Basin. Increases in concentrations of semivolatile species (e.g., nitrate) are mainly driven by increases in gas-to-particle conversion due to reduced atmospheric temperatures.

Economic globalization and concomitant growth in international trade since the late 1990s have profoundly reorganized global production activities and related CO2 emissions. Here we show trade among developing nations (i.e., South-South trade) has more than doubled between 2004 and 2011, which reflects a new phase of globalization. Some production activities are relocating from China and India to other developing countries, particularly raw materials and intermediate goods production in energy-intensive sectors. In turn, the growth of CO2 emissions embodied in Chinese exports has slowed or reversed, while the emissions embodied in exports from less-developed regions such as Vietnam and Bangladesh have surged. Although China's emissions may be peaking, ever more complex supply chains are distributing energy-intensive industries and their CO2 emissions throughout the global South. This trend may seriously undermine international efforts to reduce global emissions that increasingly rely on rallying voluntary contributions of more, smaller, and less-developed nations.

Objective

To identify common genetic variants associated with the presence of brain microbleeds (BMBs).

Methods

We performed genome-wide association studies in 11 population-based cohort studies and 3 case-control or case-only stroke cohorts. Genotypes were imputed to the Haplotype Reference Consortium or 1000 Genomes reference panel. BMBs were rated on susceptibility-weighted or T2*-weighted gradient echo MRI sequences, and further classified as lobar or mixed (including strictly deep and infratentorial, possibly with lobar BMB). In a subset, we assessed the effects of APOE ε2 and ε4 alleles on BMB counts. We also related previously identified cerebral small vessel disease variants to BMBs.

Results

BMBs were detected in 3,556 of the 25,862 participants, of which 2,179 were strictly lobar and 1,293 mixed. One locus in the APOE region reached genome-wide significance for its association with BMB (lead single nucleotide polymorphism rs769449; odds ratio [OR]_{any BMB} [95% confidence interval (CI)] 1.33 [1.21-1.45]; p = 2.5 × 10^-10). APOE ε4 alleles were associated with strictly lobar (OR [95% CI] 1.34 [1.19-1.50]; p = 1.0 × 10^-6) but not with mixed BMB counts (OR [95% CI] 1.04 [0.86-1.25]; p = 0.68). APOE ε2 alleles did not show associations with BMB counts. Variants previously related to deep intracerebral hemorrhage and lacunar stroke, and a risk score of cerebral white matter hyperintensity variants, were associated with BMB.

Conclusions

Genetic variants in the APOE region are associated with the presence of BMB, most likely due to the APOE ε4 allele count related to a higher number of strictly lobar BMBs. Genetic predisposition to small vessel disease confers risk of BMB, indicating genetic overlap with other cerebral small vessel disease markers.