PM-Attributable Mortality Burden Variability in the Continental U.S.

Epidemiologic studies have consistently observed associations between fine particulate matter (PM) exposure and premature mortality. These studies use air quality concentration information from a combination of sources to estimate pollutant exposures and then assess how mortality varies as a result of differing exposures. Health impact assessments then typically use a single log-linear hazard ratio (HR) per health outcome to estimate counts of avoided human health effects resulting from air quality improvements.

Evaluating reduced-form modeling tools for simulating ozone and PM monetized health impacts.

Reduced-form modeling approaches are an increasingly popular way to rapidly estimate air quality and human health impacts related to changes in air pollutant emissions. These approaches reduce computation time by making simplifying assumptions about pollutant source characteristics, transport and chemistry. Two reduced form tools used by the Environmental Protection Agency in recent assessments are source apportionment-based benefit per ton (SA BPT) and source apportionment-based air quality surfaces (SABAQS).

Modeling future asthma attributable to fine particulate matter (PM) in a changing climate: a health impact assessment.

Exposure to fine particulate matter (PM) is associated with asthma development as well as asthma exacerbation in children. PM can be directly emitted or can form in the atmosphere from pollutant precursors. PM emitted and formed in the atmosphere is influenced by meteorology; future changes in climate may alter the concentration and distribution of PM.

The reduction of summer sulfate and switch from summertime to wintertime PM concentration maxima in the United States.

Exposure to particulate matter air pollution with a nominal mean aerodynamic diameter less than or equal to 2.5 μm (PM) has been associated with health effects including cardiovascular disease and death. Here, we add to the understanding of urban and rural PM concentrations over large spatial and temporal scales in recent years.

Assessing Human Health PM and Ozone Impacts from U.S. Oil and Natural Gas Sector Emissions in 2025.

Incomplete information regarding emissions from oil and natural gas production has historically made it challenging to characterize the air quality or air pollution-related health impacts for this sector in the United States. Using an emissions inventory for the oil and natural gas sector that reflects information regarding the level and distribution of PM and ozone precursor emissions, we simulate annual mean PM and summer season average daily 8 h maximum ozone concentrations with the Comprehensive Air-Quality Model with extensions (CAMx). We quantify the incidence and economic value of PM and ozone health related effects using the environmental Benefits Mapping and Analysis Program (BenMAP).

The heart as an extravascular target of endothelin-1 in particulate matter-induced cardiac dysfunction.

Exposure to particulate matter air pollution has been causally linked to cardiovascular disease in humans. Several broad and overlapping hypotheses describing the biological mechanisms by which particulate matter exposure leads to cardiovascular disease have been explored, although linkage with specific factors or genes remains limited. These hypotheses may or may not also lead to particulate matter-induced cardiac dysfunction.

Lineage-specific compaction of Tcrb requires a chromatin barrier to protect the function of a long-range tethering element.

Gene regulation relies on dynamic changes in three-dimensional chromatin conformation, which are shaped by composite regulatory and architectural elements. However, mechanisms that govern such conformational switches within chromosomal domains remain unknown. We identify a novel mechanism by which cis-elements promote long-range interactions, inducing conformational changes critical for diversification of the TCRβ antigen receptor locus (Tcrb).

Peripheral subnuclear positioning suppresses Tcrb recombination and segregates Tcrb alleles from RAG2.

Allelic exclusion requires that the two alleles at antigen-receptor loci attempt to recombine variable (V), diversity (D), and joining (J) gene segments [V(D)J recombination] asynchronously in nuclei of developing lymphocytes. It previously was shown that T-cell receptor β (Tcrb) alleles frequently and stochastically associate with the nuclear lamina and pericentromeric heterochromatin in CD4(-)CD8(-) thymocytes. Moreover, rearranged alleles were underrepresented at these locations.