Evaluation of the public health impacts of traffic congestion: a health risk assessment

Background: Traffic congestion is a significant issue in urban areas in the United States and around the world. Previous analyses have estimated the economic costs of congestion, related to fuel and time wasted, but few have quantified the public health impacts or determined how these impacts compare in magnitude to the economic costs. Moreover, the relative magnitudes of economic and public health impacts of congestion would be expected to vary significantly across urban areas, as a function of road infrastructure, population density, and atmospheric conditions influencing pollutant formation, but this variability has not been explored. Methods: In this study, we evaluate the public health impacts of ambient exposures to fine particulate matter (PM2.5) concentrations associated with a business-as-usual scenario of predicted traffic congestion. We evaluate 83 individual urban areas using traffic demand models to estimate the degree of congestion in each area from 2000 to 2030. We link traffic volume and speed data with the MOBILE6 model to characterize emissions of PM2.5 and particle precursors attributable to congestion, and we use a source-receptor matrix to evaluate the impact of these emissions on ambient PM2.5 concentrations. Marginal concentration changes are related to a concentration-response function for mortality, with a value of statistical life approach used to monetize the impacts. Results: We estimate that the monetized value of PM2.5-related mortality attributable to congestion in these 83 cities in 2000 was approximately $31 billion (2007 dollars), as compared with a value of time and fuel wasted of$60 billion. In future years, the economic impacts grow (to over $100 billion in 2030) while the public health impacts decrease to$13 billion in 2020 before increasing to $17 billion in 2030, given increasing population and congestion but lower emissions per vehicle. Across cities and years, the public health impacts range from more than an order of magnitude less to in excess of the economic impacts. Conclusions: Our analyses indicate that the public health impacts of congestion may be significant enough in magnitude, at least in some urban areas, to be considered in future evaluations of the benefits of policies to mitigate congestion

IFNγ and IL-12 restrict Th2 responses during Helminth/Plasmodium co-infection and promote IFNγ from Th2 cells

Parasitic helminths establish chronic infections in mammalian hosts. Helminth/Plasmodium co-infections occur frequently in endemic areas. However, it is unclear whether Plasmodium infections compromise anti-helminth immunity, contributing to the chronicity of infection. Immunity to Plasmodium or helminths requires divergent CD4+ T cell-driven responses, dominated by IFNγ or IL-4, respectively. Recent literature has indicated that Th cells, including Th2 cells, have phenotypic plasticity with the ability to produce non-lineage associated cytokines. Whether such plasticity occurs during co-infection is unclear. In this study, we observed reduced anti-helminth Th2 cell responses and compromised anti-helminth immunity during Heligmosomoides polygyrus and Plasmodium chabaudi co-infection. Using newly established triple cytokine reporter mice (Il4gfpIfngyfpIl17aFP635), we demonstrated that Il4gfp+ Th2 cells purified from in vitro cultures or isolated ex vivo from helminth-infected mice up-regulated IFNγ following adoptive transfer into Rag1-/- mice infected with P. chabaudi. Functionally, Th2 cells that up-regulated IFNγ were transcriptionally re-wired and protected recipient mice from high parasitemia. Mechanistically, TCR stimulation and responsiveness to IL-12 and IFNγ, but not type I IFN, was required for optimal IFNγ production by Th2 cells. Finally, blockade of IL-12 and IFNγ during co-infection partially preserved anti-helminth Th2 responses. In summary, this study demonstrates that Th2 cells retain substantial plasticity with the ability to produce IFNγ during Plasmodium infection. Consequently, co-infection with Plasmodium spp. may contribute to the chronicity of helminth infection by reducing anti-helminth Th2 cells and converting them into IFNγ-secreting cells

Acute oxytocin improves memory and gaze following in male but not female nursery-reared infant macaques

Rationale: Exogenous oxytocin administration is widely reported to improve social cognition in human and nonhuman primate adults. Risk factors of impaired social cognition, however, emerge in infancy. Early interventions—when plasticity is greatest—are critical to reverse negative outcomes. Objective: We tested the hypothesis that oxytocin may exert similar positive effects on infant social cognition, as in adults. To test this idea, we assessed the effectiveness of acute, aerosolized oxytocin on two foundational social cognitive skills: working memory (i.e., ability to briefly hold and process information) and social gaze (i.e., tracking the direction of others’ gaze) in 1-month-old nursery-reared macaque monkeys (Macaca mulatta). We did not predict sex differences, but we included sex as a factor in our analyses to test whether our effects would be generalizable across both males and females. Results: In a double-blind, placebo-controlled design, we found that females were more socially skilled at baseline compared to males, and that oxytocin improved working memory and gaze following, but only in males. Conclusions: These sex differences, while unexpected, may be due to interactions with gonadal steroids and may be relevant to sexually dimorphic disorders of social cognition, such as male-biased autism spectrum disorder, for which oxytocin has been proposed as a potential treatment. In sum, we report the first evidence that oxytocin may influence primate infant cognitive abilities. Moreover, these behavioral effects appear sexually dimorphic, highlighting the importance of considering sex differences. Oxytocin effects observed in one sex may not be generalizable to the other sex

Gasoline demand with heterogeneity in household responses

Fuel demand elasticities to determine consumer responses to tax increases or price shocks are typically based on aggregate data. The literature generally provides one elasticity estimate for each country, assuming similar response for all households. However, it is possible that different households can have different responses to the same stimuli depending on the household characteristics. Assuming a single elasticity for all households may fail to capture the detailed distributional effect on different socio-economic groups, which is often needed to fully understand the impact of fuel tax measures. This paper presents results from a household level gasoline demand model which accommodates variation in price and income elasticity with increasing income as well as for different socio-economic characteristics in the USA. We find substantial heterogeneity in price and income elasticities based on demographic groupings and income groups. Results of a distributional analysis for a gasoline tax are also presented using the heterogeneous responses