A Needs-Driven, Multi-Objective Approach to Allocate Urban Ecosystem Services from 10,000 Trees.

Urban areas face challenges including vehicular emissions, stormwater runoff, and sedentary lifestyles. Communities recognize the value of trees in mitigating these challenges by absorbing pollution and enhancing walkability. However, siting trees to optimize multiple benefits requires a systems approach that may cross sectors of management and expertise. We present a spatially-explicit method to optimize tree planting in Durham, NC, a rapidly growing urban area with an aging tree stock. Using GIS data and a ranking approach, we explored where Durham could augment its current stock of willow oaks through its plans to install 10,000 mid-sized deciduous trees. Data included high-resolution landcover metrics developed by the U.S. Environmental Protection Agency (EPA), demographics from the U.S. Census, an attributed roads dataset licensed to the EPA, and sidewalk information from the City of Durham. Census block groups (CBGs) were ranked for tree planting according to single and multiple objectives including stormwater reduction, emissions buffering, walkability, and protection of vulnerable populations. Prioritizing tree planting based on single objectives led to four sets of locations with limited geographic overlap. Prioritizing tree planting based on multiple objectives tended to favor historically disadvantaged CBGs. The four-objective strategy met the largest proportion of estimated regional need. Based on this analysis, the City of Durham has implemented a seven-year plan to plant 10,000 trees in priority neighborhoods. This analysis also found that any strategy which included the protection of vulnerable populations generated more benefits than others.

Permanent, sex-selective effects of prenatal or adolescent nicotine exposure, separately or sequentially, in rat brain regions: indices of cholinergic and serotonergic synaptic function, cell signaling, and neural cell number and size at 6 months of age.

Nicotine is a neuroteratogen that disrupts neurodevelopment and synaptic function, with vulnerability extending into adolescence. We assessed the permanence of effects in rats on indices of neural cell number and size, and on acetylcholine and serotonin (5HT) systems, conducting assessments at 6 months of age, after prenatal nicotine exposure, adolescent exposure, or sequential exposure in both periods. For prenatal nicotine, indices of cell number and size showed few abnormalities by 6 months, but there were persistent deficits in cerebrocortical choline acetyltransferase activity and hemicholinium-3 binding to the presynaptic choline transporter, a pattern consistent with cholinergic hypoactivity; these effects were more prominent in males than females. The expression of 5HT receptors also showed permanent effects in males, with suppression of the 5HT(1A) subtype and upregulation of 5HT(2) receptors. In addition, cell signaling through adenylyl cyclase showed heterologous uncoupling of neurotransmitter responses. Nicotine exposure in adolescence produced lasting effects that were similar to those of prenatal nicotine. However, when animals were exposed to prenatal nicotine and received nicotine subsequently in adolescence, the adverse effects then extended to females, whereas the net effect in males was similar to that of prenatal nicotine by itself. Our results indicate that prenatal or adolescent nicotine exposure evoke permanent changes in synaptic function that transcend the recovery of less-sensitive indices of structural damage; further, prenatal exposure sensitizes females to the subsequent adverse effects of adolescent nicotine, thus creating a population that may be especially vulnerable to the lasting behavioral consequences of nicotine intake in adolescence.