Background: According to a wide variety of analyses and projections, the potential effects of global climate change on human health are large and diverse. The U.S. National Institutes of Health (NIH), through its basic, clinical, and population research portfolio of grants, has been increasing efforts to understand how the complex interrelationships among humans, ecosystems, climate, climate variability, and climate change affect domestic and global health.Objectives: In this commentary we present a systematic review and categorization of the fiscal year (FY) 2008 NIH climate and health research portfolio.Methods: A list of candidate climate and health projects funded from FY 2008 budget appropriations were identified and characterized based on their relevance to climate change and health and based on climate pathway, health impact, study type, and objective.Results: This analysis identified seven FY 2008 projects focused on climate change, 85 climate-related projects, and 706 projects that focused on disease areas associated with climate change but did not study those associations. Of the nearly 53,000 awards that NIH made in 2008, approximately 0.17% focused on or were related to climate.Conclusions: Given the nature and scale of the potential effects of climate change on human health and the degree of uncertainty that we have about these effects, we think that it is helpful for the NIH to engage in open discussions with science and policy communities about government-wide needs and opportunities in climate and health, and about how NIH’s strengths in human health research can contribute to understanding the health implications of global climate change. This internal review has been used to inform more recent initiatives by the NIH in climate and health.

Steel factor is one of the growth factors that controls the proliferation and differentiation of hematopoietic cells and SCL, also known as Tcl-5 or Tal-1, is a transcription factor involved in erythropoiesis. In this report, we studied the role of SCL in the proliferation of human peripheral blood burst-forming unit-erythroid (BFU-E) and the effects of Steel factor on SCL expression in proliferating erythroid cells. BFU-E-derived colonies increase progressively in size, as determined by cell number, from day 7 to day 14 of culture, with the greatest increase in colony size (10-fold expansion) occurring between day 7 and day 10. SCL protein levels in BFU-E-derived cells were highest in day 7 cells and decreased progressively from day 7 to day 14 of culture, suggesting an association of SCL with erythroid proliferation. In contrast, SCL mRNA levels did not decrease significantly between day 7 and day 14 cells, suggesting that posttranscriptional mechanisms are largely responsible for the decrease in SCL protein observed. The role of SCL in Steel factor-induced erythroid proliferation was then examined. In BFU-E- derived colonies cultured with Steel factor, colony size was significantly increased compared to control. In day 7 and day 10 erythroid precursors cultured with Steel factor, SCL protein was increased significantly compared to control. The increase in SCL protein levels in early erythroid precursors stimulated with Steel factor suggests one mechanism through which Steel factor may enhance normal erythroid proliferation. SCL mRNA levels assessed by Northern blot in day 7 cells did not increase significantly in response to Steel factor stimulation, suggesting that posttranscriptional mechanisms may also be important in the increase in SCL protein observed in response to Steel.

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