Water Use and Management in the Bakken Shale Oil Play in North Dakota.

Oil and natural gas development in the Bakken shale play of North Dakota has grown substantially since 2008. This study provides a comprehensive overview and analysis of water quantity and management impacts from this development by (1) estimating water demand for hydraulic fracturing in the Bakken from 2008 to 2012; (2) compiling volume estimates for maintenance water, or brine dilution water; (3) calculating water intensities normalized by the amount of oil produced, or estimated ultimate recovery (EUR); (4) estimating domestic water demand associated with the large oil services population; (5) analyzing the change in wastewater volumes from 2005 to 2012; and (6) examining existing water sources used to meet demand. Water use for hydraulic fracturing in the North Dakota Bakken grew 5-fold from 770 million gallons in 2008 to 4.3 billion gallons in 2012. First-year wastewater volumes grew in parallel, from an annual average of 1,135,000 gallons per well in 2008 to 2,905,000 gallons in 2012, exceeding the mean volume of water used in hydraulic fracturing and surpassing typical 4-year wastewater totals for the Barnett, Denver, and Marcellus basins. Surprisingly, domestic water demand from the temporary oilfield services population in the region may be comparable to the regional water demand from hydraulic fracturing activities. Existing groundwater resources are inadequate to meet the demand for hydraulic fracturing, but there appear to be adequate surface water resources, provided that access is available.

Control of TH2 polarization by the chemokine monocyte chemoattractant protein-1.

Activated T lymphocytes differentiate into effector cells tailored to meet disparate challenges to host integrity. For example, type 1 and type 2 helper (T(H)1 and T(H)2) cells secrete cytokines that enhance cell-mediated and humoral immunity, respectively. The chemokine monocyte chemoattractant protein-1 (MCP-1) can stimulate interleukin-4 production and its overexpression is associated with defects in cell-mediated immunity, indicating that it might be involved in T(H)2 polarization. Here we show that MCP-1-deficient mice are unable to mount T(H)2 responses. Lymph node cells from immunized MCP-1(-/-) mice synthesize extremely low levels of interleukin-4, interleukin-5 and interleukin-10, but normal amounts of interferon-gamma and interleukin-2. Consequently, these mice do not accomplish the immunoglobulin subclass switch that is characteristic of T(H)2 responses and are resistant to Leishmania major. These effects are direct rather than due to abnormal cell migration, because the trafficking of naive T cells is undisturbed in MCP-1(-/-) mice despite the presence of MCP-1-expressing cells in secondary lymphoid organs of wild-type mice. Thus, MCP-1 influences both innate immunity, through effects on monocytes, and adaptive immunity, through control of T helper cell polarization.