Geology topics

M.K. Clayton

Publications and source records attributed to M.K. Clayton.

3 recordsLinked to original sources

USGS2011

Terrestrial, benthic, and pelagic resource use in lakes: Results from a three-isotope Bayesian mixing model

Fluxes of organic matter across habitat boundaries are common in food webs. These fluxes may strongly influence community dynamics, depending on the extent to which they are used by consumers. Yet understanding of basal resource use by consumers is limited, because describing trophic pathways in complex food webs is difficult. We quantified resource use for zooplankton, zoobenthos, and fishes in four low-productivity lakes, using a Bayesian mixing model and measurements of hydrogen, carbon, and nitrogen stable isotope ratios. Multiple sources of uncertainty were explicitly incorporated into the model. As a result, posterior estimates of resource use were often broad distributions; nevertheless, clear patterns were evident. Zooplankton relied on terrestrial and pelagic primary production, while zoobenthos and fishes relied on terrestrial and benthic primary production. Across all consumer groups terrestrial reliance tended to be higher, and benthic reliance lower, in lakes where light penetration was low due to inputs of terrestrial dissolved organic carbon. These results support and refine an emerging consensus that terrestrial and benthic support of lake food webs can be substantial, and they imply that changes in the relative availability of basal resources drive the strength of cross-habitat trophic connections. ?? 2011 by the Ecological Society of America.

Ecology↗

USGS2007

Human influence on California fire regimes

Periodic wildfire maintains the integrity and species composition of many ecosystems, including the mediterranean-climate shrublands of California. However, human activities alter natural fire regimes, which can lead to cascading ecological effects. Increased human ignitions at the wildland-urban interface (WUI) have recently gained attention, but fire activity and risk are typically estimated using only biophysical variables. Our goal was to determine how humans influence fire in California and to examine whether this influence was linear, by relating contemporary (2000) and historic (1960-2000) fire data to both human and biophysical variables. Data for the human variables included fine-resolution maps of the WUI produced using housing density and land cover data. Interface WUI, where development abuts wildland vegetation, was differentiated from intermix WUI, where development intermingles with wildland vegetation. Additional explanatory variables included distance to WUI, population density, road density, vegetation type, and ecoregion. All data were summarized at the county level and analyzed using bivariate and multiple regression methods. We found highly significant relationships between humans and fire on the contemporary landscape, and our models explained fire frequency (R2 = 0.72) better than area burned (R2 = 0.50). Population density, intermix WUI, and distance to WUI explained the most variability in fire frequency, suggesting that the spatial pattern of development may be an important variable to consider when estimating fire risk. We found nonlinear effects such that fire frequency and area burned were highest at intermediate levels of human activity, but declined beyond certain thresholds. Human activities also explained change in fire frequency and area burned (1960-2000), but our models had greater explanatory power during the years 1960-1980, when there was more dramatic change in fire frequency. Understanding wildfire as a function of the spatial arrangement of ignitions and fuels on the landscape, in addition to nonlinear relationships, will be important to fire managers and conservation planners because fire risk may be related to specific levels of housing density that can be accounted for in land use planning. With more fires occurring in close proximity to human infrastructure, there may also be devastating ecological impacts if development continues to grow farther into wildland vegetation. ?? 2007 by the Ecological Society of America.

Ecological Applications↗

USGS1992

An egg injection method for assessing early life stage mortality of polychlorinated dibenzo- p -dioxins, dibenzofurans, and biphenyls in rainbow trout, (Oncorhynchus mykiss)

To characterize the risk that polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls (PCBs) pose to salmonid early life stage survival, we developed a method to expose rainbow trout (Oncorhynchus mykiss) eggs to graded doses of PCDD, PCDF, and PCB congeners, using 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) as a prototype. Rainbow trout eggs were injected 24–50 h post-fertilization with 0.2 μl of 50 mM phosphatidylcholine (PC) liposomes (control) or 0.2 μl of 5–7 graded doses of TCDD incorporated into 50 mM PC liposomes. Injection volume never exceeded 0.6% egg volume. Immediately following injection, the injection site was sealed with Super glue®, resulting in 92–97% of TCDD dose retained by the egg. Following both egg injection and waterborne egg exposure. TCDD toxicity in rainbow trout was manifested by half-hatching mortality but predominantly by sac fry mortality associated with hemorrhages, pericardial edema, and yolk sac edema. TCDD LD 50 s, following injection and waterborne exposure of rainbow trout eggs, were 421 (331–489) and 439 (346–519) pg TCDD/g egg (LD 50 , 95% fiducial limits), respectively. As in rainbow trout, TCDD toxicity in lake trout (Salvelinus namaycush) following the same two routes of exposure was manifested by half-hatching mortality but predominantly by sac fry mortality preceded by hemorrhages and yolk sac edema. LD 50 s, based on the dose of TCDD in lake trout eggs, were 47 (21–65) and 65 (60–71) pg/g following injection and waterborne exposure, respectively. The egg injection method is ideal for assessing the relationship between early life stage mortality in rainbow trout and graded egg doses of individual PCDD, PCDF, or PCB congeners.

Aquatic Toxicology↗