A major conservation concern is whether population size and other ecological variables change linearly with habitat loss, or whether they suddenly decline more rapidly below a "critical threshold" level of habitat. The most commonly discussed explanation for critical threshold responses to habitat loss focus on habitat configuration. As habitat loss progresses, the remaining habitat is increasingly fragmented or the fragments are increasingly isolated, which may compound the effects of habitat loss. In this review we also explore other possible explanations for apparently nonlinear relationships between habitat loss and ecological responses, including Allee effects and time lags, and point out that some ecological variables will inherently respond nonlinearly to habitat loss even in the absence of compounding factors. In the literature, both linear and nonlinear ecological responses to habitat loss are evident among simulation and empirical studies, although the presence and value of critical thresholds is influenced by characteristics of the species (e.g. dispersal, reproduction, area/edge sensitivity) and landscape (e.g. fragmentation, matrix quality, rate of change). With enough empirical support, such trends could be useful for making important predictions about species' responses to habitat loss, to guide future research on the underlying causes of critical thresholds, and to make better informed management decisions. Some have seen critical thresholds as a means of identifying conservation targets for habitat retention. We argue that in many cases this may be misguided, and that the meaning (and utility) of a critical threshold must be interpreted carefully and in relation to the response variable and management goal. Despite recent interest in critical threshold responses to habitat loss, most studies have not used any formal statistical methods to identify their presence or value. Methods that have been used include model comparisons using Akaike information criterion (AIC) or t-tests, and significance testing for changes in slope or for polynomial effects. The judicious use of statistics to help determine the shape of ecological relationships would permit greater objectivity and more comparability among studies.

Wiebe, K. L. and Swift, T. L. 2001. Clutch size relative to tree cavity size in Northern Flickers. -J. Avian Biol. 32: 167-173.We analysed clutch size versus nest size in 153 broods of the Northern Flicker Colaptes auratus, a woodpecker using natural cavities in British Columbia, Canada. Larger volume cavities were less susceptible to predation and cavity size was positively associated with the age and body size of males and with the body condition of female parents. Although clutches varied between 4 and 11 eggs, and the floor area of cavities varied about 5-fold, we found no relationship between clutch size and floor area or cavity volume. To see if there were fitness consequences to clutch size relative to nest size, we examined hatching success and nestling mortality in flicker broods. Hatching success was not related to cavity size, but crowding slightly reduced nestling survival even when clutch size was controlled statistically. However, there was no effect of cavity size on the total number of nestlings fledged. Newly excavated flicker cavities were smaller than reused cavities suggesting a cost to excavation. This cost, coupled with the minimal fitness consequences of overcrowding, may explain why flickers do not adjust clutch size to cavity size.

BackgroundExposure to swine barn air is an occupational hazard. Barn workers following an eight-hour work shift develop many signs of lung dysfunction including lung inflammation. However, the in situ cellular and molecular mechanisms responsible for lung dysfunction induced following exposure to the barn air remain largely unknown. Specifically, the recruitment and role of pulmonary intravascular monocytes/macrophages (PIMMs), which increase host susceptibility for acute lung inflammation, remain unknown in barn air induced lung inflammation. We hypothesized that barn exposure induces recruitment of PIMMs and increases susceptibility for acute lung inflammation with a secondary challenge.MethodsSprague-Dawley rats were exposed either to the barn or ambient air for eight hours and were euthanized at various time intervals to collect blood, broncho-alveolar lavage fluid (BALF) and lung tissue. Subsequently, following an eight hour barn or ambient air exposure, rats were challenged either with Escherichia coli (E. coli) lipopolysaccharide (LPS) or saline and euthanized 6 hours post-LPS or saline treatment. We used ANOVA (P < 0.05 means significant) to compare group differences.ResultsAn eight-hour exposure to barn air induced acute lung inflammation with recruitment of granulocytes and PIMMs. Granulocyte and PIMM numbers peaked at one and 48 hour post-exposure, respectively.Secondary challenge with E. coli LPS at 48 hour following barn exposure resulted in intense lung inflammation, greater numbers of granulocytes, increased number of cells positive for TNF-α and decreased amounts of TGF-β2 in lung tissues. We also localized TNF-α, IL-1β and TGF-β2 in PIMMs.ConclusionA single exposure to barn air induces lung inflammation with recruitment of PIMMs and granulocytes. Recruited PIMMs may be linked to more robust lung inflammation in barn-exposed rats exposed to LPS. These data may have implications of workers exposed to the barn air who may encounter secondary microbial challenge.