When comparing within groups, five days of low EA (15kcal·kgLBM·d) decreased bone formation and increased bone resorption in women, but not in men, and no sex specific differences were detected.

No abstract

Since the publication of the Times Beach risk assessment in 1984, which suggested that residential soils were of concern when the level of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was in excess of 1 ppb, there has been continued interest in this topic. Studies conducted within the past 5 yr on the environmental and toxicological behavior of TCDD, as well as refinement of parameters regarding human exposure, indicate that previous assessments of the risk to humans posed by TCDD-contaminated soil were overestimated. In this paper, recent information drawn from nearly 100 recently published articles regarding the histopathology interpretation of the Kociba bioassay, environmental fate and half-life of TCDD in soil, and estimates of human exposure via soil ingestion, dermal contact, inhalation, surface runoff, and the consumption of fish were incorporated into a risk assessment. Cleanup levels for TCDD in residential and industrial soils were calculated based on most likely exposure scenarios. Probability distributions of key exposure parameters were incorporated into a Monte Carlo uncertainty analysis to predict the range and probability of TCDD uptake and corresponding cleanup levels in soil. This analysis demonstrated that the most significant route of human exposure to TCDD is through dermal contact with soil, followed by soil ingestion, fish consumption, and inhalation of airborne particulates. At residential sites, soils containing 20 parts per billion (ppb) of TCDD were found to pose a lifetime cancer risk no greater than 1 in 100,000 (10(-5) risk) under typical exposure conditions. Based on the Monte Carlo analysis, soil concentrations for the 75th and 95th percentile person were 12 and 7 ppb (10(-5) risk), respectively. In industrial soils, TCDD concentrations ranged between 131 and 582 ppb (10(-5) risk), depending on the amount of time spent outdoors under typical exposure conditions. Industrial soil concentrations of approximately 93 and 46 ppb (10(-5) risk) were calculated for the 75th and 95th percentile worker, respectively, engaged in outdoor activities. The range of TCDD concentrations in industrial soils was not reduced significantly when the consumption of fish from a neighboring waterway by off-site receptors was considered. While cleanup levels for TCDD should be derived on a site-specific basis, this analysis indicated that soil cleanup standards can be generally higher than those implemented over the past 8 yr.

Changes in blood ionized calcium concentration (Ca++) appear to be dependent on the physiological state of the chicken. In the laying hen, blood Ca++ levels were affected by the ovulatory cycle; Ca++ was elevated when the shell gland was empty, declined following entry of an egg into that organ, and reached a minimum level approximately 16 hr prior to the subsequent oviposition. Pullets not in laying condition had blood Ca++ that varied with the photoperiod and/or rate of feed intake. In those pullets, blood Ca++ levels were depressed during the 9.5 hr of light, then rose in plateaued during the dark period. These studies indicate that blood Ca++ in laying hens is affected by the reproductive state first and the photoperiod and/or pattern of feed intake second.

No abstract

The incidence of KD in New Zealand is defined with significantly variable risk according to ethnicity. Most patients received appropriate rapid diagnosis and treatment but there was considerable variation in practice in regard to number and timing of echocardiograms. There was a low coronary artery aneurysm rate (2%). Accelerated vaso-occlusive disease was responsible for the single fatality in an atypical case.

The chronic bioassay of 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) reported in 1978 by Kociba et al. has been considered to be the primary evidence supporting its carcinogenicity, and is the basis for most dioxin regulations in North America and Western Europe. Because the histopathological criteria for proliferative lesions in the rat liver have changed significantly since 1978, a reevaluation of the liver slides was conducted recently by an independent panel of pathologists. Using current National Toxicology Program criteria, their study showed, in contrast to the original findings, that about two-thirds fewer tumors were present in the livers of female Sprague-Dawley rats. The no-observed-adverse-effect level (NOAEL) for hepatocellular carcinomas was 0.01 micrograms/kg/d rather than 0.001 micrograms/kg/d, which had been reported in 1978. In light of these significant findings, a quantitative dose-response assessment of 2,3,7,8-TCDD was undertaken to predict the potential carcinogenic risks to humans. Risk-specific doses (RsDs) and cancer potency factors (CPFs) were calculated by applying the linearized multistage (LMS) model to the combined incidences of hepatocellular carcinomas and adenomas, classified in accordance with the 1990 histopathological criteria. Based on the weight of evidence regarding the mechanism of action of 2,3,7,8-TCDD, body weight rather than surface area was selected as the appropriate means for scaling rodent data to predict the human response. Using the survival-adjusted data, the RsD for a 1 in 1,000,000 (10(-6)) plausible upper bound (95%) lifetime incremental cancer risk was 370 fg/kg/d based only on the incidence of hepatocellular carcinomas, and 100 fg/kg/d when hepatocellular carcinomas and adenomas were combined. The corresponding upper-bound (95%) CPFs were 2700 and 9700 (mg/kg/d)-1, respectively. These results indicate that the carcinogenic risk to humans from exposure to 2,3,7,8-TCDD is at least 16-fold lower than previous estimates derived from the Kociba et al. (1978) bioassay.

No abstract