In October 2001, the first inhalational anthrax case in the United States since 1976 was identified in a media company worker in Florida. A national investigation was initiated to identify additional cases and determine possible exposures to Bacillus anthracis. Surveillance was enhanced through health-care facilities, laboratories, and other means to identify cases, which were defined as clinically compatible illness with laboratory-confirmed B. anthracis infection. From October 4 to November 20, 2001, 22 cases of anthrax (11 inhalational, 11 cutaneous) were identified; 5 of the inhalational cases were fatal. Twenty (91%) case-patients were either mail handlers or were exposed to worksites where contaminated mail was processed or received. B. anthracis isolates from four powder-containing envelopes, 17 specimens from patients, and 106 environmental samples were indistinguishable by molecular subtyping. Illness and death occurred not only at targeted worksites, but also along the path of mail and in other settings. Continued vigilance for cases is needed among health-care providers and members of the public health and law enforcement communities.

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JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) and Brogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Bone lead levels for 367 active and 14 retired lead smelter workers were measured in vivo by X-ray fluorescence in May-June 1994. The bone sites of study were the tibia and calcaneus; magnitudes of concentration were used to gauge lead body burden. Whole blood lead readings from the workers generated a cumulative blood lead index (CBLI) that approximated the level of lead exposure over time. Blood lead values for 204 of the 381 workers were gathered from workers returning from a 10-month work interruption that ended in 1991; their blood level values were compared to their tibia and calcaneus lead levels. The resulting relations allowed constraints to be placed on the endogenous release of lead from bone in smelter workers. Calcaneus lead levels were found to correlate strongly with those for tibia lead, and in a manner consistent with observations from other lead industry workers. Relations between bone lead concentration and CBLI demonstrated a distinctly nonlinear appearance. When the active population was divided by date of hire, a significant difference in the bone lead-CBLI slope emerged. After a correction to include the component of CBLI existing before the workers' employment at the smelter was made, this difference persisted. This implies that the transfer of lead from blood to bone in the workers has changed over time, possibly as a consequence of varying exposure conditions. Key words: blood lead indices, bone lead, occupational lead exposure, smelter workers, X-ray fluorescence.

Increased hypothalamo-pituitary-adrenal axis drive has been reported in obese subjects but with paradoxically low or normal levels of plasma cortisol. Our current study was designed to investigate whether glucocorticoid feedback was altered in obesity, both under basal and stressed conditions. Plasma ACTH and cortisol concentrations in male control or obese subjects (age range 20-50 yr) were measured at frequent intervals over 24 h during infusion of saline or hydrocortisone at two physiological doses (7.5 and 15 mg/d) designed to occupy predominantly mineralocorticoid rather than glucocorticoid receptors. The same subjects then underwent insulin-induced hypoglycemia either in the morning or the evening. Obese subjects had significantly higher basal ACTH and lower cortisol concentrations throughout the 24 h infusion period, compared with controls (P < 0.05, two-way ANOVA followed by Newman-Keuls posthoc analysis). Basal plasma ACTH was decreased in obese groups given low- or high-dose hydrocortisone during the day (P < 0.05) but not during the night, unlike controls who responded to hydrocortisone both during the day and at night (P < 0.05). Obese subjects also showed resistance to steroid-induced inhibition of the ACTH response to hypoglycemia, compared with controls (P < 0.05). These data clearly show that obesity is associated with a relative insensitivity to glucocorticoid feedback, which is most marked during the night, and suggest that this condition is characterized by a decreased mineralocorticoid receptor response to circulating corticosteroids.