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Human exposure to the jet fuel, JP-8.

INTRODUCTION: This study investigates anecdotal reports that have suggested adverse health effects associated with acute or chronic exposure to jet fuel. METHODS: JP-8 exposure during the course of the study day was estimated using breath analysis. Health effects associated with exposure were measured using a neurocognitive testing battery and liver and kidney function tests. RESULTS: Breath analysis provided an estimate of an individual's recent JP-8 exposure that had occurred via inhalation and dermal routes. All individuals studied on base exhaled aromatic and aliphatic hydrocarbons that are found in JP-8. The subject who showed evidence of the most exposure to JP-8 had a breath concentration of 11.5 mg x m(-3) for total JP-8. This breath concentration suggested that exposure to JP-8 at an Air Guard Base is much less than exposure observed at other Air Force Bases. This reduction in exposure to JP-8 is attributed to the safety practices and standard operating procedures carried out by base personnel. The base personnel who exhibited the highest exposures to JP-8 were fuel cell workers, fuel specialists and smokers, who smoked downwind from the flightline. DISCUSSION: Although study-day exposures appear to be much less than current guidelines, chronic exposure at these low levels appeared to affect neurocognitive functioning. JP-8-exposed individuals performed significantly poorer than a sample of non-exposed age- and education-matched individuals on 20 of 47 measures of information processing and other cognitive functions.

Adult↗

Renal handling of drugs and amino acids after impairment of kidney or liver function--influences of maturity and protective treatment.

Renal tubular cells are involved both in secretion and in reabsorption processes within the kidney. Normally, most xenobiotics are secreted into the urine at the basolateral membrane of the tubular cell, whereas amino acids are reabsorbed quantitatively at the luminal side. Under different pathological or experimental circumstances, these transport steps may be changed, e.g., they may be reduced by renal impairment (reduction of kidney mass, renal ischemia, administration of nephrotoxins) or they may be enhanced after stimulation of transport carriers. Furthermore, a distinct interrelationship exists between excretory functions of the kidney and the liver. That means liver injury can influence renal transport systems also (hepato-renal syndrome). In this review, the following aspects were included: based upon general information concerning different transport pathways for xenobiotics and amino acids within kidney cells and upon a brief characterization of methods for testing impairment of kidney function, the maturation of renal transport and its stimulation are described. Similarities and differences between the postnatal development of kidney function and the increase of renal transport capacity after suitable stimulatory treatment by, for example, various hormones or xenobiotics are reviewed. Especially, renal transport in acute renal failure is described for individuals of different ages. Depending upon the maturity of kidney function, age differences in susceptibility to kidney injury occur: if energy-requiring processes are involved in the transport of the respective substance, then adults, in general, are more susceptible to renal failure than young individuals, because in immature organisms, anaerobic energy production predominates within the kidney. On the other hand, adult animals can better compensate for the loss of renal tissue (partial nephrectomy). With respect to stimulation of renal transport capacity after repeated pretreatment with suitable substances, age differences also exist: most stimulatory schedules are more effective in young, developing individuals than in mature animals. Therefore, the consequences of the stimulation of renal transport can be different in animals of different ages and are discussed in detail. Furthermore, the extent of stimulation is different for the transporters located at the basolateral and at the luminal membranes: obviously the tubular secretion at the contraluminal membrane can be stimulated more effectively than reabsorption processes at the luminal side.

Absorption↗

Renal tubular dysfunction in patients with inflammatory bowel disease treated with aminosalicylate.

BACKGROUND: An increasing number of case reports indicate potential nephrotoxicity of 5-aminosalicylic acid (5-ASA), which shares similarities with the chemical structures of both phenacetin and acetylsalicylic acid. AIM: In a point prevalence study the occurrence of sensitive indices indicative of early kidney malfunction was assessed in outpatients with inflammatory bowel disease. METHODS: Routine indices of kidney function (creatinine clearance, urinary protein content, pH, electrolytes, and microscopy) were investigated in 223 patients with inflammatory bowel disease as well as sensitive markers of glomerular or tubular dysfunction (microproteinuria by SDS polyacrylamide gel electrophoresis (SDS-PAGE), urinary concentrations of N-acetyl-beta-D-glucosaminidase, alpha 1-microglobulin, gamma-glutamyltransferase (GGT), alkaline phosphatase (AP), and albumin). Histories of exposure to 5-ASA were assessed by questionnaire. RESULTS: Patients receiving high amounts of 5-ASA, both actual as well as on a lifetime basis, showed an increased prevalence of tubular proteinuria by SDS-PAGE. Raised values for urinary AP and GGT indicate proximal tubular epithelial cells as the source. All other kidney function tests were normal. Analysis of covariates indicated strong associations between disease activity and size of 5-ASA doses as well as alterations in kidney tubular function. CONCLUSION: The possibility exists that high doses of 5-ASA may be associated with proximal tubular proteinuria. This point prevalence study cannot dissect the possible impact of chronic inflammation from high dose 5-ASA treatment and further prospective studies are warranted.

Adult↗