Comparison of two floor mat lead dust collection methods and their application in pre-1950 and new urban houses.

This study investigated commercial floor mats as an alternative method to assess lead in residential dust in inner-city houses. Mats were placed for 3 weeks in interior entry-ways of 34 row houses built before 1950 and 17 new row houses in Baltimore City. A high volume sampler (an HVS3 floor model cyclone-based vacuum) and a hand-held portable cyclone sampler were used in the laboratory to collect side-by-side samples of mat dust. Both devices yielded comparable estimates of lead dust deposition, dust lead concentration, and dust deposition on field mat samples and had similar sampling efficiencies on mats spiked with various types of standard reference materials. The older houses had significantly higher daily lead dust deposition (mean = 130 micrograms/ft2/day by HVS3) than the newer houses (mean = 9 micrograms/ft2/day by HVS3), due to higher dust lead concentrations (mean = 1149 ppm vs mean = 107 ppm by HVS3) and not to differences in daily dust deposition (mean = 118 mg/ft2/day vs mean = 87 mg/ft2/day by HVS3) [corrected]. Mats were found to be a feasible method for the collection of dust that has accumulated for a known amount of time. Current wipe and vacuum methods do not allow for the estimation of dust deposition rates. Further research is needed to understand the role of floor mats as a risk assessment tool.

Substrate-selective induction of rabbit hepatic UDP-glucuronyltransferases by ethanol and other xenobiotics.

Male New Zealand white rabbits were treated with various inducers of hepatic metabolism enzymes to characterize the induction of UDP-glucuronyltransferase (UDP-GT) enzymes. Rabbits were pretreated with phenobarbital, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT), 3-methylcholanthrene, beta-naphthoflavone, Aroclor 1254, ethanol, trans-stilbene oxide, pregnenolone-16 alpha-carbonitrile, or clofibric acid. Hepatic microsomes from treated and control animals were incubated with the GT1-type substrates, p-nitrophenol and 1-naphthol; the GT2-type substrate, morphine; and the steroid substrate, estrone. Compared to the rat, the rabbit was particularly resistant to UDP-GT induction. Ethanol was the most potent inducer for both GT1 and GT2 activities, but it failed to induce steroid (estrone, estradiol, and testosterone) UDP-GT activities. Ethanol pretreatment increased oxazepam-GT but it decreased bilirubin-GT activity. 3-Methylcholanthrene (3MC) and beta-naphthoflavone (BNF) are the prototypic GT1 inducers in the rat, but 3MC caused no induction of GT1 activity and BNF caused induction of both GT1 and GT2 activities in the rabbit. None of the xenobiotic pretreatments increased the hepatic microsomal glucuronidation of estrone. These results demonstrate that the induction of UDP-GT activities, and the use of this phenomenon to classify UDP-GT forms, is somewhat species-specific and cannot necessarily be extrapolated from rats to other species. In addition, the substrate selectivity of ethanol-induced microsomal UDP-GT was established.