Lead dustfall from demolition of scattered site family housing: developing a sampling methodology.

BACKGROUND: Over 3000 older homes containing lead-based paint are demolished in Chicago each year. While previous studies investigating large multifamily housing demolitions have shown high levels of lead in dustfall, dispersed single-family housing demolition have yet to be assessed. Presently, no standards exist to regulate the extent of lead dustfall from housing demolition. OBJECTIVES: We studied ten residences in Chicago undergoing demolition and debris removal and compared dustfall rates to five standing homes from March to October 2006. METHODS: Dustfall was measured using a modification of APHA Method 502; samplers consisted of plastic buckets filled with 1l of deionized water, elevated to breathing zone height and placed around the demolition site perimeter. Laboratory analysis consisted of filtration, acid digestion and analysis by ICP/MS. RESULTS: During demolition, the geometric mean lead dustfall (n=43 at 10 locations) was 64.1 microgPb/m(2)/h (range: 1.3-3902.5), while the geometric mean lead dustfall for areas with no demolition (n=18 at 6 locations) was 12.9 microgPb/m(2)/h (range: 1.8-54.5). This difference was highly statistically significant (p=0.0004). When dust suppression measures were used, dustfall lead levels were lower, although the difference was not statistically significant. The geometric mean lead dustfall with dust suppression (n=25 at five locations) and without (n=22 at six locations) was 48 Pbmicrog/m(2)/h and 74.6 microgPb/m(2)/h, respectively. CONCLUSION: Demolition dustfall lead levels are much higher than background levels of lead during demolition of single-family housing and may constitute a yet uncharacterized but important source of lead exposure to nearby residents. Simple dust suppression methods are likely to reduce the contamination considerably.

Mitochondrial transporters involved in oleic acid utilization and glutamate metabolism in yeast.

Utilization of fatty acids such as oleic acid as sole carbon source by the yeast Saccharomyces cerevisiae requires coordinated function of peroxisomes, where the fatty acids are degraded, and the mitochondria, where oxidation is completed. We identified two mitochondrial oxodicarboxylate transporters, Odc1p and Odc2p, as important in efficient utilization of oleic acid in yeast [Tibbetts et al., Arch. Biochem. Biophys. 406 (2002) 96-104]. Yet, the growth phenotype of odc1delta odc2delta strains indicated that additional transporter(s) were also involved. Here, we identify two putative transporter genes, YMC1 and YMC2, as able to suppress the odc1delta odc2delta growth phenotype. The mRNA levels for both are elevated in the presence of glycerol or oleic acid, as compared to glucose. Ymc1p and Ymc2p are localized to the mitochondria in oleic acid-grown cells. Deletion of all four transporters (quad mutant) prevents growth on oleic acid as sole carbon source, while growth on acetate is retained. It is known that the glutamate-sensitive retrograde signaling pathway is important for upregulation of peroxisomal function in response to oleic acid and the oxodicarboxylate alpha-ketoglutarate is transported out of the mitochondria for synthesis of glutamate. So, citric acid cycle function and glutamate synthesis were examined in transporter mutants. The quad mutant has significantly decreased citrate synthase activity and whole cell alpha-ketoglutarate levels, while isocitrate dehydrogenase activity is unaffected and glutamate dehydrogenase activity is increased 10-fold. Strains carrying only two or three transporter deletions exhibit intermediate affects. 13C NMR metabolic enrichment experiments confirm a defect in glutamate biosynthesis in the quad mutant and, in double and triple mutants, suggest increased cycling of the glutamate backbone in the mitochondria before export. Taken together these studies indicate that these four transporters have overlapping activity, and are important not only for utilization of oleic acid, but also for glutamate biosynthesis.