Chronic Environmental and Occupational Lead Exposure and Kidney Function among African Americans: Dallas Lead Project II.

Background: We examined the effects of lead on kidney function in occupationally and environmentally exposed adults from a Dallas lead smelter community that was the site of an Environmental Protection Agency (EPA) Superfund clean-up. All subjects were African Americans-a racial group that bears a disproportionate burden of kidney disease. Methods: A two-phase health screening was conducted. Phase II included a physical examination and laboratory tests. Study subjects were African Americans residents, aged ≥19 years to ≤89 years. Of 778 subjects, 726 were environmentally exposed and 52 were both occupationally and environmentally exposed. The effects of lead exposure on estimated glomerular filtration rate (eGFR) were examined in three groups: male and female smelter-community residents, as well as males with both occupational and environmental exposure. Multiple linear regression was used to analyze the dependence of eGFR on log (blood lead level), duration of residence in the community, type 2 diabetes, and hypertension. Results: There was a statistically significant negative effect on kidney function for all three groups. Comparison of female and male residents showed a slightly larger negative effect of blood lead level on eGFR in females versus males, with the largest effect seen in male smelter-working residents. For each unit increase (log10 10µg/dL = 1) in blood lead level, age-adjusted eGFR was reduced 21.2 mL/min/1.73 m² in male residents, 25.3 mL/min/1.73 m² in female residents and 59.2 mL/min/1.73 m² in male smelter-working residents. Conclusions: Chronic lead exposure is associated with worsening kidney function in both African American male and female residents, as well as male workers in Dallas smelter communities. This effect is slightly, but not statistically significantly, worse in female residents than male residents, and significantly worse in males that both worked and resided in the smelter community.

Pilot study of iodine-131-metaiodobenzylguanidine in combination with myeloablative chemotherapy and autologous stem-cell support for the treatment of neuroblastoma.

PURPOSE: The survival for children with relapsed or metastatic neuroblastoma remains poor. More effective regimens with acceptable toxicity are required to improve prognosis. Iodine-131-metaiodobenzylguanidine ((131)I-MIBG) selectively targets radiation to catecholamine-producing cells, including neuroblastoma cells. A pilot study was performed to examine the feasibility of a novel regimen combining (131)I-MIBG and myeloablative chemotherapy with autologous stem-cell rescue. PATIENTS AND METHODS: Twelve patients with neuroblastoma were treated after relapse (five patients) or after induction therapy (seven patients). Eight patients had metastatic and four had localized disease at the time of therapy. All patients received (131)I-MIBG 12 mCi/kg on day -21, followed by carboplatin (1,500 mg/m(2)), etoposide (800 mg/m(2)), and melphalan (210 mg/m(2)) administered from day -7 to day -4. Autologous peripheral-blood stem cells or bone marrow were infused on day 0. Engraftment, toxicity, and response rates were evaluated. RESULTS: The (131)I-MIBG infusion and myeloablative chemotherapy were both well tolerated. Grade 2 to 3 oral mucositis was the predominant nonhematopoietic toxicity, occurring in all patients. The median times to neutrophil (> or = 0.5 x 10(3)/microL) and platelet (> or = 20 x 10(3)/microL) engraftment were 10 and 28 days, respectively. For the eight patients treated with metastatic disease, three achieved complete response and two had partial responses by day 100 after transplantation. CONCLUSION: Treatment with (131)I-MIBG in combination with myeloablative chemotherapy and hematopoietic stem-cell rescue is feasible with acceptable toxicity. Future study is warranted to examine the efficacy of this novel therapy.