Gruber H E, Gonick H C, Khalil-Manesh F, Sanchez T V, Motsinger S, Meyer M, Sharp C F
Department of Orthopaedic Surgery, Carolinas Medical Center, Charlotte, NC 28232-2861, USA.
Miner Electrolyte Metab. 1997;23(2):65-73.
The skeleton, the major site for Pb accumulation, is responsible for the largest fraction of the total body burden, but long-term effects of low-level exposure in adults remain unclear. In this study rats were exposed to low (0.01%; 100 ppm, LoPb) or high (0.5%, 5,000 ppm, HiPb) Pb, low calcium, feeding regimes for 1-12 months. Both LoPb and HiPb animals showed significant 12-month blood Pb levels [LoPb 21 +/- 3 micrograms/dl; HiPb 59 +/- 18; controls 3 +/- 1 (mean +/- SEM), p = 0.001]. Dual energy X-ray densitometry of the femur detected a significant decrease in bone density in HiPb animals by 3 months which remained significantly lowered through 12 months [3 months: HiPb: 0.498 +/- 0.011 (6) vs. control: 0.546 +/- 0.012 (6), p < 0.003]. By 12 months' density was also significantly lowered in LoPb animals (p = 0.001). Mineral analyses of ashed femurs showed a significant lead content after 1, 3, 9 and 12 months' exposure [1 month: LoPb, 0.020 +/- 0.002 (4) (% ash weight) vs control 0.008 +/- 0.0004 (4); HiPb 0.016 +/- 0.001 (8); control 0.007 +/- 0.0004 (6) (p < or = 0.002)]. Ca levels (% ash weight) were significantly lowered at 9 months in HiPb and 12 months in both groups (p < or = 0.04). Quantitative histomorphometry documented significantly elevated osteoid and resorptive trabecular surface features in both Pb groups. The LoPb design produced no overt renal functional abnormalities and resulted in blood Pb values comparable to those in man with modest environmental Pb exposure. The HiPb design resulted in development of lead nephropathy (more severe from months 6-12) and produced blood lead levels comparable to those seen in past industrial exposure. Findings show that Pb is incorporated into bone mineral after only 1 month's exposure to LoPb with significant osteopenia after 12 months' exposure; HiPb caused osteopenia by 3 months. No normal compensatory mechanism was elicited to maintain bone mass. Results stress renewed concern about the effects of cumulative, low-level lead exposure in our elderly population.
骨骼是铅蓄积的主要部位，占全身铅负荷的最大部分，但成人低水平铅暴露的长期影响仍不清楚。在本研究中，将大鼠暴露于低剂量（0.01%；100 ppm，低铅组）或高剂量（0.5%，5000 ppm，高铅组）的铅、低钙饮食环境中1至12个月。低铅组和高铅组动物在12个月时血铅水平均显著升高[低铅组：21±3微克/分升；高铅组：59±18；对照组：3±1（均值±标准误），p = 0.001]。对股骨进行双能X线骨密度检测发现，高铅组动物在3个月时骨密度显著下降，且在12个月内一直保持显著降低[3个月时：高铅组：0.49·8±0.011（6），对照组：0.546±0.012（6），p < 0.003]。到12个月时，低铅组动物的骨密度也显著降低（p = 0.001）。对股骨骨灰进行矿物质分析显示，在暴露1、3、9和12个月后铅含量显著升高[1个月时：低铅组，0.020±0.002（4）（占骨灰重量百分比），对照组：0.008±0.0004（4）；高铅组：0.016±0.001（8）；对照组：0.007±0.0004（6）（p≤0.002）]。高铅组在第9个月时钙含量（占骨灰重量百分比）显著降低，两组在第12个月时钙含量均显著降低（p≤0.04）。定量组织形态计量学记录显示两组铅暴露动物的类骨质和吸收性小梁表面特征均显著升高。低铅组实验未产生明显的肾功能异常，其血铅值与环境铅暴露适度的人类相当。高铅组实验导致铅肾病的发生（6至12个月时更严重），其血铅水平与过去工业暴露时所见相当。研究结果表明，低铅组动物仅暴露1个月后铅就会掺入骨矿物质中，暴露12个月后出现明显的骨质减少；高铅组在3个月时就导致了骨质减少。未引发正常的代偿机制来维持骨量。研究结果再次强调了对老年人群累积低水平铅暴露影响的担忧。
