Air quality criteria for lead. Grant LD, ed. Research Triangle Park, NC: U.S. Environmental Protection Agency, 2006 Oct; 1:6-88 - 6-113
Chronic Pb nephropathy is a disease characterized by tubulointerstitial nephritis, which can ultimately result in small, fibrotic kidneys. It occurs in individuals who sustain chronic highlevel Pb exposure. In these individuals, Pb exposure is the primary cause of renal failure. The pathophysiologic characteristics of Pb nephropathy and the populations at increased risk for this diagnosis were the foci of the human research portion of Section 12.5, entitled Effects of Lead on the Kidney, in the 1986 Lead AQCD. The 1986 document clearly identified several high-risk groups for this diagnosis, including children in the Queensland, Australia Pb poisoning epidemic, moonshine alcohol drinkers, and Pb workers in poorly controlled settings. The section concluded that data in the latter group indicated an increased risk for Pb nephropathy associated with blood Pb levels ranging from 40 to >100 ug/dL, with adverse renal effects possibly occurring at levels as low as 30 ug/dL. The 1986 Lead AQCD noted that research at that time was not sufficient to address some of the most critical questions relating to the impact of Pb exposure on the kidney. The last paragraph of the renal section begins with "Among the questions remaining to be answered more definitively about the effects of Pb on the kidneys is the lowest blood Pb level at which renal effects occurs." The last sentence reads "Conversely, the most difficult question of all may well be to determine the contribution of low levels of Pb exposure to renal disease of non-Pb etiologies." Advances in the research conducted since that document was written allow a much more informed discussion of exactly those critical issues. As discussed below, recent research indicates that Pb nephropathy is merely the tip of the iceberg in terms of the contribution that Pb makes to renal dysfunction overall. Research increasingly indicates that Pb, at much lower doses than those causing Pb nephropathy, acts as a cofactor with other more established renal risks to increase the risk for renal dysfunction and the rate of subsequent decline. The populations at risk for renal dysfunction (diabetics and hypertensives) are increasing worldwide, particularly in countries where obesity is epidemic. Pb exposure is declining in many industrialized countries, although less so among high-risk minority populations. The extent of the public health impact of Pb on the kidney depends on the balance of these two factors.