Threshold lead exposure

These observations are important because the effects were detected at blood lead concentrations lower than the current 10 pg dl level of concern for lead in children (CDC, 1991, 2002 WHQ, 1995 AAP, 2005) and approaching current background concentrations. Thus, no threshold lead exposure has been established below which no effects can be expected on cognitive function and academic performance in children (CDC 1991 WHO 1995). 

Hearing thresholds in children may be affected adversely by lead exposure at low blood lead levels (Robinson et al. 1985 Schwartz and Otto 1987, 1991). Robinson et al. (1985) reported that hearing thresholds increased linearly with maximum historical PbB levels of 6.2-56.0 pg/dL. In the analyses by Schwartz and Otto (1987, 1991), the probability of lead levels studied (NHANES II and HHANES data, respectively), from <4 to >50 pg/dL, with no apparent threshold. There is also some evidence suggesting that lead exposure may cause postural disequilibrium in children (Bhattacharya et al. 1993). The children evaluated in that study had a geometric mean PbB for the first 5 years of life of 11.9 pg/dL, the range was 5.1 to 28.2 pg/dL. 

People with Neurologic Dysfunction or Kidney Disease. This population is unusually susceptible to lead exposure. The neurologic and renal systems are the primary target organs of lead intoxication, which may become overburdened at much lower threshold concentrations to elicit manifestations of lead intoxication (Benetou-Marantidou et al. 1988 Chisolm 1962, 1968 Lilis et al. 1968 Pollock and Ibels 1986). 

Schwartz J. 1994. Low-level lead exposure and children s IQ A meta-analysis and search for a threshold. Environ Res 65 42-55. 

Endpoint/Concentration/Rationale 15 ppm for 1 h induced a significant decrease in hematocrit levels that may be approaching a degree of hemolysis that can lead to renal failure. Given the steepness of the dose-response relationship this is justified as an estimate of the lethality threshold. An exposure of 26 ppm for 1 h resulted in 100% lethality. 

Guitart, R., J. To-Figueras, R. Mateo, A. Bertolero, S. Cerradelo, and A. Martinez-Vilalta. 1994. Lead poisoning in waterfowl from the Ebro Delta, Spain calculation of lead exposure threshold for mallards. Arch. Environ. Contam. Toxicol. 27 289-293. 

Non-thresholded chemicals that are not carcinogens are less frequently identified. For many years lead was considered to be thresholded because its effects on haemoglobin synthesis were not seen at low doses. However, recent work into the effects of lead on mental development suggest that there may be no threshold for this end-point. Food is a relatively minor source of lead exposure compared with air and dust in urban environments. For chemicals that relate to toxicological end-points that do not show thresholds it is not possible to identify a NOAEL or PTWI. In such cases it is desirable to estimate the level of risk associated with a given level of exposure. 

Royce SE, Needleman HL Lead toxicity, in Environmental Medicine Integrating a Missing Element Into Medical Education. Edited by Pope AM, Rail DP. Washington, DC, National Academy Press, 1995, pp 410-435 Schaffer SJ, Campbell JR The new CDC and AAP lead poisoning prevention recommendations consensus versus controversy. Pediatr Ann 23 592-599, 1994 Schwartz BS, Stewart WF, Bolla KI., et al Past adult lead exposure is associated with longitudinal decline in cognitive function. Neurology 55 1144-1150, 2000 Schwartz J Low-level lead exposure and children s IQ a meta-analysis and search for a threshold. Environ Res 65 42-55, 1994... 

Schwartz J, Otto D Blood lead, hearing thresholds, and neurobehavioral development in children and youth. Arch Environ Health 42 153-160, 1987 Sciarillo WG, Alexander G, Farrell KP Lead exposure and child behavior. Am J Public Health 82 1356-1360, 1992... 

Heavy metal content of ayurvedic herbal medicine products. JAMA 292 2868-2873 Saryan, L.A. and C. Zenz. (1994) Ixad and its compounds. In Occupational Medicine (third edition). L.A. Saryan and C. Zenz (editors), Mosby, St. Louis, pp. 506—541 Schwartz, J. (1994) Low-level lead exposure and children s IQ A meta-analysis and semch for a threshold. Environ. Res. 65 42-55... 

Some of the questions posed by Lin Fu in 1973 remain unanswered today. These include (a) the suitability of blood lead as an indicator of exposure, (b) normal blood levels and the possibility of a lead threshold, i.e. a safe level of lead exposure and absorption, (c) the effects of low level lead and, if any, their clinical manifestations and (d) the distinction between lead absorption in symptomatic and asymptomatic individuals. The first of these questions has been partially answered. Although blood lead measurements reflect a compromise between accuracy and convenience, despite obvious limitations, they still remain a reliable means of assessing recent absorption. The other questions remain problematic. 

If the model user seeks predictive estimates within a rather broad range and/or is using predictive data as but one element in a large cluster of criteria for risk assessment or risk management of a site, such as a hazardous waste site, the required level of agreement between empirical data and model outputs may not dictate very close concordance. If predictive data are being sought for some finite threshold value in permissible lead exposure or some... 

Communities where increased environmental lead exposures and various toxic endpoints have been explicitly incorporated into a dose—response framework currently highlight health risk characterization using case-specific evidence. Data generated in such communities typically first permit determination of distributions of risk group PbB values, specifically prevalences and incidences of PbB above an accepted health risk threshold. These PbB statistics are then incorporated into health risks using dose—toxic response relationships. 

There are several ways one can quantify human health risk characterization for humans at risk through lead exposure. The first and simplest examines the prevalences or incidences of blood lead levels above some health risk threshold, with frequencies of exceedance identifying those at more risk (compared to those with PbB values below the risk threshold). Expressions of health risk in terms of elevated PbB occurrences (e.g., 10 jig/dl) do not simultaneously provide quantitative estimates of organ- or system-specific toxic harm, such as actual loss of IQ points or increases in SBP or DBP. A health risk threshold indexed in terms of a PbB level, however, represents the synthesis of numerous empirical dose—toxic response relationships, as developed and discussed in previous chapters. 

Estimations of exposure frequencies above some health risk threshold in terms of PbB can be done using empirical data or through lead exposure modeling approaches, such as the U.S. EPA lEUBK model for childhood lead exposure simulations. Both approaches have their advantages and limitations, and a comparative look at the topic was provided by Mushak (1998). 

The flash ERG has proven to be a sensitive indicator of retinal neurotoxicity due to adult and developmental low-level lead exposure in rats. Lead exposure decreased the amplitude of the a- and b-wave components of tl ERG and increased latency (Fox, et. al., 1991 Fox and Rubenstein, 1989 Fox and Farber, 1988). ERG studies have also demonstrated a change in increment thresholds and the rate of recovery of dark adaptation with lead (Fox and Katz, 1992). Changes in the a- and b-wave amplitudes have also been noted in rats dosed with methyl mercury (Gitter, et. al., 1988 Gramoni, 1980 ). 

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