PBBs poisoning

The poisoning of the CjHg oxidation by PbB, and the permanent reactivation of a poisoned catalyst by exposure to SO2 and air was also observed in the IR experiments (see Table 2). STEM and EDX examination of the PbB poisoned 1 wt.% Pt/A Oj sample following calcination in air at 500°C revealed three types of Pb species (Figure 3) ... 

An increase in urinary coproporphyrin has long been recognized in workers and children with lead poisoning and used as an indicator of excessive exposure to lead (EPA 1986a). EPA (1986a) identified a LOAEL for elevated coproporphyrin at a PbB level of 40 pg/dL for adults and 35 pg/dL for children, but did not present the basis for this conclusion. 

In a study of 102 cases of occupational lead poisoning, 17 cases of clinically verified chronic nephropathy were found (Lilis et al. 1968). Endogenous creatinine clearance was <80 pg/dL. The mean PbB level for the entire study population was 80 pg/dL (range, 42-141 pg/dL). Nephropathy was more common among those exposed to lead for more than 10 years than among those exposed for less than 10 years. 

Full Fanconi syndrome has been reported to be present in some children with lead encephalopathy (Chisolm 1968 Chisolm et al. 1955). According to the National Academy of Sciences (NAS 1972), the Fanconi syndrome is estimated to occur in approximately one out of three children with encephalopathy and PbB levels of approximately 150 pg/dL. Aminoaciduria occurs at PbB levels >80 pg/dL in children with acute symptomatic lead poisoning (Chisolm 1962). The aminoaciduria and symptoms of lead toxicity disappeared after treatment with chelating agents (Chisolm 1962). 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Adverse effects on the thyroid have not been observed in children, however. In a study of inner-city children, linear regression analysis revealed that there was no association between PbB levels and either thyroxin or free thyroxin (Siegel et al. 1989). Similar findings were reported by Huseman et al. (1992) in a group of 12 children from the Omaha Lead and Poison Prevention Program with PbB levels in the range of 41 to 72 pg/dL. Siegel et al. (1989) offered four possible explanations to account for this apparent... 

Therefore, in spite of remarkably increased liver injury, the animals are able to overcome injury and survive the potentiated liver toxicity (Kodavanti et al. 1992 Mehendale 1990, 1991, 1992). DDT increased the sensitivity of rats to carbon tetrachloride poisoning (McLean and McLean 1966), and mice fed 100 ppm polybrominated biphenyls (PBBs) or 200 ppm polychlorinated biphenyls (RGBs) in their diet for 28 days experienced increased carbon tetrachloride hepatotoxicity (Kluwe et al. 1979). Potentiation of renal dysfunction was also found in the PBB-pretreated mice. All of these compounds are broad-spectrum MFO inducers. 

This section will describe clinical practice and research concerning methods for reducing toxic effects of exposure to PBBs and PBDEs. However, because some of the treatments discussed may be experimental and unproven, this section should not be used as a guide for treatment of exposures to PBBs and PBDEs. When specific exposures have occurred, poison control centers and medical toxicologists should be consulted for medical advice. No texts were found that provided specific information about treatment following exposures to PBBs and PBDEs. 

The polybrominated biphenyl (PBB) analogs of PCBs were the cause of massive livestock poisoning in Michigan in 1973 because of the addition of PBB flame retardant to livestock feed during its formulation. 

Phosphoric Acid Phosphorus Photoallergens Photochemical Oxidants Phthalate Ester Plasticizers Physical Hazards Picloram Picric Acid Piperazine Piperonyl Butoxide "Plants, Poisonous" Platinum (Pt) Plutonium (Pu) Poinsettia Poisoning Emergencies in Humans Pokeweed Pollutant Release and Transfer Registries (PRTRs) Pollution Prevention Act "Pollution, Air" "Pollution, Air Indoor" "Pollution, Soil" "Pollution, Water" Polybrominated Biphenyls (PBBs) Polybrominated Diphenyl Ethers (PBDEs) Polychlorinated Biphenyls (PCBs)... 

The results obtained with the engine-aged, laboratory PbB -aged, and model catalysts all clearly indicate that Pb-poisoned Pt/A Oj catalysts can be reactivated by S02. The model experiments indicate that the reactivation mechanism involves the formation of PbSO, which removes Pb from the Pt. Additional evidence for this mechanism is found in the CO adsorption experiments, described in the next section. 

The determination of PbB is of prime importance with respect to the diagnosis of lead poisoning and to the assessment of hazardous conditions both in occupationally exposed people and in the general population. It is generally agreed that the concentrations of lead in air. food and water are less relevant for assessing health hazards for humans than the amount of lead actually absorbed and this is what actually is reflected by PbB (WHO, 1977, 1980). 

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