Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation

The potential adverse effects of hazardous waste incinerators (HWI) continue to be a subject of worry. The construction of the first and up till now only HWI in Spain finished in 1999. Twenty-six subjects employed at this HWI were divided into three groups: plant, laboratory and administration. Plasma analyses of HCB, PCBs (28, 52, 101, 138, 153 and 180), and PCDD/Fs, as well as urinary analyses of 2,4- and 2,5-dichlorophenol (DCPs), 2,4,5- and 2,4,6-trichlorophenol (TCPs), pentachlorophenol (PCP), and 1-hydroxypyrene (1-HP) were carried out. Blood concentrations of Be, Mn, Hg and Pb, and urinary levels of Cd, Cr, Ni and V were also determined. In plant workers, the current levels of organic substances and metals in blood and urine did not show any increase for any of the compounds analysed (excepting urinary V). By contrast, plasma levels of PCDD/Fs and PCBs 28, 52, 101, 138 and 153 were significantly lower than the respective baseline concentrations. The current chlorophenol concentrations in urine were similar or lower than the baseline levels, with the exception of 2,5-DCP that showed a significant increase. The concentrations of organic and inorganic substances found in this study do not differ from those corresponding to non-occupationally exposed subjects.     

EXPERIMENTAL GLOMERULONEPHRITIS : THE PATHOGENESIS OF A LABORATORY MODEL RESEMBLING THE SPECTRUM OF HUMAN GLOMERULONEPHRITIS

Daily injections of any one of several foreign serum proteins produced in rabbits functional and morphological alterations similar to those seen in acute, subacute, and chronic human glomerulonephritis. The critical factor determining whether a rabbit would develop renal disease and the type of disease developed was the amount of antibody the rabbit formed. Those responding with much antibody were likely to develop an acute, self-limited glomerulonephritis and to be subsequently immune to further renal damage. Those responding with antibody barely sufficient to neutralize the antigen injected developed subacute and chronic glomerulonephritis. In the circulation of the rabbits with chronic glomerulonephritis, there was a daily recurring antigen-antibody reaction in the region of near antigen excess to near antibody excess which presumably led to the disease. Antigen apparently in the form of antigen-antibody complexes was deposited along the renal capillary basement membranes coincident with the development of subacute and chronic glomerulonephritis. Once developed, the morphologic stigmata of chronic glomerulonephritis persisted even after injections of antigen were stopped. However, in milder instances the renal function recovered in part after stopping antigen. This experimental model has several implications: first, the renal injury is precipitated by antigens with no known affinity for, or immunologic relationship to, kidney; second, antigen antibody complexes localize in the kidney, apparently on the basis of non-immunologic factors, and may be an etiologic agent of renal injury; third, severe hypersensitivity disorders can be related specifically to relatively poor as well as to good antibody responses; and finally, the pathogenesis suggested here offers an alternative to that of nephrotoxic serum nephritis for the experimental approach to the study of human glomerulonephritis.