The humoral and cell-mediated immune responses of murine lymphocytes exposed to lead in vivo and in vitro were investigated. In vivo Pb was administered via the drinking water (0 to 10 mM) for 1 to 10 weeks. In vivo exposure of the mice to Pb did not alter significantly their plaque-forming cell response to sheep erythrocytes; however, their susceptibility to Listeria infection was reduced significantly with Pb dosages of greater than 0.4 mM. Although the in vivo plaque-forming cell responses did not appear to be altered, in vitro assessment of the reactivity of these in vivo Pb-exposed lymphocytes indicated that intermediate doses enhanced, but a high dose (10 mM) was suppressive. The 10 mM in vivo Pb dose suppressed the in vitro plaque-forming cell response, the mixed-lymphocyte culture response, and lipopolysaccharide-induced proliferation, but it did not affect concanavalin A- or phytohemagglutinin-induced proliferation. Interestingly, in vitro Pb exposure (10(-6) to 10(-4) M) of murine spleen cells caused an enhancement of most activities even though these in vitro concentrations of Pb were slightly above the in vivo concentrations. Direct in vitro Pb effects on the lymphocytes could be measured, and Pb consistently enhanced humoral and cell-mediated immunity.

In vivo and in vitro effects of lead on humoral and cell-mediated immunity.

DURING an evaluation of the Limulus lysate assay procedure1–6 for the detection of Gram negative endotoxins, deionized water was found to be contaminated with endotoxins. Endotoxins were also present in samples of New Orleans tap water, which comes from deep levels of the Mississippi River. To appreciate the environmental distribution of endotoxins, studies were undertaken to compare the Gram negative endotoxin content of New Orleans water with that of other cities, as well as endotoxin distribution in various beverages and biological fluids.

Bacterial Endotoxins in the Environment

Tissue-specific lead accumulation rates were determined in the estuarine teleost fish,Gillichthys mirabilis, as a function of four variables; sea water lead concentration, duration of exposure to lead, salinity, and temperature. Distinct tissue-specific accumulation rates were found. Spleen, gills, fins, and intestine accumulated the greatest amounts of lead; liver and muscle accumulated the least lead. Decay of lead from tissues of lead-exposed fish was observed only for gills, fins, and intestine, tissues which all possess an outer or inner covering of mucus. Our data suggest that the rapid turnover of lead in these mucus-covered tissues is a result of lead complexing with mucus and subsequent loss of lead when the mucus layer is sloughed off. In spleen and vertebrae, lead levels continued to rise in fish returned to natural (unspiked) sea water from lead-spiked sea water. The rate of lead accumulation was dependent on both the holding salinity and the temperature. Fish held at high temperature accumulated lead more rapidly than fish held at low temperature. The rate of lead accumulation was inversely proportional to the salinity of the medium. Both of these environmental effects on lead accumulation rates could be significant in estuarine habitats where lead concentrations, salinity, and temperature are all apt to vary seasonally.

Lead accumulation rates in tissues of the estuarine teleost fish, Gillichthys mirabilis: salinity and temperature effects.

Simultaneous exposure to lead and cadmium is highly probable due to common environmental sources of exposure. Mice were exposed simultaneously for 10 wk to lead and cadmium and effects were observe...

Jaime Lamberty

Papers

Ultrastructural alterations of liver and spleen following acute lead administration in rats.