Lead toxicity manifestations

Frape, D.L. and J.D. Pringle. 1984. Toxic manifestations in a dairy herd consuming haylage contaminated by lead. Vet. Rec. 114 615-616. 

This is a widely used antiepileptic drug, which occasionally causes liver dysfunction. There are two types of dysfunction, the first type is a mild transient elevation of the transaminases (ALT, AST), which resolves the second type is of a more severe hepa to toxicity, manifested as fatty liver with jaundice and necrosis, which may lead to fatal liver failure. 

A report from the European literature describes the findings in a 19-year-old woman who committed suicide by taking 40 Letigen tablets (200 mg of caffeine and 20 mg of ephedrine) amounting to 10 g of caffeine and 1 g of ephedrine. She developed severe toxic manifestations from the heart, CNS, muscles, liver, and kidneys leading to several cardiac arrests, and died subsequently of cerebral edema and incarceration on the fourth day of hospitalization. Postmortem blood concentrations were not given (134). 

Nondietary sources of cyanide include sodium nitro-prusside (a hypotensive agent), succinonitrile (an antidepressant agent), acrylonitrile (used in the plastic industry and as a fumigant to kill dry-wood termites), and tobacco smoke. Chronic exposure to cyanogenic compounds leads to toxic manifestations such as demyelination, lesions of the optic nerves, ataxia (failure of muscle coordination), and depressed thyroid functions. This last effect arises from accumulation of thiocyanate, the detoxified product of cyanide in the body (see below). Thiocyanate inhibits the active uptake of iodide by the thyroid gland and, therefore, the formation of thyroid hormones (Chapter 33). 

FIGURE 65-2 Manifestations of lead toxicity associated with varying concentrations of lead in blood of children and adults, 8-ALA = 5-aminolevulinate. 

Initial interest in lead intoxication as a clinical phenomenon was focussed on encephalopathy and the gross neuropathological changes that can be ascribed to lead exposure only more recently have the less obvious consequences, like behavioural effects and their possible basis, been studied in depth. Attention has been focussed on children as the group most at risk from lead intoxication. As they appear to be more sensitive than adults with respect to the more obvious manifestations of lead toxicity, the same has been presumed to be true for more subtle effects. 

However, careful attention must be given to calibration and quality control procedures. Limited data on blood lead-ZPP correlations and the ZPP levels which are associated with the adverse health effects discussed in Section 2 are the major limitations of the test. Also it is difficult to correlate ZPP levels with environmental exposure and there is some variation of response with age and sex. Nevertheless, the ZPP promises to be an important diagnostic test for the early detection of lead toxicity and its value will increase as more data is collected regarding its relationship to other manifestations of lead poisoning. 

Excessive retinol intake by animals and humans produces distinct toxic manifestations, as discussed in other chapters (Chapter 6, Vol. 1 Chapter 13, Vol. 2). Considerable information is available about the mechanism of the toxic effects of vitamin A on tissues..Studies both in vivo and in vitro have shown that excess retinol results in increased lability of biological membranes (Roels et al., 1969 Fell, 1970). This effect of retinol is believed to be due to its surface-active membranolytic properties (Bangham et al., 1964). In particular, excess retinol has been shown to lead to increased synthesis and release of lysosomal enzymes, and these hydrolases have been shown to be critically involved in the effects of vitamin A on cartilage and limb-bone rudiments (Fell, 1970 Fell and Dingle, 1963 Dingle e/a/., 1971). 

Within the control limits, increased intakes of vitamin D lead to increased blood levels of 25-OHD but not of l,25-(OH)2D and homeostasis is maintained. However, at higher dietary levels of vitamin D, toxic manifestations of hypercalcaemia become increasingly evident with deformation of bone and even calcification of soft tissues. Thus vitamin D is toxic at dietary levels which overload the control processes. 

In humans, acute intoxieation by PAHs is related with expositions to concentrations around 100 to 200 ppm. These eoneentrations promote nonspeeifie elinic signs and symptoms such as dizziness, nausea, headaches and difficulties in the motor coordination, by the action of these substanees in the nervous system. Chronis effects can lead to toxic manifestations in several organs and systems, mainly, hematopoietic, renal, hepatic and nervous (Pedrozo et al., 2002). The effeets of the B[a]P inhalation by humans result in patch opacities, prominent bronchiovascular markings and pleural effusions, besides vomits with blood, problems in the respiration, pain and irritation on the chest, irritation in the throat and cough (Gupta et al. 1993). 

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