Chronic exposure to lead

Reiter LW, Anderson GE, Laskey JW, et al. 1975. Developmental and behavioral changes in the rat during chronic exposure to lead. Environ Health Perspect 12 119-123. 

Borgmann, U., 0. Kramar, and C. Loveridge. 1978. Rates of mortality, growth, and biomass production of Lymnaea palustris during chronic exposure to lead. Jour. Fish. Res. Board Canad. 35 1109-1115. 

Nation, J.R., D.E. Clark, A.E. Bourgeois, and J.K. Rogers. 1982. Conditioned suppression in the adult rat following chronic exposure to lead. Toxicol. Lett. 14 63-67. 

Acute exposure to inorganic lead can cause reversible damage to the kidneys, manifested as tubular dysfunction. Chronic exposure to lead, however, causes permanent interstitial nephropathy, which involves tubular cell atrophy, pathological changes in the vasculature, and fibrosis. The most pronounced changes occur in the proximal tubules. Indeed, lead-protein complexes are seen as inclusion bodies in tubular cells, and the mitochondria in such cells have been shown to be altered with impaired oxidative phosphorylation. Clearly, this will influence the function of the proximal tubular cells in reabsorption and secretion of solutes and metabolites. Consequently, one indication of renal dysfunction is amino aciduria, glycosuria, and impairment of sodium reabsorption. 

Chronic exposures to lead by inhalation or the oral route cause adverse effects that include damage to the peripheral and central nervous system, anemia, and chronic kidney damage. Lead accumulates in the soft tissues and bones, with the highest accumulation in the liver and kidneys, and elimination is slow. Lead has shown developmental and reproductive toxicity in both male and female... 

Both acute and chronic exposure to lead became more common with the advent of the Industrial Revolution and there were as many as a thousand cases per year of lead poisoning in the UK at the end of the nineteenth century. During the nineteenth century there were also many cases of lead poisoning due to contamination of domestic drinking water in areas such as the north of England where slightly acidic water was delivered to houses in lead pipes. Lead was also used in fungicides in the form of lead arsenate. 

Eels LM, C. Herbort C, Pergande M, Jung K, Hotter G, Rosello J, Gelpi E, Mutti A, De Broe M, Stolte H. Nephron target sites in chronic exposure to lead Nephrol Dial Transplant. 1994 9 1740-1746. 

Fiedler, N., WelsefC., Lynch, R., Kelly-McNeil, K.,Wedeen, R., Jones, K., Udasin, L, Ohman-Strickland, P.,and Gochfeld, M.Cognitive effects of chronic exposure to lead and solvents. Am. J. Indust. Med. 2003 4 413-423. 

Chronic exposure to low levels of lead results in lead accumulation within the body. Workers who have been chronically exposed to lead develop interstitial fibrosis, vascular and glomerular sclerosis, and tubular atrophy and/or hypertrophy. Although acute lead nephropathy is reversible with chelator therapy and/or removal from exposure, chronic effects may be irreversible. In addition, chronic exposure to lead may result in a gouty nephropathy as lead reduces uric acid excretion and elevates blood uric acid levels. 

Pergande M, Jung K, Precht S, Eels LM, Herbort C, Stolte H. Changed excretion of urinary proteins and enzymes by chronic exposure to lead. Nephrol Dial Transplant 1994 9 613-8. 

Although the Consumer Product Safety Commission (CPSC) banned the residential use of lead-based paint in 1978, millions of children remain at risk for exposure to lead from deteriorating paint in older homes. Lead poisoning is especially harmful to children under the age of 5 years because it interferes with growth and development and it has been shown to lower IQ. Symptoms of chronic exposure to lead include diminished appetite, nausea, malaise, and convulsions. Blood lead level fBLL), expressed as micrograms per deciliter (p.g/dL), is used to monitor the effect of chronic exposure. A BLL < 10 p.g/dL is considered normal a BLL > 45 xg/dL requires medical and environmental intervention. At high levels (>70 p.g/dL), lead can cause seizures, coma, and death. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

The nonvisual or subtle effects of air pollutants involve reduced plant growth and alteration of physiological and biochemical processes, as well as changes in the reproductive cycle. Reduction in crop yield can occur without the presence of visible symptoms. This type of injury is often related to low-level, long-term chronic exposure to air pollution. Studies have shown that field plantings exposed to filtered and unfiltered ambient air have produced different yields when no visible symptoms were present (5). Reduction in total biomass can lead to economic loss for forage crops or hay. 

Beeause the diisoeyanate is used in exeess, there is usually free monomer present. Isoeyanates are hazardous materials particularly upon inhalation and skin contact. Chronic exposure ean lead to sensitization. The adhesives must therefore be used with proper ventilation and should not come in eontact with the skin in the unreaeted state. Vapor monitoring badges for employees and periodie real time vapor monitoring around process equipment is reeommended. 

At one time, benzene was widely used as a solvent, both commercially and in research and teaching laboratories. Its use for that purpose has largely been abandoned because of its toxicity. Chronic exposure to benzene vapor leads to various blood disorders and, in extreme cases,... 

The first case is based on a hypothetical stream receiving a metal-poUuted source (for instance the outlet of a metal factory). In this case, metal concentration is expected to be driven by dilution, being higher under low-flow than under base-flow conditions and minimum during floods. Metal accumulation is expected to be maximum under low-flow conditions and proportional to the duration of this water scarcity situation. Chronic exposure will lead to community adaptation, which is often related to changes in species composition. Metals will therefore be bioaccumulated in fluvial biofihns and transferred to higher trophic levels in the fluvial food web. 

Acute exposure to cadmium may lead to chemical pneumonitis and edema, but is rare nowadays (Herber 1994b). Chronic exposure to Cd affects mostly the renal tubules and the lung. Exposure to Cd can take place both in the occupational and environmental area. 

PbB concentrations reflect the absorbed dose of lead. However, the interpretation of PbB data depends on a knowledge of the past history of exposure to lead. This is because in the body, bone constitutes the major lead sink and this results in lead having a long body half-life. Thus, in the absence of intense exposure to lead for a considerable period up to its body half-life, the PbB concentrations reflect recent lead exposures. However, if intermittent exposure to lead is occurring in several distinct environments, the PbB concentration reflects both recent and past exposures to lead. Thus, biological effects for populations with the same PbB concentrations may not be the same since different exposure times scales may be involved. This is the reason why free erythrocyte protoporphyrin (FEP) and erythrocyte zinc protoporphyrin (ZPP) have been used as additional biological markers since their elevation is more related to chronic lead exposure than acute lead exposure (see Section 2.7). 

Renal Effects. Exposure to lead that results in PbB ranging from approximately 60 to >100 pg/dL has been associated with nephropathy in some studies of lead-exposed workers (e.g., Chia et al. 1995a). The characteristics of early or acute lead-induced nephropathy in humans include nuclear inclusion bodies, mitochondrial changes, and cytomegaly of the proximal tubular epithelial cells dysfunction of the proximal tubules (Fanconi s syndrome) manifested as aminoaciduria, glucosuria, and phosphaturia with hypophosphatemia and increased sodium and decreased uric acid excretion. These effects appear to be reversible. Characteristics of chronic lead nephropathy include progressive interstitial fibrosis, dilation of tubules and atrophy or hyperplasia of the tubular epithelial cells, few or no nuclear inclusion bodies,... 

Iannaccone A. Carmignani M, Boscolo P. 1981. [Cardiovascular reactivity in the rat following chronic exposure to cadmium and lead.] Ann 1st Super Sanita 17 655-660. (Italian)... 

Kimber I, Stonard MD, Gidlow DA, et al. 1986b. Influence of chronic low- level exposure to lead on plasma immunoglobin concentration and cellular immune function in man. Int Arch Occup Environ Health 57 117-125. 

Chronic exposure to Pb has been shown to cause anaemia, neurotoxic effects, such as reduced cognitive performance and reduced peripheral nerve conduction velocity, and nephrotoxicity. Children are more sensitive to exposure to Pb than adults, especially during the first 2 years of life [41], For children, exposure to lead can cause growth retardation, affect the neuropsychological development and cause encephalopathy [39]. Adverse reproductive effects due to lead exposure have been observed for both men and women. Exposure of pregnant women to low concentrations of lead is associated with miscarriages and low birth weights [40],... 

Janssens de Bisthoven, L., A. Vermeulen, and F. Ollevier. 1998. Experimental induction of morphological deformities in Chironomus riparius larvae by chronic exposure to copper and lead. Arch. Environ. Contam. Toxicol. 35 249-256. 

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