Blood lead levels and major depressive disorder, panic disorder, and generalized Relationship of Bone and Blood Lead Levels to Psychiatric Symptoms: The. Psychiatric manifestations may include increased depression, anxiety, and irritability. Lead in the body is measured with both blood and bone levels. . been noted, with results suggesting a dose-dependent relationship. Lead poisoning is a type of metal poisoning caused by lead in the body. The brain is the most . At blood lead levels between 25 and 60 μg/dL, neuropsychiatric effects such as . A fetus may be poisoned in utero if lead from the mother's bones is There is apparently no lower threshold to the dose- response relationship.
Residual lead in soil contributes to lead exposure in urban areas. However, this is not always the case, as there are several other reasons for lead contamination in soil. The city of Madison, Wisconsin addressed the issue and replaced all of their piping, but there are still others that have yet to follow suit.
While there are chemical methods that could help reduce the amount of lead in the water distributed, the sure fix would be replacing the pipes completely. Experts say that if the city were to replace their pipes and the citizens were to keep the old pipes located in their homes, there would be a potential for more lead to flow into their drinking water. The ultimate goal is for a total overhaul to take place, but this would require the citizens to buy into the pipe replacement.
Such a move would allow the preservation of present health and secure greater health for the future. Ceramic glaze often contains lead, and dishes that have been improperly fired can leach the metal into food, potentially causing severe poisoning.
BioMed Research International
Bullets[ edit ] Contact with ammunition is a source of lead exposure. As oflead-based ammunition production is the second largest annual use of lead in the US, accounting for over 84, metric tons consumed in Because game animals can be shot using lead bullets, the potential for lead ingestion from game meat consumption has been studied clinically and epidemiologically. In a recent study conducted by the CDC,  a cohort from North Dakota was enrolled and asked to self-report historical consumption of game meat, and participation in other activities that could cause lead exposure.
The study found that participants' age, sex, housing age, current hobbies with potential for lead exposure, and game consumption were all associated with blood lead level PbB. According to a study published in1. However, the biggest impediment to using the vast majority of alternatives relates to current laws in the United States pertaining to armor-piercing rounds.
Laws and regulations relating to armor-piercing ammunition expressly prohibit the use of brass, bronze, steel, tungsten, and nearly every metallic alternative in any bullet that can be shot by a handgun, which at this time is nearly every caliber smaller than 50BMG including the popular.
Some lead-based bullets are resistant to fragmentation, offering hunters the ability to clean game animals with negligible risk of including lead fragments in prepared meat. Other bullets are prone to fragmentation and exacerbate the risk of lead ingestion from prepared meat. In practice, use of a non-fragmenting bullet and proper cleaning of the game animal's wound can eliminate the risk of lead ingestion from eating game;  however, isolating such practice to experimentally determine its association with blood lead levels in study is difficult.
Bismuth is an element used as a lead-replacement for shotgun pellets used in waterfowl hunting although shotshells made from bismuth are nearly ten times the cost of lead. Pathophysiology[ edit ] Tetraethylleadstill used as an additive in some fuels, can be absorbed through the skin. Pathophysiology Plumbum Pba chemical element in the carbon group otherwise known as lead, is a soft and malleable metal, which is considered a heavy metal.
The remaining lead binds to red blood cells, is distributed throughout the soft tissues of the body, and eventually accumulates in bone.
Pb Neurotoxicity: Neuropsychological Effects of Lead Toxicity
The half-life of bone-deposited lead ranges from 20 to 30 years. Turnover of bone tissue releases lead back into the bloodstream, and such processes as pregnancy, menopause, or lactation may increase blood lead levels by speeding bone tissue turnover.
Lead in the body is measured with both blood and bone levels. Blood lead levels are more reflective of acute exposure, whereas bone lead levels better reflect cumulative exposure over time [ 5 ].
The presence of lead in the human body causes damage to the nervous system through several mechanisms. Direct effects on the nervous system may be classified as either morphological or pharmacological [ 6 ]. Morphological effects alter the development of the nervous system, particularly from the prenatal period through childhood.
Such effects include disruption of key molecules during neuronal migration and differentiation [ 7 ]; interference with synapse formation, mediated by a reduction in neuronal sialic acid production [ 8 ]; and premature differentiation of glial cells [ 9 ]. Pharmacological effects result from the action of lead as a pharmacological agent in the CNS. Lead substitutes for calcium and, to a lesser extent, zinc and inappropriately triggers processes reliant on calmodulin [ 10 ].
Lead also interferes with neurotransmitter release, disrupting the function of GABAergic, dopaminergic, and cholinergic systems as well as inhibiting NMDA-ion channels during the neonatal period [ 1112 ]. Within the cell, lead appears to interfere with calcium release from the mitochondria [ 14 ], resulting in formation of reactive oxygen species, speeding mitochondrial self-destruction through formation of the permeability transition pore, and priming activation of programmed cell death processes [ 15 ].
Indirect effects on the nervous system result from interference with other body systems that support nervous system function. Lead exposure has been found to increase risk of numerous conditions that may have adverse effects on nervous system function, including hypertension, impaired renal function, impaired thyroid function, vitamin D deficiency, and preterm birth [ 5 ].
There has been some debate as to whether lead exposure affects peripheral nerve conduction velocity, with some reviews concluding a lack of toxic effect [ 16 ] and others finding significant population-based changes [ 17 ]. The literature appears, at best, to support consistent subclinical lead effects on nerve conduction velocity [ 18 ].
The most severe neurological effect of lead exposure is lead encephalopathy [ 19 ], a response to very high doses of lead that results in development of irritability, headache, mental dullness and attention difficulty, memory loss, tremor, and hallucinations within weeks of exposure.
Symptoms abruptly worsen to paralysis, convulsions, delirium, coma, or death. Children may develop lead encephalopathy at lower doses of lead than adults. Postmortem pathological findings include edema, capillary disruption, proliferation of glia, and diffuse anoxic injury [ 17 ]. Etiology Acute high-dose exposure to lead is not the only source of lead-based neurotoxicity.
Acute low-dose exposure also appears to produce measurable, if less dramatic, effects on nervous system function.
Chronic exposure to environmental lead also has measurable effects on the nervous system due to the propensity for lead to accumulate in the bone over time. For instance, in an MRI study of former lead workers, high tibia lead was associated with reduced total brain volume, lower volume of gray matter in the insula and cingulum, and diminished white matter volume in the parietal lobes [ 23 ]. Historically, the main sources of lead exposure were leaded gasoline, lead-based paint and plumbing, and solders used in food packaging.
Leaded gasoline was thoroughly phased out of use by and is no longer a means of exposure. Similarly, lead solder in food cans was banned by the FDA in Lead plumbing still exists in buildings erected beforeand lead paint, though banned in the United States inis still found in some older buildings.
These two latter sources perhaps explain the frequent association of lead exposure with low socioeconomic status [ 52425 ]. Some evidence suggests that effects of chronic exposure may persist long after exposure has ended, which is further discussed in Section 4 of this paper.
Prenatal exposure presents an additional risk for lead neurotoxicity. Maternal exposure to lead and overall maternal body burden of lead are closely associated with lead levels in the fetus, likely because lead appears to cross the placenta freely and because pregnancy increases systemic demand for calcium, resulting in higher bone turnover and consequent lead release into the bloodstream [ 2627 ].
Animal studies of brain lead content have demonstrated that the blood-brain barrier is particularly ineffective against lead in the prenatal stage, becoming more effective during weaning and even more so after weaning [ 2829 ]. Poor nutrition appears to increase risk of toxic effects of lead when exposure is held constant. Deficiencies in calcium, iron, and zinc have been specifically identified as risk factors. Calcium deficiency appears to increase both retention of lead and the severity of its toxic effects [ 30 ].
Low intake of dietary iron has similar effects and is perhaps more important because of relatively high risk of iron deficiency in childhood [ 3132 ]. At least one large-scale longitudinal study has shown that iron deficiency worsens the effects of lead exposure on neurobehavioral measures and blood cell production in infants, children, and pregnant women [ 33 ]. Zinc deficiency appears to result in a vicious cycle in that it increases lead absorption, which in turn increases zinc excretion [ 34 ].
The role of nutrition perhaps accounts for the finding that low socioeconomic status increases risk for persistence of cognitive deficits after prenatal lead exposure [ 35 — 37 ]. Moreover, the distribution of blood lead levels among children exhibited a shift toward lower levels; the majority of US children are no longer in the range of concern for risk of toxicity [ 24 ]. These results suggest that public health reforms targeting lead exposure were largely successful. Inner-city poor children are at the highest risk, presumably due to the presence of lead in older building materials and reduced access to sources of nutrition.
Analyzed according to racial background, African American children appear to be at the highest risk, followed by Mexican American children, and then European American children [ 24 ]. Increased blood lead has also been associated with living in a rural area, though research on this factor is limited [ 38 ]. Incidence of concerning levels among adults almost halved from tofalling from According to the same study, occupational exposure was the primary source of lead exposure for adults, particularly in the mining and battery manufacturing industries.
Risk was found to be higher among men than women because of occupational differences; there is no such gender difference consistently found among children. Epidemiological research on international populations is currently very limited.
Neuropsychology of Pb Toxicity Lead exposure has effects on neuropsychological functioning that vary across the lifespan.
Prospective studies have found that prenatal exposure, as measured by lead levels in umbilical cord blood, predicted slower development in the sensorimotor and visuomotor domains, as measured by the Bayley Scales of Infant Development [ 4041 ].
Numerous studies of children have shown that lead exposure reduces overall cognitive functioning in children, both cross-sectionally and longitudinally, but most such studies examine omnibus measures of intellectual functioning rather than domain-specific effects [ 3542 — 44 ].
Relationship of bone and blood lead levels to psychiatric symptoms: the normative aging study.
In adulthood, it is apparent that chronic exposure to lead is more harmful to cognition than acute exposures. In a sample of demographically diverse, primarily middle-aged US adults, bone lead levels predicted worse cognitive performance in several domains, whereas blood lead level did not [ 45 ]. Researches on domain-specific cognitive effects are presented below.
Intelligence Lowered intellectual scores have been most commonly noted in children following lead exposure. These results suggest a dose-dependent decrease in intellectual ability following lead exposure, with higher lead exposure producing larger point decreases.
Relationship of bone and blood lead levels to psychiatric symptoms: the normative aging study.
While less consistently noted than pediatric effects, some decreased intellectual abilities have also been suggested in adults. Further supporting a dose-dependent effect on intelligence in adults, increased levels of occupational lead exposure have been associated with lower overall cognitive scores and intelligence scores [ 49 ].
While initial studies of the cognitive effects following lead exposure focused on overall cognitive or intellectual effects, more recent research suggests the importance of examining domain-specific effects following lead exposure. Memory Some research has demonstrated lowered learning and memory scores in occupational lead-exposed adults [ 4950 ]. These results suggest that lead exposure is particularly detrimental in older adults, with individuals of age 55 and older producing lower learning and memory scores, among other cognitive declines.
Despite this vulnerability in older adults, decreased memory performances have also been noted in adults younger than 55 years of age who have been exposed to high levels of lead.
These individuals demonstrated decreased performances on verbal memory and visual memory tasks following lead exposure [ 50 ]. Lower visuospatial memory scores have been consistently documented [ 49 ], suggesting that lead exposure disrupts visuospatial skills and the ability to remember visual stimuli. Occupational lead exposure is also associated with lowered visual memory scores, specifically delayed recall of a complex figure [ 51 ]. Lowered verbal memory scores have also been noted following lead exposure, resulting in worsened immediate recall, delayed recall, and recognition.
Not only does chronic exposure appear to affect both verbal and nonverbal memories, but it also appears to produce progressive decline. In this sample, both verbal and nonverbal memory tests scores further declined in subsequent years. This suggests that progressive memory decline may ensue for years following prolonged exposure [ 51 ]. Executive Functioning and Attention Several studies have demonstrated declines in executive functioning following occupational lead exposure.
Decreased executive functioning abilities on switching and inhibition tasks Trails Making Test B and Stroop Task, resp. Lowered executive functioning scores were also found in earlier research using similar assessments and scores [ 52 ]. Unfortunately, much of the research related to executive functioning is confounded by a visual-motor component.
Overall, the evidence is mixed regarding specific executive functioning deficits following lead exposure. Processing Speed Processing speed deficits following lead exposure have been noted, with results suggesting a dose-dependent relationship. Individuals exposed to high levels of lead have shown slowed decision-making abilities and reaction times.
These results also demonstrated subtle deficits in classification speed and accuracy in a category search task. A follow-up study with the same participants and testing battery confirmed this dose-dependency in neurobehavioral deficits [ 53 ].