Benzene and lead exposure assessment among occupational bus drivers in Bangkok traffic

Four environmental and biological monitoring sites were strategically established to evaluate benzene and lead exposure assessment at various traffic zones of Bangkok Metropolitan Region(BMR). Biological measurement of 48 non air-conditioned, male bus drivers was carried to study the relationship between individual exposure levels and exposure biomarkers. The study group was further sub-divided into four age groups(16—25, 26—35, 36—45 and 46—55 years old) to monitor the age—related exposure effects. A total of 12 unexposed persons were deliberately chosen as the control group. Measurement of unmetobolized benzene in blood and analysis of urinary tt-Muconic acid urine and urinary creatinine are recommended as biomarkers of benzene exposure. Measurement of lead in blood and urine is also recommended for the biological monitoring of lead exposure. During the monitoring period, benzene and lead levels at Yaowarat Road was C_6H_6: 42.46±3.88 μg/m 3, Pb: 0.29±0.03 μg/m 3 and decreased to C_6H_6: 33.5±1.35 μg/m 3, Pb: 0.13±0.01 μg/m 3 at Phahonyothin Road. Significant difference was established between the nonsmoking exposed group and nonsmoking control group for blood benzene concentrations ( P <0.001, two-tailed, Mann-Whiteney U test). Strong correlations were also found between trans-trans-Muconic acid concentrations in post shift samples and atmospheric benzene concentrations. Similarly, good correlation between all of biomarkers and lead level in air is established from automobile emissions.The analysis revealed that among the occupational population in the urban sites, the driver groups were found to have the highest risk of benzene and lead exposures derived from automobile emission.

Assessment of Lead Exposures during Abrasive Blasting and Vacuuming in Ventilated Field Containments: A Case Study

Painting contractors have struggled with implementation and assessment of lead exposure controls leading to persistently elevated blood lead levels in this high-risk group of workers. The objective of this study was to assess the intensity of lead exposures based on commonly used air velocities inside field containment structures during abrasive blasting and vacuuming. Exposures were assessed over 14 days from April to July 2021 at a tainter gate and bridge lead paint removal project. Personal air samples, skin wipes, air velocity readings, and blood lead samples were collected. The geometric mean (GM) lead exposure for abrasive blasters and vacuumers was ≥4 × the OSHA Lead Permissible Exposure Limit (PEL) of 50 μg/m3. There was high variability in the personal lead exposures (Geometric standard deviation (GSD) 4.0 - 5.0). The GM hand wipe exposures exceeded a Dermal PEL of 500 μg/wipe (abrasive blaster 564 μg/wipe and vacuumer 754 μg/wipe). Residual lead was measured on workers’ hands in 67% of the post hand washing samples. Air velocities measured inside of the field containments ranged from 107 feet per minute to 229 feet per minute. The effect of air velocity on the concentration of lead on workers’ hands after work (F = 0.58, p = 0.35) and airborne lead concentration was not significant (F = 0.36, p = 0.48). Six of the eight workers’ blood lead levels increased after exposure to lead. There was a non-statistically significant relationship between lead remaining on workers’ hands after handwashing and an increase in blood lead level. This is the first study that assessed both ventilation flow rates used in the industrial painting industry and measurements of airborne and dermal (hands) lead exposures. For the projects evaluated, the collected exposure data indicate that air velocities frequently used in the industrial painting industry to ventilate field containment structures did not tend to prevent an increase in worker blood lead and were ineffective for adequately controlling elevated concentrations of airborne lead and preventing contact with workers’ hands.

Multi-biological defects caused by lead exposure exhibit transferable properties from exposed parents to their progeny in Caenorhabditis elegans

Whether the multi-biological toxicity from lead exposure could be transferred to progeny has not been clarified. In the present study, we explored the Caenorhabditis elegans to analyze the multiple toxicities from lead exposure and their possibly transferable properties. The lead exposure could cause series of severe multi-biological defects with a concentration-dependent manner by affecting the endpoints of life span, development, reproduction and locomotion behaviors in nematodes. Moreover, most of these toxicities could be transferred to progeny from lead exposed animals and some of the defects in progeny appeared even more severe than in their parents, such as the body sizes and mean life spans. We summarized the defects caused by lead exposure into three groups according to their transferable properties or rescue patterns. That is, the defects caused by lead exposure could be largely, or partially, or became even more severe in progeny animals. Therefore, our results suggest that lead exposure can cause severely multi-biological defects, and most of these multiple toxicities can be considered as transferable for exposed animals in C. elegans.

Study on the neurotoxic effects of low-level lead exposure in rats

Objective: To investigate effects of developmental lead exposure on nitric oxide synthase (NOS) activity in different brain regions and on N-methyl-D-aspartate (NMDA) receptor mRNA expression in the hippocampus of rats. On the basis of these observations, we explored possible mechanisms by which lead exposure leads to impaired learning and memorizing abilities in children. Methods: A series of rat animal models exposed to low levels of lead during the developing period was established (drinking water containing 0.025%, 0.05% and 0.075% lead acetate). NOS activities in the hippocampus, the cerebral cortex, the cerebellum and the brain stem were determined with fluorescence measurement and levels of mRNA expression of the NMDA receptor 2A (NR2A) subunit and NMDA receptor 2B (NR2B) subunit in the rat hippocampus were measured with Retro-translation (RT-PCR). Results: There were no differences in the body weight of rat pups between any of the groups at any given time (P>0.05). The blood lead level of Pb-exposed rat pups showed a systematic pattern of change: at 14 d of age, it was lower than that at 7 d of age, then rising to the peak level at 21 d and finally falling to lower levels at 28 d. The hippocampal NOS activities of lead-exposed groups were all lower than that of the control group on the 21 st and 28th day (P<0.01). NOS activities in the cerebellum of lead-exposed groups were all lower than that of the control group on the 21 st and 28th day (P<0.001) and the NOS activity of the 0.025% group was significantly lower than that of the 0.05% and 0.075% groups on the 28th day (P<0.05).NOS activity in the cerebral cortex of the 0.075% group was significantly lower than that of the control, 0.025% and 0.05% groups on the four day spans (P<0.001). There was no significant difference of NOS activity in the brain stem between any lead-exposed group and the control group on the four day spans. In the 0.05% and the 0.075% groups, the level of NR2A mRNA expression was higher than that in the control group at 7 d and 14 d of age (P<0.05). In the 0.025% group, the level of NR2A was found to be higher than that in the control group at 7 d of age only (P<0.05). No significant differences were found for the levels of NR2B mRNA expression between any of the groups at any given time. Conclusions: NOS activity in the hippocampus, the cerebral cortex and the cerebellum are inhibited by lead exposure. The degree of the inhibitory effect depends on the time span of exposure and the lead concentration. Developmental low-level lead exposure was found to raise the level of NR2A mRNA expression in the hippocampus of rats. Developmental low-level lead exposure does not affect the level of NR2B mRNA expression in the hippocampus.

Beta-amyloid precursor protein cleavage enzyme-1 expression in adult rat retinal neurons in the early period after lead exposure

Previous studies have reported that non-human primates and rodents exposed to lead during brain development may become dependent on the deposition of pre-determined β-amyloid protein （Aβ）,and exhibit upregulation of β-site amyloid precursor protein expression in old age.However,further evidence is required to elucidate the precise relationship and molecular mechanisms underlying the effects of early lead exposure on excessive Aβ production in adult mammals.The present study investigated the effects of lead exposure on expression of β-amyloid precursor protein cleavage enzyme-1 （BACE-1） in the rat retina and the production of Aβ in early development,using the retina as a window for studying Alzheimer＇s disease.Adult rats were intraocularly injected with different doses of lead acetate （10μmol/L,100μmol/L,1 mmol/L,10 mmol/L and 100 mmol/L）.The results revealed that retinal lead concentration,BACE-1 and its cleavage products β-C-terminal fragment and retina Aβ1-40 were all significantly increased in almost all of the lead exposure groups 48 hours later in a dose-dependent manner.The only exception was the 10μmol/L group.The distribution of BACE-1 in the retina did not exhibit obvious changes,and no distinctive increase in the activation of retinal microglia was apparent.Similarly,retinal synaptophysin expression did not exhibit any clear changes.These data suggest that lead exposure can result in the upregulation of retinal neuron BACE-1 expression in the early period of development and further increase the overproduction of Aβ1-40 in the retina.Our results provided novel insight into the molecular mechanisms underlying environmentally-induced Alzheimer＇s disease.

Non-occupational lead exposure and hypertension in Pakistani adults

Hypertension is one of the most prevalent diseases in the developed and developing countries. Based on the long historical association and the provocative findings of blood pressure effects at low level of lead exposure a study was carried out to determine if an association existed between low blood lead concentration and hypertension. In this study the effects of low-level exposure to lead on blood pressure were examined among 244 adults using atomic absorption spectrometer. For quality assurance purpose certified reference materials i.e., Animal blood A-13, Bovine liver 1577 and cotton cellulose V-9 from IAEA （International Atomic Energy Agency） and NIST （National Institute of Standard Technology） were analyzed under identical experimental conditions. The mean age of hypertensive adults was 52 years （range 43-66）. The mean values of systolic and diastolic blood pressure were （209±11.7） （range 170-250） and （117±3.9） （range 105-140） mmHg respectively. Blood lead concentration ranged from 78-201 μg/L with a mean of 139 μg/L and 165-497 μg/L with a mean of 255 μg/k in normal and hypertensive adults respectively. Increase in systolic blood pressure was significantly predictive with increase in blood lead levels. Body mass index （BMI） and lipid profile including total cholesterol, low density lipoprotein cholesterol, high density lipoprotein cholesterol and triglyceride correlated with blood pressure.

Potential Association of Lead Exposure During Early Development of Mice With Alteration of Hippocampus Nitric Oxide Levels and Learning Memory

Objective Chronic lead （Pb） exposure during development is known to produce learning deficits. Nitric oxide participates in the synaptic mechanisms involved in certain forms of learning and memory. This study was designed to clarify whether Pb-induced impairment in learning and memory was associated with the changes of nitric oxide levels in mice brains. Methods Sixty Balb/c mice aged l0 days were chosen. A model of lead exposure was established by drinking 0.025%, 0.05% 0.075% lead acetate, respectively for 8 weeks. The controls were orally given distilled water. The ability to learn and memorize was examined by open field test, T-water maze test. In parallel with the behavioral data, NO level of hippocampus tissue was detected by biochemical assay. Results Compared with control groups, （1） the weight of 0.075% group was significantly reduced （P〈0.05）; （2） The number of times in mice attaining the required standards in T-water maze test was lower in 0.075% group （P〈0.01）. No significant difference was found between experimental and control groups in open field test （P〉0.05）; （3） NO level of mouse hippocampus tissue was decreased in 0.075% group （P〈0.01）. Conclusions The findings suggest that decreased hippocampus NO level may contribute to the Pb-induced deficits in learning and memory processes.

Effect of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children

Objective: To investigate the influence of lead exposure on the immune function of lymphocytes and erythrocytes in preschool children. Materials and methods: A group of 217 children three to six years of age from a rural area were given a thorough physical examination and the concentration of lead in blood samples taken from each subject was determined. The indices of lymphocyte immunity (CD^+3CD^+4, CD^+3CD^+8, CD^+4CD^+8, CDˉ3CD^+19) and erythrocyte immunity (RBC-C3b, RBC-IC, RFER, RFIR, CD35 and its average fluorescence intensity) of 40 children with blood lead levels above 0.483 μmol/L were measured and compared with a control group. Results: The blood lead levels of the 217 children ranged from 0.11 μmol/L to 2.11 μmol/L. The CD^+3CD^+4and CD^+4CD^+8 cells were lower (P＜0.01) and the CD^+3CD^+8 cells were higher in the lead-poisoned subjects than those in the control group (P＜0.05). CD^+3 and CDˉ3CD^+19 did not show significant differences. Although the RBC-C3b rosette forming rate was lower and the RBC-IC rosette forming rate was higher in the lead-poisoned group, this difference could not be shown to be statistically significant (P＞0.05). RFIR was found to be lower in the lead-poisoned group (P＜0.01). Compared with the control group, the positive rate of CD35 was not found to be significantly different in a group of 25 lead-poisoned children (P＞0.05), while the average fluorescence intensity was lower in the lead-poisoned group (P＜0.05). Conclusion: Lead exposure can result in impaired immune function oft lymphocytes and erythrocytes in preschool children.

Developmental Lead Exposure Alters the Distribution of Protein Kinase C Activity in the Rat Hippocampus

Chronic low-level lead (Pb) exposure in children is known to cause a deficit in learning and memory. In vitro studies have demonstrated that Pb altered protein kinase C (PKC) activityt Especially, hippocampal PKC has been correlated with performance in several learning tasks. The effects of Pb exposure on hippocampal PKC were investigated during development at various postnatal ages: postnatal day (PN) 7, 14, 28, and 56. Two-tenth % Pb acetate was administered to pregnant and lactating dams and then administered to weanling rats in drinking water. PKC activity was measured in both membrane and cytosolic fractions from the hippocampi of the controls and Pb-exposed animals. Pb-induced increase in PKC activity in the cytosolic fraction was obsereved in the PN56 rats. In contrast, PKC activity was decreased by Pb at PN7 in the membrane fraction. Furthermore, a significant decrease in the ratio of membrane to cytosolic PKC activity which is representative of PKC distribution was observed in the PN28 and PN56 Pb-exposed rats relative to the same-age controls. This study indicates that chronic Pb exposure during development influences hippocampal PKC activity and distribution. These changes may be involved in the subclinical neurotoxicity of chronic Pb exposure in young children.

Lead Exposure and Oxidative Stress in Coal Miners

We aimed to investigate the short-term correlation between blood lead levels and oxidative stress generation in coal miners. The study involved 94 male coal miners from the Velenje Coal mine, arranged into four groups： three groups according to the number of consecutive working days, and a fourth control group. Miners who worked for three consecutive days had higher blood levels of lead and 8-isoprostane than the control group（P 〈 0.001）. Correlation between lead and 8-isoprostane was of medium strength（r = 0.512, P 〈 0.001）. Short-term lead environmental exposure can potentially harmful and should be considered when formulating improvements in working processes.

Evaluation of Lead Exposure by Hand Wipes: A Review of the Effectiveness of Personal Hygiene on Industrial Sites

To evaluate the effectiveness of personal hygiene (handwashing) amongst workers at industrial sites to remove lead from their hands, a retrospective analysis of hand wipe samples was conducted using data collected by two contractors from two bridge painting projects for total lead using method ASTM E-1979-17/EPA SW846 7000B. Exposures resulted from the removal of lead-based paint from the structure and trace elements of lead found in the abrasive blast media. In total, six work tasks were evaluated and sixty unique hand wipe samples were evaluated. Thirty samples were collected during the worker’s lunch break, after they had reportedly washed their hands with a further 30 collected at the end of the workday following the same protocol. To be included in this evaluation, the contractors were required to follow NIOSH Method 9105 (Lead in Dust Wipes-Dermal Surfaces) with subsequent analysis of samples for total lead by an American Industrial Hygiene Association (AIHA) accredited laboratory. All 60 samples contained detectable lead. The lead exposures ranged from 19.5 μg to 3420 μg. The geometric mean for the samples collected was 337 μg. These results indicate that current personal hygiene practices at the evaluated sites are not effective at removing lead from worker’s hands during and after the workday. They also suggest that the residual lead measured on the workers’ hands, at the end of the shift, is likely contributing to the elevated blood lead levels in this population.

Maternal Lead Exposure Induces Down-regulation of Hippocampal Insulin-degrading Enzyme and Nerve Growth Factor Expression in Mouse Pups

Lead exposure is a known potential risk factor for neurodegenerative diseases such as Alzheimer’s disease （AD）. Exposure to lead during the critical phase of brain development has been linked with mental retardation and hypophrenia in later life.

Surveillance of Childhood Blood Lead Levels in 14 Cities of China in 2004-2006

Objective To investigate the blood lead level in children aged 0-6 years in urban areas of China. Methods Fourteen cities were selected as sites under surveillance. A total of 44 045 peripheral blood specimens were collected from 2004 to 2006, during which 15 727, 14 737, and 13 584 specimens were tested in 2004, 2005, and 2006, respectively. Tungsten atomizer absorption spectrophotometer was employed to determine blood lead level. Results The geometric mean blood lead level in the tested children was 47.10 μg/L with 10.10% ≥100 μg/L, 46.17 μg/L with 7.78% ≥100 μg/L, and 47.03 μg/L with 7.30% ≥ 100μg/L in 2004, 2005, and 2006, respectively. The blood lead levels seemed to tend to rise in parallel with the increase of age of the children and were higher in boys （48.84 μg/L, 47.56μg/L, and 47.78 μg/L in the 3 respective years） than in girls （45.00 μg/L, 44.53μg/L, and 46.13 μg/L）. Conclusion The blood lead levels in children in cities of China are lower than those in previous national studies, but higher than those in developed countries. Childhood lead poisoning remains a public health problem in China.

Blood Lead Levels During Pregnancy and Its Influencing Factors in Nanjing,China

Objective To investigate the blood lead levels （BLLs） in the duration of pregnancy and 6-12 weeks after delivery, and analyze the influencing factors of BLLs in healthy pregnant women. Methods Pregnant women were recruited from September 2009 to February 2010 at the prenatal clinic in Nanjing Maternity and Child Health Care Hospital. Altogether 174 healthy pregnant women without pregnant or obstetric complications or abnormal pregnancy outcomes were enrolled as the gravida group, and 120 healthy non-pregnant women as the control group. BLLs during pregnancy were determined by flame atomic absorption spectroscopy. Results BLLs in all the three pregnancy trimesters and postpartum were 59.8±24.3, 55.4±20.1, 55.9±19.7, and 67.6±17.4 μ/L, respectively, and the mean BLL in control group was 67.5±21.3 μg/L. BLLs during all the three trimesters were lower in the gravida group than in the control group （P=0.043, 0.021, and 0.028）. Furthermore, occupations, nutrients supplementation, and time of house/apartment painted were associated with BLLs in pregnant women. Lead-related occupations, cosmetics use, and living in a house painted less than 1 year before are risk factors of high BLLs among pregnant women, while calcium, iron, zinc, and milk supplements are protective factors. Conclusion Supplementing calcium, iron, zinc, and milk, or avoiding contact with risk factors may help people, especially pregnant women, to reduce lead exposure.

Navigating the Lead Laws/Rules/Standards for Renovation and Repair Activities: A Guide for Contractors and Laborers

Children and adults are often exposed to lead in homes as a result of deteriorating lead-based paint surfaces and any disturbance to those surfaces. There are a number of laws, regulations, standards and guidance documents in place aimed at minimization of lead dust contamination following renovation and repair activities. These laws and regulations are oftentimes confusing and conflicting for the maintenance contractor who has limited time and resources for researching the right and appropriate course of action. This paper provides a comprehensive review and discussion of the lead laws, regulations, standards and guidelines for contractors.

Increased hippocampal Disrupted-In-Schizophrenia 1 expression in mice exposed prenatally to lead

Disrupted-in-Schizophrenia 1 is a susceptibility gene for schizophrenia and other psychiatric disorders. Developmental lead exposure can cause neurological disorders similar to hyperactivity disorder, dyslexia and schizophrenia. In the present study, we examined the impact of developmental lead exposure, administered in vitro and in vivo, on hippocampal Disrupted-In- Schizophrenia 1 expression. Our results show that in cultured hippocampal neurons, in vitro exposure to 0.1-10 pM lead, inhibited neurite growth and increased Disrupted-In-Schizophrenia 1 mRNA and protein expression dose-dependently. In addition, blood lead levels in mice were increased with increasing mouse maternal lead （0.01-1 mM） exposure. Hippocampal neurons from these mice showed a concomitant increase in Disrupted-in-Schizophrenia 1 mRNA and protein expression. Overall our findings suggest that in vivo and in vitro lead exposure increases Disrupted-In-Schizophrenia 1 expression in hippocampal neurons dose-dependently, and consequently may influence synapse formation in newborn neurons.

Contribution of Soil Lead to Blood Lead in Children: A Study from New Orleans, LA

In recent years, a significant number of environmental studies have been conducted in New Orleans, LA and surrounding Gulf Coast areas due in part to the occurrence of hurricanes Katrina and Rita. Data collected from studies in the New Orleans area indicate that inorganic contaminants including arsenic (As), iron (Fe), lead (Pb), and vanadium (V);high concentration of bioaerosols, particularly Cladosporium and Aspergillus, and several organic pollutants (PAHs, pesticides, and volatiles) may pose a risk to human health in New Orleans. While many of these results resemble historical data, a current quantitative exposure assessment has not been conducted. We engaged in one such assessment for lead (Pb) contamination in surface soils. We used Pb concentrations in surface soils ( μg/day to 102 μg/day for our study area within urbanNew Orleans. These data are concerning because children exposed to >33.5 μg/d Pb may cause their blood-Pb levels to exceed the Centers for Disease Control and Prevention (CDC) threshold for blood-Pb of 10 μg/dL. It has generally been accepted that a more protective blood Pb concentration threshold of 6 - μg/dL is warranted. Using the 6-μg/dL threshold puts children exposed to as little as 20.2 μg/day Pb at risk.

Lead acetate in drinking water is toxic to hippocampal tissue Measuring relative protein changes using tissue array detection

BACKGROUND： Lead can cause structural changes in the hippocampus, followed by damage to learning and memory functions, but its specific mechanisms are not yet clear. OBJECTIVE： To observe long-term toxicity of high-dose lead in drinking water on hippocampal tissue in rats, and analyze the potential association of oxidative damage, cell apoptosis, and pathology. DESIGN, TIME AND SETTING： A randomized, controlled animal experiment was performed at the Center for Medical Experiment, Lanzhou General Hospital of Lanzhou Military Area Command of Chinese PLA from May 2007 to October 2008. MATERIALS; Rabbit anti Bcl-2, Bax, and inducible nitric oxide synthase （iNOS） polyclonal antibodies were purchased from Santa Cruz Biotechnology, USA. An streptavidin-peroxidase immunohistochemistry kit and concentrated DAB kit were purchased from Beijing Zhongshan Biotechnology Company Limited, China. Crystal violet was purchased from Sigma, USA. METHODS： A total of 72 Wistar rats, aged 3 months, were randomly divided into control, low-, middle-, and high-dose lead groups, with 18 rats per group. Animal models were established through free drinking water contaminated by Pb2＋ for 1, 3, and 6 months, respectively. MAIN OUTCOME MEASURES： The general toxicity of lead was dynamically observed; the levels of Pb2＋ in the blood and brain tissue homogenete were detected using atomic absorption method; pathological changes were observed using hematoxylin-eosin staining and tigroid body staining; the protein expression levels of Bcl-2, Bax, and iNOS were dynamically observed using streptavidin-peroxidase immunohistochemistry of the hippocampus. RESULTS： Lead exposure reduced autonomic activities, produced a slumped appearance, slow responses, and lusterless fur, especially in the high-dose group. The amount of ingestion and hydroposia showed a decreasing trend, especially in middle- and high-dose groups. Lead levels in whole blood and brain homogenate were higher than controls （P 〈 0.01）. Lead caused degeneration of hippocampal neurons and pyknosis, with fewer tigroid bodies, especially in high-dose lead group. Bcl-2 expression decreased with increasing lead dose （P 〈 0.01）, whereas lead dose-dependently increased Bax levels （P 〈 0.01） and iNOS levels （P 〈 0.05）. CONCLUSION： High levels of Pb^2＋ may disrupt hippocampal structure by passing through the blood brain barrier. Oxidative damage and apoptosis may be a toxicity mechanism of Pb^2＋ on the hippocampus.

Exacerbation of Soft Tissue Lesions in Lead Exposed Virus Infected Mice

Objective To investigate the effect of Lead (Pb) acetate exposure on Semliki forest virus (SFV) pathogenesis in mice. Methods Different doses (62.5, 125, 250 and 500 mg/Kg body weight) of Pb dissolved in normal saline were given to mice by oral intubation in a sub-acute (28 days) and sub-chronic (90 days) regimen followed by SFV infection. Morbidity, mortality, clinical symptoms, mean survival time (MST), changes in body and organ weight, accumulation of lead in soft tissues, virus titre in brain and histopathological alterations were compared between lead exposed and infected groups. Results Early appearance of virus symptoms, increased mortality, decreased MST, enhanced SFV titre and greater tissue damage were observed in lead exposed-SFV-infected mice. Conclusion Pre-exposure to lead increases the susceptibility of mice towards SFV infection. Further studies are suggested in view of the persistence of lead in the environment and the possibility of infection by microbial pathogens.

N-methyl-D-aspartate receptor subunit expression in memory-related brain areas of lead-exposed rats

Lead exposure induces decreased hippocampal N-methyI-D-aspartic acid （NMDA） receptor gene and protein expressions, which influences the molecular mechanisms of learning and memory. However, lead poisoning-induced differences in NMDA subunit expression, and the correlation of lead poisoning with learning and memory, remain poorly understood. The present study measured differences in expression of NMDA receptor subunits NR1, NR2A, and NR2B in memory-related brain regions of rats who underwent different doses of lead exposure. Results demonstrated decreased NR1, NR2A, and NR2B subunit expressions in some memory-related brain areas. The inhibitory effect of 4.8 mmol/L lead exposure on hippocampal NR2B was most significant, although NR2A expression also significantly decreased following 14.4 mmol/L lead exposure. There was no difference in NR1 expression following exposure to 〈 4.8 mmol/L lead, although the inhibitory effect of 19.6 mmol/L lead exposure was strongest for NR1 expression in the hippocampus. Inhibitory avoidance test results revealed that greater concentrations of lead exposure resulted in decreased learning and memory. Therefore, lead toxicity was dependent on NMDA receptor subunit composition, and NR1, NR2A, and NR2B expressions were associated with time and concentration of lead exposure.