Effects Of Chronic Lead Exposure Research Articles

Chronic Lead Exposure Impairment of Hypothalamic-Pituitary-Gonadal Axis in Adult Male Wistar Rats: Biochemical and Histomorphological Evidence

Introduction: The upsurge in male infertility has been associated with impaired hypothalamic-pituitary-gonadal (HPG) axis. There is a dearth of conclusive empirical data as to the deleterious impacts of heavy metal intoxication on male reproductive functioning through the HPG axis. Objective: This study seeks to elucidate the possible effects of chronic lead exposure on HPG signalling activities via biochemical and histopathological assessment. Experimental Section/Material and Methods: Forty adult male Wistar rats were randomised into four experimental groups (n=10). Group A, the control group received standard feed and water ad libitume. In Groups B, C and D, animals were orally administered lead acetate at concentrations of 2.5% 3.0% and 3.5%, respectively, using a stock solution of 150mg/kg once daily for 35 days. After the treatment period, all animals were fasted overnight and euthanized by cervical dislocation. Blood levels of anterior pituitary hormones (FSH and LH) were analysed using standard methods. Statistical analyses was done on graph pad prism. Testicular tissue was processed routinely for histopathological analyses using different stains. Results: Hormonal assays showed no significant changes in follicle-stimulating hormone (FSH) and luteinizing hormone (LH) (p>0.05) levels across groups. However, histological examination revealed alterations in testicular architecture, including disrupted spermatogonia cell arrangement and reduced Sertoli cell numbers, indicative of adverse effects on spermatogenesis. Conclusion: Chronic lead exposure adversely affects testicular histomorphology in adult male Wistar rats, potentially impacting reproductive function. While hormonal levels remain relatively unaffected, alterations in testicular structure suggest a direct impact on gonadal functions at a cellular level.

The Effects of Chronic Lead Exposure on Testicular Development of Japanese Quail (Coturnix japonica): Histopathological Damages, Oxidative Stress, Steroidogenesis Disturbance, and Hypothalamus-Pituitary-Testis Axis Disruption.

Lead (Pb) becomes a global public health concern for its high toxicology. Birds are sensitive to environmental pollution and Pb contamination exerts multiple negative influences on bird life. Pb also impacts on avian reproductive system. Thus, in this study, we attempted to determine toxicological effects and possible mechanistic pathways of Pb on avian testicular development by using the model species-Japanese quail (Coturnix japonica). Male quail chicks of 1-week-old were exposed to 0, 50, 500, and 1000ppm Pb concentrations in drinking water for 5weeks when reaching sexual maturation. The results showed that high Pb doses (500 and 1000ppm) induced testis atrophy and cloacal gland shrinkage. Microstructural damages of both hypothalamus and testis indicated the disruption of the hypothalamus-pituitary-gonadal (HPG) axis by Pb exposure. The decrease of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and testosterone (T) may also imply HPG axis disruption. Moreover, excess testicular oxidative damages featured by increasing reactive oxygen species (ROS) and malondialdehyde (MDA) and decreasing catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), glutathione-S-transferase (GST), and total antioxidant capacity (T-AOC) indicated increasing risks of reproductive dysfunction by Pb. Furthermore, increasing apoptosis and upregulation of gene expression associated with cell death suggested testicular abnormal development. In addition, molecular signaling involved with steroidogenesis in the testis was disturbed by Pb treatment. The study showed that Pb could impair testicular development and reproductive function by morphological and histological injury, hormone suppression, oxidative stress, cell death, and HPG axis disruption.

Intestinal Protective Efficacy of Gamma Co-60 Irradiated Chitosan and Vitamin E Combination on Lead acetate-induced Rats

As an organ that absorbs food, the intestine can be damaged when interacting directly with lead (Pb). Gamma Co-60 irradiated chitosan, and vitamin E combination potentially can help reduce free radical damage to intestinal organs. This study examines the efficacy of gamma Co-60 irradiated chitosan and vitamin E combination in protecting the intestinal tissue of rats exposed to Pb acetate. The 24 rats were grouped into 6 groups, each 4 rats; were induced with Pb acetate, except the control group. The negative control group was only induced Pb acetate. The positive control group had additional treatment of irradiated chitosan. The treatment group (1-3) was treated using the combination of gamma Co-60 irradiated chitosan at a dose of 64 mg/kg BW and vitamin E 1000 IU at a dose of 1.44; 2.16, 3.00 mg/kg BW, respectively, for forty days. The research parameters observed are edema, degeneration, necrosis, erosion of the intestinal villi, and lysis of the intestinal villi. Intestinal histology appearance data in all groups were analyzed descriptively. The result shows that a combination of Gamma Co-60 irradiated chitosan at a dose of 64 mg/kg BW and vitamin E at a dose of 1.44 mg/kg BW effectively reduced lead cytotoxicity in the intestinal tissue of Pb acetate-induced rats. The larger the dose of vitamin E has the potential to produce pro-oxidants, which will increase the toxic effect on intestinal tissue. Gamma Co-60 irradiated chitosan, and vitamin E combination at the right dose has the potential to be developed as a supplement to reduce the toxic effects of chronic lead exposure. Especially for people who, for some reason, cannot avoid chronic lead exposure.

Effect of occupational exposure to lead on serum levels of lipid profile and liver enzymes: An occupational cohort study

The present study was performed to know the effects of chronic lead exposure on serum lipids, lipoproteins, and liver enzymes in a cohort study among of lead mine workers. We followed of 200 Iranian workers for 3- years (2018–2020), 100 of them with known occupational exposure to lead thorough their work in lead mine while the others 100 were with no such exposure. Blood lead level (BLL), serum lipids, lipoproteins, and liver enzymes of the exposure group for 3- years were measured and compared with those attained in the non-exposed workers. The BLL levels of the lead-mine workers were higher than with recommended level and the non-exposed group (24.15 and 6.35 µg/dL, respectively). The findings indicated a positive and significant relationship between BLL and lactate dehydrogenase, aspartate transaminase, alkaline phosphatase, alanine transaminase, and bilirubin levels (P < 0.01). Also while we found a negative and significant correlation between BLL and triglyceride, total protein, albumin, and globulin levels (P < 0.01). This report depicted that chronic lead exposure is a risk factor for hematological, liver, and cardiovascular diseases. Despite the fact that the level of liver function parameters was in the normal range, the results of 3- years follow-up show a significant relationship between BLL and alteration of biochemical parameters levels.

Chronic Lead Exposure Alters Mineral Properties in Alveolar Bone

The objective of the present study was to investigate the effects of chronic lead exposure on the mineral properties of alveolar bone. For this purpose, female Wistar rats (n = 8) were exposed to 1000 ppm lead acetate in drinking water for 90 days, while the control group (n = 5) was treated with sodium acetate. The alveolar bone structure and chemical composition of the dissected mandibles were examined using micro-computed tomography (micro-CT), scanning electron microscopy (SEM), inductively coupled plasma optical emission spectrometry (ICP-OES), attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR), and X-ray diffraction (XRD) techniques to determine possible alterations in alveolar bone due to lead exposure. In addition, changes in bone mechanical properties were analysed using a three-point bending test. Exposure to lead induced notable changes in bone mineralization and properties, specifically a reduction of the trabecular thickness and bone mineral density. Furthermore, there was a reduction in carbonate content and an increase in bone mineral crystallinity. These changes in bone mineralization could be explained by an alteration in bone turnover due to lead exposure. Three-point bending showed a trend of decreased displacement at failure in the mandibles of lead-exposed rats, which could compromise the mechanical stability and normal development of the dentition.

The effects of chronic lead exposure on the ovaries of female juvenile Japanese quails (Coturnix japonica): Developmental delay, histopathological alterations, hormone release disruption and gene expression disorder

Lead (Pb) is well-recognized for its great hazards to human and wildlife health. It has negative influences on multiple organs and systems of birds. Especially, lead exposure caused adverse impacts on bird reproduction. In this study, one week old female Japanese quails were randomly allocated into four groups and each group was respectively fed with 0, 50 ppm, 500 ppm and 1000 ppm Pb in drinking water for 36 days to determine the effects of chronic lead exposure on ovarian development and function. The results showed that Pb did accumulate in the ovary and ovarian development was delayed by high dose lead exposure (500 ppm and 1000 ppm). Moreover, high Pb dosage induced ovarian histopathological damages characterized by granulosa cells disorganization, follicle atresia and interstitial cell degeneration. Meanwhile, the concentration of estradiol (E2) was significantly decreased and mRNA levels of genes involved with ovarian steroidogenesis were significantly down-regulated by high concentration Pb. In addition, Pb exposure caused increasing cell apoptosis and significant changes of the expression of genes involved with cell death in the ovary. High dose Pb exposure also inhibited thyroid hormone release and disrupted ovarian thyroid deiodination apart from causing thyroid histopathological injury such as follicular deformation and atrophy. The study indicated that Pb might cause ovarian malfunction by inducing ovary and thyroid microstructural damages, thyroid hormone and estrogen release inhibition and ovarian steroidogenesis disruption.

The effects of chronic lead exposure on the liver of female Japanese quail (Coturnix japonica): Histopathological damages, oxidative stress and AMP-activated protein kinase based lipid metabolism disorder.

Lead (Pb) is one of the most toxic metals to human and wildlife. It also had multiple negative influences on birds with physical, neurological and hematological clinical signs. However, the impacts of lead on bird liver lipid metabolism are still unclear. In this study, female Japanese quails were used to examine the effects of chronic lead exposure on liver histology, oxidative stress and AMPK (AMP-activated protein kinase) based lipid metabolism. Quails were randomly divided into 5 groups and each group was respectively fed with 0, 50, 250, 500 and 1000ppm lead solution for 49 days. The result showed that exposure to 250, 500 and 1000ppmPb induced severe histopathological damages characterized by liver lipid vacuoles and accumulation, hepatic cytoplasmic hyalinization and vacuolization, hepatocytes necrosis, hepatic sinusoid congestion, and it also caused ultrastructural alterations featured by swelling and vacuolar mitochondria, the depolymerization of polyribosome, and lipid droplets accumulation. Moreover, significant decrease of activities of GPx (glutathione peroxidase), SOD (superoxide dismutase), CAT (catalase) and level of T-AOC (total antioxidant capacity) while significant increase of MDA (malondialdehyde) content were found in livers of all Pb groups. In addition, the expressions of genes related to fatty synthesis were significantly upregulated in livers of all Pb groups while the expressions of genes related to fatty β-oxidation were significantly downregulated in livers of 250ppmPb group. The present study indicated lead exposure does cause bird health damages through inducing liver microstructural and ultrastructural injury, oxidative damages and lipid metabolism disorder.

Chronic lead exposure induces histopathological damage, microbiota dysbiosis and immune disorder in the cecum of female Japanese quails (Coturnix japonica)

Lead (Pb) is one of the most hazardous metals to human and wildlife and it also has multiple negative impacts on birds. However, its influences on bird gut morphology and intestinal microbiota were still unclear. We used female Japanese quails (Coturnix japonica) to examine the effects of chronic lead exposure (0, 50 ppm and 1000 ppm) on cecal histology, microbial communities and immune function. The results showed 50 ppm lead exposure caused subtle damages of cecum cell structure. However, 1000 ppm lead exposure caused severe cecum histopathological changes characterized by mucosa abscission, Lieberkühn glands destruction and lymphocyte proliferation. Moreover, both lead concentrations induced ultrastructural damages featured by nucleus pyknosis, mitochondrial vacuolation and microvilli contraction. Meanwhile, microbial community structure, species diversity, taxonomic compositions and taxa abundance in the cecum were affected by lead exposure. Furthermore, the mRNA relative expression of immunity-related genes such as interleukin 2 (IL-2) and gamma interferon (IFN-γ) was significantly downregulated while that of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and natural killer kappa B (NF-κB) was significantly upregulated in the cecum of 50 and 1000 ppm lead exposure groups. We concluded that lead exposure may cause gut health impairment of female Japanese quails by inducing cecal histopathological changes, microbiota dysbiosis and cecal immune disorder.

Effects of chronic lead exposure on the sympathoexcitatory response associated with the P2X7 receptor in rat superior cervical ganglia.

Chronic lead exposure frequently brings about increased blood pressure and other cardiovascular diseases associated with autonomic nervous dysfunction. Purinergic signaling is involved in the development of abnormal sympathoexcitatory response due to myocardial ischemic injury. However, the potential implication of P2X7 receptor in altered sympathoexcitatory response caused by chronic lead exposure and the underlying mechanisms remain unclear. In this study, a rat model of chronic lead exposure was used to explore the changes in sympathoexcitatory response and possible involvement of P2X7 receptor in the superior cervical ganglion (SCG). Rats were divided into three groups called control, low lead and high lead groups according to daily lead exposure levels, i.e. 0, 0.5 and 2 g/L respectively. One year later, changes in P2X7 receptor expression in SCG, sympathetic nerve activity and myocardial function were measured for these rats. Our results showed that increased blood pressure and heart rate, decreased heart rate variability, enhanced cervical sympathetic nerve discharge, higher phosphorylation of ERK1/2, and up-regulated protein and mRNA levels of P2X7 expression in SCG occurred after lead exposure. In addition, double-label immunofluorescence staining of P2X7 receptor and glutamine synthetase (GS) revealed activation of the satellite glial cells of SCG by lead exposure. Moreover, knockdown of P2X7 could effectively relief the effect of lead exposure on enhanced expression of P2X7 receptor and GS. Thus our data suggest that the up-regulation of P2X7 receptor activity in satellite glial cells of SCG may contribute to the raised sympathoexcitatory response due to chronic lead exposure.

Lead Induced Ototoxicity and Neurotoxicity in Adult Guinea Pig.

Lead exposure causes or aggravates hearing damage to human or animal, but the detailed effects of lead exposure on auditory system including injury sites of the cochlea in mammal remain controversy. To investigate the effect of chronic lead exposure on auditory system, 40 adult guinea pigs with normal hearing were randomly divided into five groups. They were fed 2 mmol/L lead acetate in drinking water for 0, 15, 30, 60, and 90 days (n = 8), respectively. Lead concentrations in blood, cochlea, and brainstem were measured. Auditory function was measured by auditory brainstem response (ABR) and distortion product otoacoustic emission (DPOAE). The morphology of cochlea and brainstem was observed, and expression of autophagy-related protein in brainstem was also assessed. The blood lead concentration reached a high level at the 15th day and kept stable, but the lead level in brainstem and cochlear tissue increased obviously at the 60th day and 90th day of lead exposure, respectively. There was no significant difference in the morphology of hair cells and stria vascularis (SV) among these five groups, but the number of spiral ganglion neuron (SGN) gradually decreased after 60 days. The differences of ABR thresholds and DPOAE amplitudes were not statistically significant among each group, but I wave latency, III latency, and I-III wave interval of ABR were delayed with the prolonging of time of lead exposure. The expressions of autophagy-related protein ATG5, ATG6, and LC3B in brainstem were increased after 30 days. These results suggest that the key target of lead toxicity was the auditory nerve conduction pathway including SGNs and brainstem, rather than cochlear hair cells and SV. Autophagy may play a very important role in lead toxicity to auditory nervous system.

Psychiatric benefits of lithium in water supplies may be due to protection from the neurotoxicity of lead exposure

IntroductionLithium is a medication used to treat bipolar disorder and may also prevent cognitive decline and suicide. Lithium is also found naturally, in levels well below clinical doses, in drinking water worldwide, and levels have been inversely associated with rates of psychiatric disorders. Lead (Pb) is another element in the environment but is a toxin of public health concern. Negative effects of chronic lead exposure and possible benefits of environmental lithium exposure appear complementary. HypothesisExposure to environmental lithium has associated benefits, which may be due to the mitigation of lead toxicity by lithium. MethodsA series of reviews tested each element of the hypothesis. A systematic review clarified the psychiatric and medical correlates of lithium in drinking water. Non-systematic reviews clarified the harms of environmental lead, summarized experimental studies of lithium used to prevent lead toxicity, and explored overlapping biological mechanisms in lithium and lead exposure. ResultsHigher levels of lithium in drinking water were associated with lower suicide rates in 13 of 15 identified studies. While fewer studies were available for other outcomes, lithium was associated with lower rates of homicide, crime, dementia, and mortality. Lead was reported to be ubiquitous in the environment, and chronic low-level exposure has been associated with adverse effects, including effects opposite to the outcomes associated with lithium. Animal studies demonstrated that lithium pre-treatment mitigates lead toxicity. Neurophysiological correlates of lead and lithium exposure overlap. ConclusionsMicrodose lithium is associated with better psychiatric and medical outcomes, which are complementary to harms of environmental lead exposure. Experimental animal evidence is supportive, and lead and lithium impact overlapping neurophysiologic pathways. Therefore, several lines of circumstantial evidence suggest that lithium protects against the neurotoxic effects of lead. Further studies are required to clarify the benefits and mechanisms of low-dose lithium. There are significant public health implications if this paper's hypothesis is true.

Effects of chronic lead exposure on bone mineral properties in femurs of growing rats.

Lead exposure has been associated with several defective skeletal growth processes and bone mineral alterations. The aim of the present study is to make a more detailed description of the toxic effects of lead intoxication on bone intrinsic material properties as mineral composition, morphology and microstructural characteristics. For this purpose, Wistar rats were exposed (n=12) to 1000ppm lead acetate in drinking water for 90days while control group (n=8) were treated with sodium acetate. Femurs were examined using inductively coupled plasma optical emission spectrometry (ICP-OES), Attenuated Total Reflection Fourier transform infrared spectroscopy (ATR-FTIR), X-ray diffraction (XRD), and micro-Computed Tomography (μCT). Results showed that femur from the lead-exposed rats had higher carbonate content in bone mineral and (Ca2++Mg2++ Na+)/P ratio values, although no variations were observed in crystal maturity and crystallite size. From morphological analyses, lead exposure rats showed a decreased in trabecular bone surface and distribution while trabecular thickness and cortical area increased. These overall effects indicate a similar mechanism of bone maturation normally associated to age-related processes. These responses are correlated with the adverse actions induced by lead on the processes regulating bone turnover mechanism. This information may explain the osteoporosis diseases associated to lead intoxication as well as the risk of fracture observed in populations exposed to this toxicant.

More evidence of unpublished industry studies of lead smelter/refinery workers.

Lead smelter/refinery workers in the US have had significant exposure to lead and are an important occupational group to study to understand the health effects of chronic lead exposure in adults. Recent research found evidence that studies of lead smelter/refinery workers have been conducted but not published. This paper presents further evidence for this contention. To present further evidence of industry conducted, unpublished epidemiologic studies of lead smelter/refinery workers and health outcomes. Historical research relying on primary sources such as internal industry documents and published studies. ASARCO smelter/refinery workers were studied in the early 1980s and found to have increased risk of lung cancer and stroke in one study, but not in another. Because occupational lead exposure is an on-going concern for US and overseas workers, all epidemiologic studies should be made available to evaluate and update occupational health and safety standards.

The pharmacological effect of Artemisia absinthium extract in protecting adult rats against lead neurotoxicity

Lead (Pb) is a heavy metal with no apparent biological function. It is recognized as a dangerous neurotoxin, since it induces morphological and functional abnormalities in the brain. Several studies reported, in the rat brain, the antioxidant and anti-inflammatory effects /INS;of aqueous extracts of Artemisia absinthium. Here, we investigated the potential role of A. /INS;absinthium aqueous extract in protecting brain against the effect of chronic lead exposure, especially on the dopaminergic neurons together with the glial system.

Chronic Exposure to Lead: A Cause of Oxidative Stress and Altered Liver Function in Plastic Industry Workers in Kolkata, India

It is well known that chronic exposure of lead leads to adverse health effects. Workers for plastic industry are generally exposed to high concentration of lead as fume, dust, and additive that protect PVC. This study was done on them to find out the detrimental effects of chronic lead exposure on hepatic and hematological toxicity. Blood and 24h urine sample was collected from 47 plastic industry workers and matched against 42 controls for various parameters. The study group shows significant increase in blood (p<0.0001) and urinary level of lead (p<0.0001). Hemoglobin levels were significantly decreased (p<0.0001), and the liver enzymes like ALP, ALT, AST and y-GT were significantly increased (p<0.0001) in all cases exposed for >10years. Serum lipid peroxide by quantitative assay of thiobarbituric acid reactive substances was also found increased in the study group (p<0.0001). The observations point towards the acute health risk faced by plastic industry workers, in whom chronic exposure to lead increases the absorption and accumulation, over a period of time, of this highly toxic element in their body. This increases oxidative stress, causes metabolic damage to RBC and cell membranes, and also suggests necrosis of liver cell, hepatocellular injury and presence of space occupying lesions. Considering the data immediate health and hygiene monitoring and proper rehabilitation for the suffering population seem to be of paramount need in plastic industry to minimize occupational hazards.

Effects of chronic lead exposure on functions of nervous system in Chinese children and developmental rats

Lead pollution is a very serious problem in China with the rapid economic development. A large amount of lead has been released into the environment due to mineral processing activities and has impacted water resources, soils, vegetables, and crops. The gasoline with lead has been banned in China since July 1, 2000. Though a noticeable decrease of lead poisoning rates has been evidenced, the children's blood lead levels are still significantly higher than those in developed countries. Therefore, lowering the lead exposure in childhood continues to be an important public health objective in China. There is also a lot that remains to be done to reduce children's exposure to lead. In this section, five scientists from China presented latest research results regarding the current situation of lead poisoning in China, the mechanisms involved in lead-induced neurotoxicity, and the new advances related to the potential therapy methods. Their researches may pave new way not only for the prevention of lead poisoning but also for the treatment of affected children in China and other countries.

Effect of chronic lead exposure on pro-apoptotic Bax and anti-apoptotic Bcl-2 protein expression in rat hippocampus in vivo.

Despite reduction in environmental lead, chronic lead exposure still possess a public health hazard, particularly in children, with devastating effects on developing CNS. To investigate the mechanism of this neurotoxicity, young and adult rats were used to study whether exposure to 500 ppm concentrations of lead could induce apoptosis in hippocampus. 2-4 and 12-14-week-old rats received lead acetate in concentration of 500 ppm for 40 days. Control animals received deionized distilled water. In lead-treated groups, the blood lead levels were increased by 3-4 folds. Light and electron microscopical study of hippocampus revealed increased apoptotic cells. Western blot analysis of Bax and Bcl-2 (pro- and anti-apoptotic gene products, respectively) indicated higher expression of Bax protein and no significant change in bcl-2 expression and accordingly increased the Bax/Bcl-2 ratio compared to control group, confirming the histological study. In conclusion, these data suggest that neurotoxicity of chronic lead exposure in hippocampus in vivo may partly be due to facilitation of apoptosis.

Effects of lead exposure on acid-sensing ion channel in hippocampus of baby-rats

To observe the effects of chronic lead exposure on mRNA and protein expression of ASIC1a, ASIC2a, ASIC2b in hippocampus of baby-rats. The Wistar pregnant rats were randomly divided into 3 groups fed with distilled water or lead contained water (0.2% and 1.0% lead acetate) respectively, 5 rats in each group. The lead-exposure ranged from the 0 day of pregnancy to the offspring weaned. Then the baby-rats were fed with lead water like their mothers and killed at postnatal day 8 or 50. Atomic absorption spectrometry was used to determine lead content in the brain. RT-PCR and Western blotting were used to observe mRNA and protein expression of ASIC1a, ASIC2a and ASIC2b in their hippocampus respectively. The brain lead content of test groups was higher than that of the control group (P < 0.01), and the lead content of the postnatal day 50 was higher than that in postnatal day 8 (P < 0.01). Compared with the control group, ASIC1a mRNA expression of 1.0% lead exposure in the hippocampus was uptrend (P < 0.01), ASIC1a protein expression of each test group was downtrend (P < 0.05), while for ASIC2a and ASIC2b mRNA and protein, there was no significant differences observed (P > 0.05). ASIC1a expression in hippocampus can be changed by chronic lead exposure.

Low Dose Effect of Chronic Lead Exposure on Neuromotor Response Impairment in Children is Moderated by Genetic Polymorphisms

Low Dose Effect of Chronic Lead Exposure on Neuromotor Response Impairment in Children is Moderated by Genetic Polymorphisms

Chronic Lead Exposure may be Associated with Erectile Dysfunction

Heavy metals constitute significant potential threats to human health in both occupational and environmental settings. Research examining the etiology of lead toxicity-induced hypertension reveals that the free radical production and lowering of inherent antioxidant reserves resulting from lead toxicity are directly related to vasoconstriction underlying lead-induced hypertension. A similar mechanism would affect smooth muscle relaxation in the cavernous tissue leading to erectile dysfunction (ED). Is to study the possible hazardous effect of chronic lead exposure on the erectile function, and to document the deposition of lead in the cavernous tissue. The study group consisted of 34 men with ED, consecutively scheduled for penile implant insertion at Cairo University Hospital, as well as 15 controls. We determined the blood lead level for the two groups by the use of atomic absorption spectrophotometry. Sixteen of the 34 patients, and none of the 15 controls, had elevated lead serum levels (above 25 [g/dL]). We estimated the levels of two reactive oxygen species (ROS) and four antioxidants in peripheral blood for the two groups. At the time of penile implant insertion, we prepared cavernous tissue paraffin sections stained with Mallory-Parker stain to study lead deposition. We also prepared ultrathin sections for electron microscopy. We estimated cavernous tissue lead level. The ED group had significantly higher blood lead level when compared with the control group. A significant positive correlation was found between the blood lead level and cavernous tissue lead level of the ED group. Individuals with high blood lead had significantly higher levels of serum ROS and significantly lower levels of serum antioxidants, compared with those having low blood lead. Histological sections from patients with high blood lead showed deposition of grayish lead granules in the cavernous tissue. Chronic lead exposure may be associated with ED.