Occupational Lead Research Articles

THE ATTRIBUTABLE COSTS OF US OCCUPATIONAL LEAD POISONING

Background: Occupational standards for lead in the US have not been changed for decades, during which the knowledge about lead’s health effects has grown substantially, and new health outcomes and lower exposures associated with those outcomes are a general pattern. Objective: We estimated the health and economic benefits that would accrue from a reduction in occupational lead levels in the United States. Methods: We reviewed the literature on both occupational and general population studies of the effects of lead, and found substantial evidence for multiple health endpoints. We took data from the cost of illness literature to estimate avoided costs by reducing these effects and estimated the benefits that might be expected. To estimate exposure, we used US government data on the number of workers exposed; this is likely to be a significant underestimate of actual exposures. Results: Payer and private medical costs alone are estimated at $40 million (09US$) per year, and total direct and indirect costs are estimated at $117-142 million (09US$) per year for the 11,000 or so workers with occupational lead exposures. This does not include increased mortality, a valuation of all health effects associated with lead exposures and quality of life decrements. Conclusions: Reducing allowable lead limits would result in benefits of approximately $10,000 per worker per year, suggesting that cost effective reductions are likely to be possible. Given underreporting of actual exposures and the omission of important health effects, this is likely a significant underestimate of the true benefits of reducing occupational lead exposures in the US.

THE LEAD-ACID BATTERY FACTORY HARM TO THE SURROUNDING ENVIRONMENT AND POPULATION HEALTH

Background and Aims: To explore the effects of lead-acid battery factory on surrounding air, water and soil, as well as the impacts to population health neighboring, in order to provide scientific evidences to the strategy of protection and governance. Methods Literatures in the almost two decades concerning occupational lead contact, lead harm and lead poisoning level in battery manufacturers are analyzed and summarized to investigate the harm status. Results Lead concentration in air, water and soil exceeds the allowed limit more slightly than before since 1998, and lead accumulation in the body of occupational population and children were higher than the resident around. According to the references, Children’s BBL exceeded the allowed level above 70%, and the lead burden of occupational population arranged from 4.8% to 66.7%. Conclusion The harm of occupational lead contact in our country is relatively serious, so the supervision should be strengthened to ensure the health of workers, staffs and all people involved.

Comprehensive Analysis of 5-Aminolevulinic Acid Dehydrogenase (ALAD) Variants and Renal Cell Carcinoma Risk among Individuals Exposed to Lead

BackgroundEpidemiologic studies are reporting associations between lead exposure and human cancers. A polymorphism in the 5-aminolevulinic acid dehydratase (ALAD) gene affects lead toxicokinetics and may modify the adverse effects of lead.MethodsThe objective of this study was to evaluate single-nucleotide polymorphisms (SNPs) tagging the ALAD region among renal cancer cases and controls to determine whether genetic variation alters the relationship between lead and renal cancer. Occupational exposure to lead and risk of cancer was examined in a case-control study of renal cell carcinoma (RCC). Comprehensive analysis of variation across the ALAD gene was assessed using a tagging SNP approach among 987 cases and 1298 controls. Occupational lead exposure was estimated using questionnaire-based exposure assessment and expert review. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using logistic regression.ResultsThe adjusted risk associated with the ALAD variant rs8177796CT/TT was increased (OR = 1.35, 95%CI = 1.05–1.73, p-value = 0.02) when compared to the major allele, regardless of lead exposure. Joint effects of lead and ALAD rs2761016 suggest an increased RCC risk for the homozygous wild-type and heterozygous alleles (GGOR = 2.68, 95%CI = 1.17–6.12, p = 0.01; GAOR = 1.79, 95%CI = 1.06–3.04 with an interaction approaching significance (pint = 0.06).. No significant modification in RCC risk was observed for the functional variant rs1800435(K68N). Haplotype analysis identified a region associated with risk supporting tagging SNP results.ConclusionA common genetic variation in ALAD may alter the risk of RCC overall, and among individuals occupationally exposed to lead. Further work in larger exposed populations is warranted to determine if ALAD modifies RCC risk associated with lead exposure.

Occupational Health Management in the Lead Industry: The Korean Experience

In 1967, the problem of occupational lead exposure came to public attention in Korea. Since then, regular progress has been made in lowering workplace lead exposures, instituting new workplace controls, and implementing health examinations of exposed workers. Past serious lead poisoning episodes made it possible to introduce biological monitoring programs on a voluntary basis in high-lead-exposure facilities in Korea. Industry-specific occupational health services for lead workers in Korea during the last 22 years can be categorized into three phases. During the first phase (1988-1993), efforts were directed at increasing awareness among workers about the hazards of lead exposure, biological monitoring of blood zinc protoporphyrin began, and a respiratory protection program was introduced. During the second phase (1994-1997), a computerized health management system for lead workers was developed, blood-lead measurement was added to biologic monitoring, and engineering controls were introduced in the workplace to lower air-lead levels to comply with air-lead regulations. Finally, during the third phase (1998-present), a new biomarker, bone-lead measurement by X-ray fluorescence, was introduced. Bone-lead measurement proved to be useful for assessing body burden and to demonstrate past lead exposure in retired workers. Occupational health service practice for lead workers, including the industry-specific group occupational health system, has brought considerable success in the prevention of lead poisoning and in reducing the lead burden in Korean lead workers during the last several decades. The successful achievement of prevention of lead poisoning in Korea was a result of the combined efforts of lead workers, employers, relevant government agencies, and academic institutes.

Abnormal increase in CD8(low) T lymphocyte in patients with occupational chronic lead poisoning

To analyze the changes in CD8(low) T lymphocyte subsets in patients with occupational chronic lead poisoning. Flow cytometric analysis was used to count the numbers of CD8+ cells. 23 patients with occupational chronic lead poisoning and 20 controls were examined. Compared with control group (8.21% ± 3.02%), the CD8(low) T lymphocyte (12.98% ± 5.62%) were significantly increased in patients with occupational chronic lead poisoning. Although the ratio of CD+ T lymphocyte is normal, the CD8 level is significantly decreased. The increase of CD8(low) T lymphocyte may be an important phenomenon of immuno-injury induced by lead. CD8(low) T lymphocyte could be an new direction for research of lead immuno-toxicity.

Environmental and Occupational Lead Effect on Hearing

Environmental and Occupational Lead Effect on Hearing

The Association of Lead Exposure and Impairment of Brainstem Auditory-evoked Response and Cochlea Function

PP-31-156 Background/Aims: On the basis of some researches, the heavy metals (including lead, mercury, and tin) may be toxic on hearing in human beings and animals. Complex exposures to lead and noise were the 2 common sources of occupational exposures in the factories. The aim of the study was to investigate the effect of occupational lead on the auditory system. Methods: We measured the auditory brainstem-evoked response and cochlea function with distortion product otoacoustic emissions (DPOAEs) that are preneural responses of the outer hair cells of the inner ear in 12 adult lead-workers and 12 age- and sex- matched persons who were not exposed to lead and noise. Results: The results showed that the auditory brainstem-evoked response latency of wave I, II, III, and III–V significantly increased in the group of lead-workers (blood lead: 36.13 ± 4.52 μg/dL), as compared with the group without lead exposure (blood lead: 4.09 ± 1.41 μg/dL). The latency of wave I, II, III, V, and interpeak latency I–III were correlated to blood lead levels. Mean DPOAEs of the lead workers were significantly different from the reference group at DP frequencies of 812, 1000, 1281, 1593, 2031, 2562, and 3187 Hz. However, the DPOAEs for the lead workers were within the normal ranges of the reference group only at 4031 Hz. Although there was a tendency for the lead workers to have diminished DPOAEs, no consistent correlation of DPOAEs with lead level was found. The prevalence of normal DPOAEs in the lead workers was up to 79%. Conclusion: We concluded that lead should be otoneural toxic, especially, in the workers exposed to lead and noise both. The hearing conservation program should enhance more for the worker exposing to both ototoxic agents.

Occupational and Environmental Lead Exposure in Port Harcourt, Nigeria: Analysis of its association with renal function indices

In spite of the high risk of lead exposure in Nigeria, there is a paucity of data on the occupational and environmental burden of lead exposure and its impact on human health especially its nephrotoxic effects. This study aims to assess the degree of occupational and environmental lead exposure in Port Harcourt Nigeria and the relationship between lead exposure and indices of renal function. A cross sectional comparative study of 190 aduIt subjects with occupational lead exposure and 80 matched controls. Blood lead was used as the biomarker of lead exposure. Serum urea, creatinine, uric acid, urine albumin and glomerular filtration rate were the renal function indices measured. Occupationally lead exposed subjects had higher mean blood lead 50.37 +/- 24.58 ug/dI, than controls 41.40 +/- 26.85 ug/dl (p = 0.008). The mean values of serum urea, creatinine and uric acid were significantly higher in study subjects compared to controls 3.06 +/- 0.81 mmol/L vs. 2.7 +/- 0.84 mmol/L (p = 0.002), 87.2 +/- 14.30 umol/L vs. 80.68 +/- 14.70 umol/L (p = 0.001) and 271.93 +/- 71.18 umol/L vs. 231.1 +/- 62.70 umol/L (p = 0.000) respectively. Creatinine clearance was significantly lower in subjects compared to controls 98.86 +/- 21.26 mI/min/1.72m2 vs. 108.18 +/- 25.16 mI/min/1.72m2 (p = 0.002). Blood lead correlated positively only with blood urea [r = .031, r2 = .017, p = .031] and negatively [r = -.144, r2 = .02 1, p = .018] with serum phosphate. The level of environmental and occupational lead exposure in Port Harcourt, Nigeria is high, with occupational lead exposure increasing the risk of lead toxicity and renal function impairment.

Abstract PR-8: Gene-environment interactions between JAZF1 and occupational and neighborhood lead exposure in African American prostate cancer cases

Abstract African American men have the highest incidence of prostate cancer in the world and have substantially higher rates of prostate cancer when compared to white men in the U.S. The cause(s) for this race disparity remains elusive. A single nucleotide polymorphism (SNP), rs10486567, in intron 2 of juxtaposed with another zinc finger protein 1 (JAZF1) has been associated with increased risk of prostate cancer in genome-wide association studies (GWAS) and may be key to uncovering reasons for disparities in the disease. JAZF1 is a cysteine-hystidine structured zinc finger protein, a type of protein that has been shown to interact with lead in vitro. Lead is recognized as a probable carcinogen in humans and African American men who are residentially segregated to industrialized urban environments in the U.S. have higher blood lead levels on average compared to white men. In a case-only study of 228 African American men with prostate cancer diagnosed at a large health system in the Detroit Metropolitan area, we assessed gene-environment interactions (GxE) between rs10486567 (CC vs. CT/TT genotype) and two sources of lead exposure. Lifetime occupational lead exposure was determined through industrial hygiene review of extensive face-to-face interviews. Neighborhood lead exposure, defined as the median proportion of census tract housing built before 1950 (≥ 47% vs. <47%), was derived from subjects address at time of diagnosis. Generalized estimating equation (GEE) modeling was used for analyses that included nested census data. In younger African American cases (<62 years of age), we found a significant gene-environment interaction between rs10486567 CC carriers and high occupational-respiratory lead exposure when compared to those with no respiratory lead exposure (OR 2.68, CI 1.05-6.88, p=.04). A significant GxE interaction was also observed between CC carriers and residence in a neighborhood with a large proportion of older housing in all cases and younger cases (all OR 1.92, CI 1.12-3.29, p=.017, younger OR 2.64, CI 1.21-5.73, p=.014, older OR 1.64, CI 0.73-3.70, p=.23). The interaction between rs10486567 and housing remained significant even after adjustment for occupational lead exposure. Combining lead exposure from occupation and neighborhood housing into a four category index showed even stronger interactions between the polymorphism and the highest lead exposed group compared to the lowest exposure group (all OR 3.13, CI 1.22-7.99, p=.017). These findings indicate that lead may be an important risk factor for prostate cancer in carriers of the rs10486567 CC genotype. Future studies of race disparities in prostate cancer should further assess interactions between lead and JAZF1 and lead and other zinc containing proteins. Focusing on genes and polymorphisms identified in GWAS studies might help to identify environmental risk factors for prostate cancer. Citation Information: Cancer Epidemiol Biomarkers Prev 2010;19(10 Suppl):PR-8.

Executive function modifies the relationship between occupational lead exposure and complex figure test performance

ObjectivesTo determine if chronic lead exposure is associated with non-verbal memory performance and if this association is affected by organisation strategies, a component of executive functions.MethodsWe administered the Rey–Osterrieth Complex...

Effects of occupational lead exposure on renal and nervous system of workers of traditional tile factories in Mashhad (northeast of Iran)

Occupational lead poisoning is a health problem in Iran. Renal and neuropsychiatric complications of occupational lead poisoning are the main concerns for the workers and their employers. It was thus aimed to investigate the renal and neurotoxic effects of lead poisoning in the workers of two traditional-tile-factories. Researchers visited the workers in the factories and collected data by taking direct history and physical examinations in summer of 2005. Data were recorded in previously designed forms. Blood and urine lead concentrations were measured by an atomic absorption technique. A neurologist examined all workers and electrophysiological investigations were undertaken as clinically indicated. Data were analyzed by SPSS software and chi-square, student t test and Pearson correlation tests were used accordingly. The numerical data were expressed as mean ± standard deviation and p < 0.05 was considered as the significant level. Overall, 108 male subjects aged 37 ± 7.8 years were studied. Duration of lead exposure was 9.8 ± 6 years. Lead concentration in 2005 was 361.5 ± 176.9 μg/L. The main objective clinical findings were lead line (64.8%), peripheral neuropathy of upper limb (37%), suppression of deep tendon reflexes (DTR) in upper limbs (25.7%), tremor (23.3%), peripheral neuropathy of lower limbs (17%) and abdominal tenderness (15.1%). The subjective findings were mainly on the central nervous system, such as loss of memory (57%), moodiness (56.1%), agitation (47.7%), drowsiness (36.4%), and headache (29.9%). There was no significant correlation between blood lead concentration and glomerular filtration rate (GFR). But there were significant correlations between the blood lead concentrations and urine lead concentration (p < 0.001). This study showed that lead had toxic effects on the teeth (bone), central and peripheral nervous system, more than renal function. Prophylactic and treatment measures were performed.

Risk assessment of renal dysfunction caused by occupational lead exposure

To assess the risk of renal dysfunction caused by occupational lead exposure through epidemiological investigation. The workers in a battery factory were selected as the subjects for the exposure and effect assessment. The occupational environmental monitoring data was collected and used to calculate the total external dose of lead. The relationship between external dose and internal dose of lead was analyzed. The external dose, blood lead (BPb) and urinary lead (UPb) were used as exposure biomarkers while the urinary N-acetyl-D-glucosaminidase (UNAG), and urinary albumin (UALB) were used as the effect biomarkers for the renal dysfunction caused by lead. Software of BMDS (BMDS 11311) was used to calculate BMD. The external and internal does of lead was positively correlated (BPb: r = 0.466, P < 0.01; UPb: r = 0.383, P < 0.01). The levels of BPb, UPb in exposure group (654.03 microg/L, 143.45 microg/g Cr) were significantly higher than those in the control group (57.12 microg/L, 7.20 microg/g Cr), so were UALB, UNAG; in addition, all of them presented significant dose-response relationship. The BPb BMD of UALB, UNAG were 607.76, 362.56 microg/L respectively and the UPb BMD of UALB, UNAG were 117.79, 78.79 microg/gCr respectively. Occupational lead exposure can cause renal dysfunction, which presents dose-response relationship; the risk assessment of renal dysfunction caused by occupational lead exposure is performed by BMD calculation of BPb and UPb.

Risk assessment of nerve conduction velocity in workers exposed to lead

To explore the dose-effect relationship between lead exposure and nerve conduction velocity, and to assess risk characteristics of nerve conduction velocity induced by lead exposure. The external dose, internal dose (blood lead, urine lead) and the conduction velocity of peripheral nerve were examined. The benchmark dose of a population exposed to occupational lead was estimated to develop risk assessment of nerve conduction velocity in worker exposed to lead by use of BMDS (version 1.3.3). The BMDL in terms of blood lead and urine lead was calculated. There was correlation between blood lead and urine lead. The sense nerve conduction velocity was decreased significantly in the group of lead exposure workers (P < 0.05). The BMDLs-05 for median nerve conduct velocity, ulnar nerve conduction velocity, and superficial peroneal nerve conduction velocity in terms of blood lead were 456.99, 332.36 and 468.38 microg/L respectively; the BMDLs-05 in terms of urine lead were 14.1, 9.2 and 13.6 microg/gCr respectively. The internal dose is the better index to reflect the level of lead exposure. Blood lead is identified as a specific and sensitive biomarker for sense nerve conduction velocity reduction. Ulnar nerve conduction velocity can be used as highly sensitive biomarkers to screen the high risk population of lead exposure.

Occupational Lead Exposure and Severe CKD: A Population-Based Case-Control and Prospective Observational Cohort Study in Sweden

The role of low-level lead exposure in the cause of chronic kidney disease (CKD) is unsettled. Case-control study and prospective observational cohort study. 926 cases with incident severe CKD (serum creatinine > 3.4 mg/dL for men and > 2.8 mg/dL for women for the first time) and 998 population controls were included. Cases represented nearly all patients with incident severe CKD in Sweden during 2 years. Cases also were followed up prospectively for 7-9 years. Exposed and nonexposed cases were compared with regard to rate of change in estimated glomerular filtration rate (eGFR) and renal survival. Lead exposure was assessed using the expert rating method. Associations between lead exposure and risk of CKD, adjusted for factors associated with this outcome, were analyzed using multivariable logistic regression modeling, whereas links to the rate of change in eGFR were analyzed in mixed-effects multivariable models based on up to 6 measurements. Renal survival in relation to lead exposure was analyzed in a Cox proportional hazards model. The adjusted OR for incident severe CKD was 0.97 (95% CI, 0.68-1.38) in lead-exposed compared with nonexposed participants. The OR for individuals with the highest average exposure (>0.0075 mg/m(3)) was 1.09 (95% CI, 0.64-1.85). ORs for CKD caused by glomerulonephritis, nephrosclerosis, and diabetic nephropathy did not differ importantly. In patients with CKD ever exposed and most exposed to lead, eGFRs changed by -4.27 and -3.39 mL/min/1.73 m(2)/y compared with -4.55 mL/min/1.73 m(2)/y in nonexposed patients, respectively. Only native Swedes were included, which may limit generalizability. Blood lead was not measured to confirm the validity of the expert rating method. Our data provide no evidence of an important role of low-level occupational lead exposure in the cause or progression of severe CKD.

Lead Nephropathy: Revisiting an Overlooked Cause of Kidney Disease

Despite the recognition of lead nephropathy as a consequence of environmental and occupational lead exposure, lead nephropathy still appears to be underrecognized by physicians as a cause and promoter of chronic kidney disease (CKD), especially in people with more apparent causative factors such as diabetes and hypertension. This review focuses on the clinical, pathophysiological and epidemiological perspectives of lead nephropathy with the objective of promoting the awareness of this important but overlooked cause of CKD among physicians. Literature was reviewed using available medical journals and online literature search through Google, Pubmed, Medline, Medscape and HINARI databases. The key words employed were: Lead Nephropathy, Environmental and Occupational lead exposure and chronic kidney disease. Lead nephropathy which is a tubulointerstitial nephritis, may present acutely or chronically in association with hypertension. The clinical diagnosis of lead nephropathy is complex, because the symptoms are varied and non-specific especially with subclinical nephrotoxicity. The recognition of lead nephropathy can be enhanced if physicians have a high index of suspicion in the assessment of patients with renal disease. It is recommended that the evaluation of environmental and occupational nephrotoxins like lead be incorporated into programs for the prevention of CKD, especially in developing countries where lead exposure and toxicity still remain largely unchecked and the prevalence and burden of CKD is increasing.

Individual susceptibility associated with enzymatic and cytogenetic biomarkers in occupational exposure to inorganic lead

More consideration is given to occupational lead exposure, especially from ecogenetic and molecular epidemiology point of view. Lead causes genotoxic effects and influences some important metabolic pathways by inhibiting key enzymes, a good reason for researchers to assess individual susceptibility through specific biomarkers. The present paper emphasizes the relationship between occupational lead exposure, biochemical indicators (δ-aminolevulinic acid dehydratase), cytogenetic biomarker, hematological indicators (hemoglobin, hematocrit) and frequency of hospitalizations for saturnism. The study comprised 12 male workers occupationally exposed to inorganic lead from a non- ferrous metallurgical factory, Romania. Exposure to inorganic lead was assessed by determination of lead concentration in the workplace and by biotoxicological analyses (blood lead level, urine lead level, urine δ-aminolevulinic acid). Blood δ- aminolevulinic acid dehydratase level was measured. We found a statistically significant correlation between micronucleus score, level of δ-aminolevulinic acid dehydratase and frequency of hospitalizations for lead poisoning. We propose these indicators as an accessible instrument in evaluating individual susceptibility to lead poisoning, more practical than laborious polymorphism genes assessment and less ethically debatable issue.

Gruppenvergiftung mit Blei am Arbeitsplatz

Seventeen East-European workers with a suspected lead-intoxication presented themselves to the Department of Toxicology. All of them had worked on the renovation of pylons of a high-tension line. The old paint, known to contain lead was removed with needle descalers. The patients had blood lead concentrations between 325 and 1124 microg/l, but no specific symptoms. The workers neglected the protective measures at their working-place. 12 of 17 workers had lead-concentrations above 400 microg/l (Reference < 90 microg/l). 10 of 17 patients showed an increased level of free protoporphyrins and all workers showed a decreased activity of delta-aminolaevulinacid-dehydratase (ALAD). Patients with lead-concentration above 700 microg/l were treated with the chelating agent meso-2,3-dimercaptosuccinic acid (DMSA) 3 x 200 mg/d for nine days. The patients with lead concentrations between 400 and 700 microg/l were treated which DMSA 3 x 100 mg/d. After the DMSA-treatment the lead-concentrations had dropped (p < 0.001). During the DMSA-therapy one patient had to be treated in the hospital because of a generalised allergic exanthema. We report seventeen patients with high lead concentration in their blood due to occupational exposure. The high blood lead levels showed that the workers had not been protected adequately. This examplifies that occupational lead exposure still occurs, also in Germany. By patients with unspecific symptoms connected with lead exposure a biomonitoring for lead is necessary.

Lead Exposure, Polymorphisms in Genes Related to Oxidative Stress, and Risk of Adult Brain Tumors

There is some evidence that oxidative stress plays a role in lead-induced toxicity. Mechanisms for dealing with oxidative stress may be of particular relevance in the brain given the high rate of oxygen metabolism. Using a hospital-based case-control study, we investigated the role of oxidative stress in the potential carcinogenicity of lead through examination of effect modification of the association between occupational lead exposure and brain tumors by single nucleotide polymorphisms in genes with functions related to oxidative stress. The study included 362 patients with glioma (176 of which had glioblastoma multiforme), 134 patients with meningioma, and 494 controls. Lead exposure was estimated by expert review of detailed job history data for each participant. We evaluated effect modification with 142 single nucleotide polymorphisms using likelihood ratio tests that compared nested unconditional logistic regression models that did and did not include a cross-product term for cumulative lead exposure and genotype. When the analyses were restricted to cases with glioblastoma multiforme, RAC2 rs2239774 and two highly correlated GPX1 polymorphisms (rs1050450 and rs18006688) were found to significantly modify the association with lead exposure (P <or= 0.05) after adjustment for multiple comparisons. Furthermore, the same GPX1 polymorphisms and XDH rs7574920 were found to significantly modify the association between cumulative lead exposure and meningioma. Although the results of this study provide some evidence that lead may cause glioblastoma multiforme and meningioma through mechanisms related to oxidative damage, the results must be confirmed in other populations.

Detection of DNA damage of workers occupationally exposed to lead with flow cytometer assay

To study DNA damage of workers occupationally exposed to lead with flow cytometer assay. The lymphocytes were obtained from 41 workers occupationally exposed to lead (comparable group) and another 50 from control group. Flow cytometer (FCM) assay was used to detect DNA damage. DNA damage rate and geometric mean fluorescence intensity in the comparable group were significantly higher than those in the control group (P<0.05). There were no significant differences in the DNA damage and geometric mean fluorescence intensity between different age groups (P>0.05). The differences in correlation analysis between blood lead, urine lead, delta-ALA and DNA damage rate were not significant (P>0.05). The correlation analysis showed no statistical significance between concentration of blood lead, urine lead, delta-ALA and geometric mean fluorescence intensity (P>0.05). There was positive correlations not only between the high concentration of blood lead, delta-ALA and damage rate of DNA, but also between the high concentration of blood lead and geometric mean fluorescence intensity. The coefficient r showed statistical significance (P<0.05). Occupational lead exposure can cause DNA damage. Gamma H2AX flow cytometer assay is a sensitive, objective and effective method for detection of DNA damage of peripheral blood lymphocytes.

Membrane, intracellular, plasma and urinary sodium and potassium in occupational lead exposure: effects of Vitamin C supplementation

Membrane, intracellular, plasma and urinary sodium and potassium in occupational lead exposure: effects of Vitamin C supplementation