Association between blood lead exposure and mental health in pregnant women: Results from the Japan environment and children's study.

OBJECTIVE: Although environmental lead exposure has decreased, several studies have shown that low-level lead exposure can result in adverse psychological symptoms. However, few studies have examined lead neurotoxicity in pregnant women. We investigated the association between lead exposure and psychological symptoms in pregnant women, and between socio-economic status and blood lead levels. METHODS: Blood lead levels were measured in 17,267 pregnant women in the Japan Environment and Children's Study. Odds ratios (ORs) for high blood lead levels were calculated using multinomial logistic regression. Psychological symptoms were assessed using the Kessler Psychological Distress Scale (K6). ORs for depression (K6 ≥ 13 or ≥5) were calculated using logistic regression with adjustment for potential confounders. RESULTS: The geometric mean of whole blood lead levels was 0.58 µg/dl (range 0.14-6.75 µg/dl). Higher blood lead levels were associated with older age (OR 1.79, 9 5% confidence interval [CI] 1.46-2.19), unmarried status (OR 1.75, 95 % CI 1.31-2.33), lower household income (OR 1.76, 95 % CI 1.38-2.24), and lower educational attainment (OR 1.34, 95 % CI 1.20-1.48). The percentage of women with K6 scores ≥13 and ≥5 was 3 % and 28.2 %, respectively. There was no significant association between lead exposure and K6 score (K6 ≥ 13: OR 1.00, 95 % CI 0.76-1.32; K6 ≥ 5: OR 0.98, 95 % CI 0.88-1.09). CONCLUSION: Our results indicate a small but significant association between higher blood lead levels and lower socio-economic status in a population with low blood lead levels, but no association between low-level lead exposure and psychological symptoms.

Environmental and Occupational Lead Exposure Among Children in Cairo, Egypt: A Community-Based Cross-Sectional Study.

The aim of this study was to assess childhood lead exposure in a representative sample of Cairo, and to investigate the possible risk factors and sources of exposure. This cross-sectional study was conducted from November 2014 through April 2015. The target population was children aged 6 to 18 years, recruited into 4 groups, garbage city, moderate-living standard area, urban and suburban schools, and workshops in the city of Cairo. Blood lead levels (BLLs) and hemoglobin (Hb) concentrations were measured. Also, potential local environmental sources were assessed for hazardous lead contamination. Analysis on 400 participants has been carried out. A total of 113 children had BLLs in the range 10 to 20 µg/dL. Smoking fathers, housing conditions, playing outdoors, and exposure to lead in residential areas were significantly correlated with high BLLs. The mean values of hemoglobin were inversely correlated with BLLs. Children involved in pottery workshops had the highest BLLs and the lowest Hb values with a mean of (43.3 µg/dL and 8.6 g/dL, respectively). The mean value of environmental lead in workshop areas exceeded the recommended levels. Also, those values measured in dust and paint samples of garbage city were significantly high. Moreover, the mean lead levels in the soil samples were significantly higher in urban schools (P = 0.03) than the suburban ones. Childhood lead poisoning accounts for a substantial burden in Egypt, which could be preventable. Development of national prevention programs including universal screening program should be designed to reduce incidence of lead toxicity among children.

Developmental origins of adult diseases and neurotoxicity: epidemiological and experimental studies.

To date, only a small number of commercial chemicals have been tested and documented as developmental neurotoxicants. Moreover, an increasing number of epidemiological, clinical and experimental studies suggest an association between toxicant or drug exposure during the perinatal period and the development of metabolic-related diseases and neurotoxicity later in life. The four speakers at this symposium presented their research results on different neurotoxic chemicals relating to the developmental origins of health and adult disease (DOHaD). Philippe Grandjean presented epidemiological data on children exposed to inorganic mercury and methylmercury, and discussed the behavioral outcome measures as they relate to age and stage of brain development. Donald A. Fox presented data that low-dose human equivalent gestational lead exposure produces late-onset obesity only in male mice that is associated with neurodegeneration. Didima de Groot presented results on prenatal exposure of rats to methylazoxymethanol and discussed the results in light of the etiology of western Pacific amyotrophic lateral sclerosis and Parkinson-dementia complex. Merle G. Paule addressed the long-term changes in learning, motivation and short-term memory in aged Rhesus monkeys following acute 24 h exposure to ketamine during early development. Overall, these presentations addressed fundamental issues in the emerging areas of lifetime neurotoxicity testing, differential vulnerable periods of exposure, nonmonotonic dose-response effects and neurotoxic risk assessment. The results indicate that developmental neurotoxicity results in permanent changes, thus emphasizing the need to prevent such toxicity.

Effect of the delta-aminolevulinic acid dehydratase gene polymorphism on renal and neurobehavioral function in workers exposed to lead in China.

Effects of delta-aminolevulinic acid dehydratase (ALAD) polymorphisms on the renal and neurobehavioral functions were investigated in Chinese workers from a storage battery plant exposed to inorganic lead. Blood and urine were collected from each worker to determine the ALAD genotypes, blood lead levels (PbB), urinary beta2-MG and urinary NAG activity. The World Health Organization Neurobehavioral Core Test Battery (WHO-NCTB) was used. Of the 135 lead workers tested for ALAD genotype, 126 were ALAD1-1, 9 were ALAD1-2 but none were ALAD2-2. The gene frequencies of ALADl-1 and ALADl-2 were 93.33% and 6.67%, respectively. The workers with ALAD1-2 genotype had significantly higher concentrations of PbB (62.52microg/dl vs. 41.02microg/dl), urinary NAG (22.01U/gCr vs. 13.49U/gCr), urinary beta2-MG (194.98microg/gCr vs. 112.88microg/gCr), and digit span backward (DSB) score (6.67 vs. 5.33) than those of ALAD1-1 genotype. Urinary NAG of ALAD1-2 genotype carriers was significantly higher than that of ALAD1-1 genotype under the same blood lead level (b(i) 0.75 vs. b(i) 0.29). Interaction between PbB and ALAD genotypes has a significant influence on NAG (P=0.02) and beta(2)-MG (P=0.01). It is postulated that the workers with the ALAD2 allele appear to be more susceptible to the effects of lead on renal injury, whereas neurobehavioral functions in ALAD1 homozygote tend to be more vulnerable.

Association of cumulative lead and neurocognitive function in an occupational cohort.

Lead is a neurotoxicant that accumulates in bone with a half life of 25-30 years. To evaluate the association of lead biomarkers and cognitive function, a cohort of exposed and nonexposed workers who had been previously assessed in 1982 was retested approximately 22 years later. For the current assessment, both blood lead and tibia bone lead levels were determined. In addition, cognitive function was tested with the Pittsburgh Occupational Exposures Test battery, which had previously been administered in 1982. In exposed workers, bone lead level predicted lower current cognitive performance and cognitive decline over 22 years. In those lead-exposed workers older than age 55, higher levels of bone lead predicted poorer cognitive scores, suggesting vulnerability for older workers with higher past lead exposure. Finally, there was no association with bone lead level and recency of exposure, suggesting that cumulative body burden is most likely responsible for the progressive cognitive decrement evidenced with vulnerability because of aging.

Are brain volumes based on magnetic resonance imaging mediators of the associations of cumulative lead dose with cognitive function?

The authors used cross-sectional data (2001-2003) to consider the pathway through which past occupational lead exposure impacts cognitive function. They were motivated by studies linking cumulative lead dose with brain volumes, volumes with cognitive function, and lead dose with cognitive function. It was hypothesized that the brain regions associated with lead mediate a portion of the relation between lead dose and cognitive function. Data were derived from an ongoing US study of 513 former organolead manufacturing workers. Magnetic resonance imaging was used to perform a novel analysis to investigate mediation. Volumes associated with cognitive function and lead dose were derived by using registered images and were used in a subsequent mediation analysis. Cumulative lead dose was associated with adverse function in the visuo-construction, executive function, and eye-hand coordination domains. Regarding these domains, there was strong evidence of volumetric mediation of lead's effect on cognition in the visuo-construction domain and a moderate amount for executive function and eye-hand coordination. A second path-analysis-based approach was also used. To address the possibility that chance associations explained these findings, a permuted analysis was conducted, the results of which supported the mediation inferences. The approach to evaluating volumetric mediation may have general applicability in epidemiologic neuroimaging settings.

Intoxicação por chumbo no ambiente de trabalho / Lead poisoning in the workplace

O presente estudo tem por objetivo abordar a intoxicação por chumbo no ambiente ocupacional. Inicialmente, buscou-se contemplar a etiopatogenia do saturnismo, onde se pode afirmar que os efeitos tóxicos do chumbo dependem não só da quantidade absorvida como da tolerãncia individual e de sua distribuição no organismo: foi visto o processo de absorção, distribuição e eliminação do chumbo, sua epidemiologia, quadro clínico, diagnóstico, tratamento e prevenção. O estudo conclui qua as medidas de primeira linha na prevenção das exposições a chumbo estão no plano da prevenção primária, ou seja, trata-se de medidas que buscam eliminar ou reduzir a exposição excessiva. A quelação com EDTA (Ácido Etileno Diamino tetra-acético) é o que melhores resultados apresentam para o tratamento da intoxicação por chumbo, sendo considerado o de escolha principalmente nas intoxicações graves.

Neuropathies associated with excessive exposure to lead.

Exposure to lead is a ubiquitous problem of the modern era. The majority of cases of all forms of lead intoxication, especially lead neuropathy, result from industrial exposure. In the Western world meticulous monitoring in industry has reduced the risk of overt lead neuropathy. The classic form of lead neuropathy consists of weakness that primarily involves the wrist and finger extensors but which later spreads to other muscles. There is only minimal sensory involvement. Less commonly, there is a more typical toxic neuropathy with distally accentuated sensory and motor involvement. The motor neuropathy is more likely to develop following relatively short-term exposure to high lead concentrations and evolves in a subacute fashion. Prognosis for recovery is good as long as exposure is terminated promptly. The distal sensory and motor neuropathy develops after many years of exposure, evolves more slowly, and recovery is less certain. There is a generally weak relationship between the development of lead neuropathy and blood lead levels, at least for the subacute motor neuropathy, leading to speculation that the metabolic basis for the neuropathy is interference with porphyrin metabolism. Lead intoxication in humans causes axonal degeneration, but in some other species it causes a primarily demyelinating neuropathy. It should be possible to prevent lead neuropathy by good industrial hygiene. Close monitoring should identify excessive lead exposure before it causes overt neuropathy. If evidence of excessive exposure is found or if overt neuropathy develops, exposure must be terminated immediately. The role of chelation therapy in the treatment of lead neuropathy is controversial.

Occupational lead exposure and longitudinal decline in neurobehavioral test scores.

BACKGROUND: No previous longitudinal studies have compared and contrasted associations of blood lead and tibia lead with declines in cognitive function over the course of time in a large sample of subjects with current and past occupational exposure to inorganic lead. METHODS: From 1997 through 2001, we conducted a longitudinal study of 803 current and former lead workers in South Korea to evaluate effects on the central and peripheral nervous systems. Three study visits occurred during a mean follow-up duration of 2.20 years. Neurobehavioral test scores, peripheral nervous system function, and blood lead were measured at each of the 3 study visits, whereas tibia lead was measured by x-ray fluorescence at the first and second visits. We limited our analysis to the 576 lead workers who completed testing at all 3 visits. We performed regression analyses using generalized estimating equations. RESULTS: There were consistent associations of blood lead with test scores at baseline and of tibia lead with declines in test scores over the next year, mainly in executive abilities, manual dexterity, and peripheral vibration threshold. CONCLUSIONS: The results support the inference that occupational lead exposure can cause declines in cognitive function over the course of time. Lead likely has an acute effect on neurobehavioral test scores as a function of recent dose and a longer-term (possibly progressive) effect on cognitive decline as a function of cumulative dose.

Associations of blood lead, dimercaptosuccinic acid-chelatable lead, and tibia lead with neurobehavioral test scores in South Korean lead workers.

The authors performed a cross-sectional study to evaluate associations between blood lead, tibia lead, and dimercaptosuccinic acid (DMSA)-chelatable lead and measures of neurobehavioral and peripheral nervous system function among 803 lead-exposed workers and 135 unexposed controls in South Korea. The workers and controls were enrolled in the study between October 1997 and August 1999. Central nervous system function was assessed with a modified version of the World Health Organization Neurobehavioral Core Test Battery. Peripheral nervous system function was assessed by measuring pinch and grip strength and peripheral vibration thresholds. After adjustment for covariates, the signs of the beta coefficients for blood lead were negative for 16 of the 19 tests and blood lead was a significant predictor of worse performance on eight tests. On average, for the eight tests that were significantly associated with blood lead levels, an increase in blood lead of 5 microg/dl was equivalent to an increase of 1.05 years in age. In contrast, after adjustment for covariates, tibia lead level was not associated with neurobehavioral test scores. Associations with DMSA-chelatable lead were similar to those for blood lead. In these currently exposed workers, blood lead was a better predictor of neurobehavioral performance than was tibia or DMSA-chelatable lead, mainly in the domains of executive abilities, manual dexterity, and peripheral motor strength.