Synergistic effects of iron deficiency and lead exposure on blood lead levels in children

Background  

Lead poisoning is a well recognized environmental health problem in children. Independent association of iron deficiency and lead exposure with elevated blood lead level (BLL) has been reported. Whether iron deficiency in combination with chronic lead exposure increases BLL and susceptibility to its harmful effects in children needs to be elucidated.     

Effect of living in lead mining area on growth

Objective Blood lead level BLL and growth parameters including weight and height, in children, living in lead mining area was surveyed. Methods Two groups of 7–11 yr old children, including 45 from a lead mining area (Angooran-Zanjan Province-Iran) and 36 from control area (similar area to the study area, but not lead mining: Ijrood-the same province), were selected to assess BLL (by atomic absorption spectrometry) and growth parameters. Results In the children of the study and control areas, mean BLLs were 36.97±24.67 (μg/dL; mean ± SD) and 15.57 ± 13.35 (μg/dL; mean±SD), respectively (P=0.0005). No significant correlation was found between BLL in children and their fathers’ occupation. In addition, there was no significant difference in growth parameters, including weight and height, in the children of two groups. Conclusion Regarding the results of this study, environmental exposure due to living in lead mining area can lead to increased BLL in children. In addition, our results suggest there is no significant effect of BLL on growth parameters in children in lead mining area. Since some clinical and sub clinical problems are strongly probable when BLL is increased, special attention of the relevant organizations, and more research about the problem and its outcome, is recommended.     

Childhood passive smoking, race, and coronary artery disease risk: the MCV Twin Study. Medical College of Virginia.

BACKGROUND: Children with long-term exposure to passive cigarette smoke may be at elevated risk for the development of premature coronary artery disease (CAD). OBJECTIVE: To examine how CAD risk factors, exposure to passive smoking, sex, and race are related in pubertal children and to determine if there is an identifiable childhood risk profile (i.e., does passive smoking interact with other coronary risk factors to increase the risk of developing premature CAD). DESIGN: Cohort analytic study. SETTING: The Medical College of Virginia (MCV) Twin Study, Richmond, Va. SUBJECTS: Randomly selected twins from 408 11-year-old twin pairs recruited from nearby schools. METHODS: Data collection occurred at 18-month intervals on family and health histories, smoking and alcohol consumption, blood pressure, anthropometrics, and biochemical assays. Data from cohorts of 11-year-olds studied through age 15 years were analyzed by repeated-measures analyses of variance using a mixed modeling approach. Models for high-density lipoprotein cholesterol (HDL-C) included race, sex, passive smoking status, weight, systolic and diastolic blood pressures, and all interactions. RESULTS: Passive smoke exposure was greater in white families than in black families. Levels of HDL-C and HDL2-C (HDL subfraction 2 cholesterol) were lower in white children than in black children (visit 1: HDL-C, mean +/- SD, 1.21+/-0.26 vs. 1.31+/-0.26 mmol/L [47.0+/-10.1 vs. 50.6+/-10.1 mg/dL], P< or =.01; HDL2, mean +/- SD, 0.31+/-0.18 vs. 0.41+/-0.19 mmol/L [12.3+/-7.0 vs. 15.9+/-7.4 mg/dL], P< or =.001). Children with a family history of cardiovascular disease had differences in HDL-C levels related to race that were worsened by exposure to cigarette smoke. In these children, HDL-C level was lower in those exposed to passive smoking (visit 1: 1.18+/-0.23 vs. 1.25+/-0.23 mmol/L [45.6+/-9 vs. 48.2+/-9 mg/dL] and visit 4: 0.98+/-0.10 vs. 1.19+/-0.18 mmol/L [37.8+/-4 vs. 46.0+/-7 mg/dL]; P<.001), with white children having lower HDL-C levels than black children (visit 1: 1.12+/-0.21 vs. 1.36+/-0.23 mmol/L [43.2+/-8 vs. 52.7+/-9 mg/ dL] and visit 4: 0.97+/-0.31 vs. 1.01+/-0.31 mmol/L [37.6+/-12 vs. 39.0+/-12 mg/dL]; P = .004). In white families, as weight increased, boys exposed to passive smoking showed the greatest decrease in HDL-C level (P<.01 for weight by sex and passive smoking interaction). Risk factors for CAD, such as blood pressure, interacted with HDL-C and these relationships varied by race and sex. CONCLUSIONS: Pubertal children with long-term passive cigarette smoke exposure have lower HDL-C levels. Racial differences in HDL-C levels are related to passive smoke exposure. In children with a family history of cardiovascular disease, interactions exist between passive smoking, HDL-C level, and blood pressure that differ by sex and race. White males exposed to passive smoking who have a family history of cardiovascular disease and higher weights and diastolic blood pressures may be at special risk for premature CAD.     

Evaluation of risk assessment questions used to target blood lead screening in Illinois

OBJECTIVE: Beginning in 1995, Illinois law permitted targeted-as opposed to universal-blood lead screening in low-risk areas, which were defined by ZIP code characteristics. State guidelines recommended specific lead risk assessment questions to use when targeting screening. This study was designed to evaluate the sensitivity and specificity of Illinois lead risk assessment questions. DESIGN: Parents bringing their 9- or 10- or 12-month and 24-month-old children for health supervision visits at 13 pediatric practices and parents of children (aged 6 through 25 months and who needed a blood lead test) receiving care at 5 local health departments completed a lead risk assessment questionnaire concerning their child. Children had venous or capillary blood lead testing. Venous confirmation results of children with a capillary level >/=10 micrograms/dL were used in analyses. CHILDREN: There were 460 children with both blood and questionnaire data recruited at the pediatric practices (58% of eligible) and 285 children (51% of eligible) recruited at local health departments. Of the 745 children studied, 738 provided a ZIP code that allowed their residence to be categorized as in a low-risk (n = 456) or high-risk (n = 282) area. RESULTS: Sixteen children (3.5%) living in low-risk areas versus 34 children (12.1%) living in high-risk areas had a venous blood lead level (BLL) >/=10 micrograms/dL; 1.8% and 5.3%, respectively, had a venous BLL >/=15 micrograms/dL. For children living in low-risk areas, Illinois mandated risk assessment questions (concerning ever resided in home built before 1960, exposure to renovation, and exposure to adult with a job or hobby involving lead) had a combined sensitivity of.75 for levels >/=10 micrograms/dL and.88 for levels >/=15 micrograms/dL; specificity was.39 and.39, respectively. The sensitivity of these questions was similar among children from high-risk areas; specificity decreased to.27 and.28, for BLLs >/=10 micrograms/dL and >/=15 micrograms/dL, respectively. The combination of items requiring respondents to list house age (built before 1950 considered high risk) and indicate exposure to renovation had a sensitivity among children from low-risk areas of.62 for BLLs >/=10 micrograms/dL with specificity of.57; sensitivity and specificity among high-risk area children were.82 and.36, respectively. For this strategy, similar sensitivities and specificities for low and high-risk areas were found for BLLs >/=15 micrograms/dL. CONCLUSIONS: The Illinois lead risk assessment questions identified most children with an elevated BLL. Using these questions, the majority of Illinois children in low-risk areas will continue to need a blood lead test. This first example of a statewide screening strategy using ZIP code risk designation and risk assessment questions will need further refinement to limit numbers of children tested. In the interim, this strategy is a logical next step after universal screening.     

Parental smoking: asthma and wheezing illnesses in infants and children

Parental smoking has an important impact on asthma and wheezing illnesses in infants and children. In utero exposure is associated with impaired lung growth and wheezing illnesses, particularly in preschool children. Exposure to environmental tobacco smoke is associated with increased wheezing illnesses and increased symptoms in asthmatics. There are no consistent data to confirm an effect of in utero or postnatal cigarette smoke exposure on the prevalence of asthma but there is evidence of increased severity of symptoms. The detrimental effects of parental smoking on lung growth will have an impact on respiratory health throughout life.     

Promoting bone health in children and adolescents following solid organ transplantation

Solid organ transplantation in children and adolescents provides many benefits through improving critical organ function, including better growth, development, cardiovascular status, and quality of life. Unfortunately, bone status may be adversely affected even when overall status is improving, due to issues with pre‐existing bone disease as well as medications and nutritional challenges inherent post‐transplantation. For all children and adolescents, bone status entering adulthood is a critical determinant of bone health through adulthood. The overall health and bone status of transplant recipients benefits from attention to regular physical activity, good nutrition, adequate calcium, phosphorous, magnesium and vitamin D intake and avoidance/minimization of soda, extra sodium, and obesity. Many immunosuppressive agents, especially glucocorticoids, can adversely affect bone function and development. Minimizing exposure to “bone‐toxic” medications is an important part of promoting bone health in children post‐transplantation. Existing guidelines detail how regular monitoring of bone status and biochemical markers can help detect bone abnormalities early and facilitate valuable bone‐directed interventions. Attention to calcium and vitamin D supplementation, as well as tapering and withdrawing glucocorticoids as early as possible after transplant, can provide best bone outcomes for these children. Dual‐energy X‐ray absorptiometry can be useful to detect abnormal bone mass and fracture risk in this population and newer bone assessment methods are being evaluated in children at risk for poor bone outcomes. Newer bone therapies being explored in adults with transplants, particularly bisphosphonates and the RANKL inhibitor denosumab, may offer promise for children with low bone mass post‐transplantation.     

Growth hormone treatment in children with cystic fibrosis

Children with cystic fibrosis (CF) have problems with poor linear growth and inadequate weight gain. Nutritional augmentation has been the mainstay of therapy for improving both weight and height in CF; however inadequate growth continues to be a problem. Furthermore, protein catabolism has been documented even in non-acutely ill adults and children with CF, and could adversely affect longitudinal growth. Human recombinant growth hormone (GH) has positive effects on nitrogen balance, and multiple studies have demonstrated improved height and weight in children treated with GH. The purpose of this article is to summarize studies evaluating GH use in children with CF.     

Relationship between Blood Pressure and Passive Smoking in Elementary School Children

Objective

Many diseases form their basis during childhood. One example is the changes in vascular structure and function, leading to atherosclerosis. In this study, we have assessed the impact of exposure to cigarette smoke on blood pressure of elementary school children in Kermanshah.

Methods

80 elementary school children exposed to cigarette smoke and 80 not exposed to smoke were studied in fall 2010. Information regarding the smoking status of parents and the children’s health were obtained through questionnaires completed by parents. After physical examination and exclusion of those children with acute and chronic diseases as well as those consuming medicine, we measured and compared blood pressure in the exposure and non-exposure groups. Data were analyzed using the ANOVA statistical test. Values are expresses as Mean±SD.

Findings

The mean systolic and diastolic blood pressures of the exposure group were higher than those of the non-exposure group (109.3±9.97/64.92±7.36 vs105.47±8.98/62.5±7.01, respectively; CI: 0.95, P<0.05). Meanwhile, difference between two groups according to sex was not statistically significant.

Conclusion

Our study indicates that systolic and diastolic blood pressures are higher in those elementary school children exposed to cigarette smoke compared to those who are not.     

Early developmental origins of impaired lung structure and function

Epidemiological studies show that exposure to factors that restrict fetal growth or lead to low birthweight can alter lung development and have later adverse effects on lung function and respiratory health. The major causal factors include reduced nutrient and oxygen availability, nicotine exposure via maternal tobacco smoking and preterm birth, each of which can affect critical stages of lung development. Experimental studies show that these environmental insults can permanently alter lung structure and hence lung function, increasing the risk of respiratory illness and accelerating the rate of lung aging. Further studies are required that address the molecular and cellular mechanisms by which these factors adversely affect lung development and whether such effects can be blocked or reversed. Ultimately however, a major goal should be to prevent prenatal compromises through clinical monitoring, and in the case of smoking through education, thereby ensuring that each fetus has the best possible environment in which to develop.     

Long-term sleep disturbances in children: A cause of neuronal loss

Short-term sleep loss is known to cause temporary difficulties in cognition, behaviour and health but the effects of persistent sleep deprivation on brain development have received little or no attention. Yet, severe sleep disorders that last for years are common in children especially when they have neurodevelopmental disabilities. There is increasing evidence that chronic sleep loss can lead to neuronal and cognitive loss in children although this is generally unrecognized by the medical profession and the public. Without the restorative functions of sleep due to total sleep deprivation, death is inevitable within a few weeks. Chronic sleep disturbances at any age deprive children of healthy environmental exposure which is a prerequisite for cognitive growth more so during critical developmental periods. Sleep loss adversely effects pineal melatonin production which causes disturbance of circadian physiology of cells, organs, neurochemicals, neuroprotective and other metabolic functions. Through various mechanisms sleep loss causes widespread deterioration of neuronal functions, memory and learning, gene expression, neurogenesis and numerous other changes which cause decline in cognition, behaviour and health. When these changes are long-standing, excessive cellular stress develops which may result in widespread neuronal loss. In this review, for the first time, recent research advances obtained from various fields of sleep medicine are integrated in order to show that untreated chronic sleep disorders may lead to impaired brain development, neuronal damage and permanent loss of developmental potentials. Further research is urgently needed because these findings have major implications for the treatment of sleep disorders.     

Blood lead levels and risk factors for lead toxicity in children from schools and an urban slum in Delhi

This cross-sectional study was conducted to estimate the mean blood lead levels (BLL) and prevalence of lead toxicity in a representative sample of schoolchildren and children residing in an urban slum. In addition, the association of potential environmental risk factors with elevated BLL was studied. Children aged 4-6 years were selected from schools of the South zone of Delhi (n = 125) and from an urban slum (n = 65). Risk factors were recorded using a pre-tested questionnaire and blood lead and zinc protoporphyrin (ZPP) levels were estimated. The mean BLL was 7.8 microg/dl (SD 3.9) and the proportion of children with blood lead > or = 10 microg/dl was 18.4 per cent. Distance of the residence or school from a main road appeared to be associated with higher blood lead concentrations, but these differences were not statistically significant. In our setting, vehicular pollution may be a major contributing factor in lead contamination of the environment.     

Blood lead concentration and children's anthropometric dimensions in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994

OBJECTIVE: To assess the association between lead exposure and children's physical growth. DESIGN: Cross-sectional analysis of data from the Third National Health and Nutrition Examination Survey, 1988-1994. PARTICIPANTS: A total of 4391 non-Hispanic white, non-Hispanic black, and Mexican-American children age 1 to 7 years. Measurements and Results: We investigated the association between blood lead concentration and stature, head circumference, weight, and body mass index with multiple regression analysis adjusting for sex, ethnic group, iron status, dietary intake, medical history, sociodemographic factors, and household characteristics. Blood lead concentration was significantly negatively associated with stature and head circumference. Regression models predicted reductions of 1. 57 cm in stature and 0.52 cm in head circumference for each 0.48 micromol/L (10 micrograms/dL) increase in blood lead concentration. We did not find significant associations between blood lead concentration and weight or body mass index. CONCLUSIONS: The significant negative associations between blood lead concentration and stature and head circumference among children age 1 through 7 years, similar in magnitude to those reported for the Second National Health and Nutrition Examination Survey, 1976-1980, suggest that although mean blood lead concentrations of children have been declining in the United States for 2 decades, lead exposure may continue to affect the growth of some children.     

Blood lead levels of maternal-cord pairs, children and adults who live in a central urban area in Turkey

Lead levels were measured in blood samples of 99 adults, 180 children and 143 pregnant women living in Eski?ehir, an urban area in Turkey. One hundred and twenty 120 cord blood and 93 breast-milk samples were also obtained. Mean lead level in blood of adults, children, pregnants, cord blood and in breast-milk samples were 3.13 +/- 1.4 microg/dl, 3.56 +/- 1.7 microg/dl, 2.8 +/- 1.5 microg/dl, 1.65 +/- 1.4 microg/dl and 2.34 +/- 1 microg/L, respectively. It was higher in men than in women in adults (p<0.05) and in iron-deficient children than in those not deficient (p<0.01), and was negatively correlated with body weight (BW) and hemoglobin (Hb) in children (p<0.05 for both). Maternal lead level was strongly related with cord blood and breast-milk lead contents (p<0.001, p<0.0001, respectively). The lead exposure in this region is much lower than the critical level defined for lead poisoning as >10 microg/dl by the Centers for Disease Control and Prevention iron deficiency poor nutrition are the risk factors to lead exposure in children.     

Lead levels in Canadian children: Do we have to review the standard?

Research indicates that the blood lead levels that were once considered safe can adversely affect the neurodevelopment of children. The purpose of the present article is to review issues surrounding lead exposure in Canadian children, including sources, chronic low levels of exposure, and recommendations for prevention. Information was obtained through searches of MEDLINE and Web of Science using a combination of: “Canada” or “Canadian” plus “child” or “paediatrics” plus “lead” or “lead poisoning” or “blood lead”. Centers for Disease Control and Prevention data and American peer-reviewed literature were also used. On-line Health Canada advisories (available since 1995), as well as relevant reports from nongovernmental organization and the media, were reviewed. The present review found that there has been limited surveillance of blood lead levels of Canadian children and, mainly, among high-risk groups. Harmful health effects may occur below the current standards and the threat of lead in consumer products remains. The current regulation seems to be inadequate to protect Canadian children.     

Maternal tobacco smoking, nicotine replacement and neurobehavioural development

Abstract The adverse effects of prenatal cigarette smoke exposure on human reproductive outcomes are a major scientific and public health concern. In the United States, approximately 25% of women of childbearing age currently smoke cigarettes, and only a small percentage of these individuals quit after learning of their pregnancy. Women interested in smoking cessation during pregnancy have a number of options, including behavioural and pharmacological aids, but nicotine replacement therapy (NRT) is by far the most common approach. While NRT avoids exposure to the myriad compounds present in tobacco smoke, nicotine itself causes damage to the developing nervous system. The purpose of this article is to review the detrimental effects of developmental tobacco smoke exposure on short- and long-term outcomes with particular emphasis on neurobehavioural consequences. In conclusion based on the clear, adverse effects of nicotine on brain development observed in human and animal studies, we suggest that safer alternatives for smoking cessation in pregnancy are badly needed.     

儿童铅暴露对骨密度影响的研究进展

铅暴露对儿童机体多个系统都会产生不利影响.随着工业化社会的发展,铅污染引起的儿童铅暴露现象日趋严重,而骨骼则是铅负荷的最重要靶器官.儿童期是峰值骨量形成的关键时期.正常骨密度的维持对儿童骨骼健康及减少儿童成年后骨质疏松病的发生有重要作用.高水平铅暴露对儿童骨骼健康的负面效应主要是通过抑制成骨细胞的活性及功能,阻碍钙磷代谢导致的儿童骨密度异常,及抑制儿童骨骼生长.该文系统总结儿童铅暴露的来源、危害、以及铅暴露对儿童骨密度的影响及其机制.     

Maternal and fetal influences on blood pressure.

To study maternal and fetal influences on blood pressure in childhood 405 children aged 4 years who were born and still resident in the Salisbury health district were visited at home for blood pressure and growth measurements. Information on the pregnancy, delivery, and baby was abstracted from the routine obstetric notes. Similar to recent findings in adults, the child's systolic pressure was inversely related to birth weight and positively related to placental weight. Systolic pressure at 4 years increased by 1.2 mm Hg for every SD decrease in the ratio of head circumference to length at birth, and by 1.1 mm Hg for every SD decrease in ponderal index at birth. Mothers whose haemoglobin concentrations fell below 100g/l during pregnancy had children whose systolic pressures were on average 2.9 mm Hg higher than the children of mothers with higher haemoglobin concentrations. Patterns of placental weight, birth weight, head circumference, and length that are associated with high blood pressure in adults are also associated with higher blood pressure in 4 year old children. Identification of the intrauterine influences that lead to these patterns of fetal growth could lead to the primary prevention of hypertension.     

Environmental risk factors for attention-deficit hyperactivity disorder

Attention-deficit hyperactivity disorder (ADHD) is the most common cognitive and behavioural disorder diagnosed among school children. It is characterized by deficient attention and problem solving, along with hyperactivity and difficulty withholding incorrect responses. This highly prevalent disorder is estimated to affect 5-10% of children and in many cases, persists into adulthood, leading to 4% prevalence among adults. Converging evidence from epidemiologic, neuropsychology, neuroimaging, genetic and treatment studies shows that ADHD is a valid medical disorder. The majority of studies performed to assess genetic risk factors in ADHD have supported a strong familial nature of this disorder. Family studies have identified a 2- to 8-fold increase in the risk for ADHD in parents and siblings of children with ADHD. Various twin and adoption studies have also highlighted the highly genetic nature of ADHD. In fact the mean heritability of ADHD was shown to be 0.77, which is comparable to other neuropsychiatric disorders such as schizophrenia or bipolar disorder. However, several biological and environmental factors have also been proposed as risk factors for ADHD, including food additives/diet, lead contamination, cigarette and alcohol exposure, maternal smoking during pregnancy, and low birth weight. Many recent studies have specifically examined the relationships between ADHD and these extraneous factors. This review describes some of these possible risk factors. CONCLUSION: Although a substantial fraction of the aetiology of ADHD is due to genes, the studies reviewed in this article show that many environmental risk factors and potential gene-environment interactions also increase the risk for the disorder.     

Prevention of disability in children: elevating the role of environment

Much public attention and many resources are focused on medical research to identify risk factors and mitigate symptoms of disability for individual children. But this focus will inevitably fail to prevent disabilities. Stephen Rauch and Bruce Lanphear argue for a broader focus on environmental influences that put entire populations at risk. They argue that identifying and eliminating or controlling environmental risk factors that incrementally increase the prevalence of disability is the key to preventing many disorders. Rauch and Lanphear examine emerging evidence that many disabilities of childhood have their roots in the environment--from toxins in air, water, and soil, to the stressors of poverty, to marketing practices that encourage unhealthy choices or discourage healthy ones. They review research on well-known environmental causes of disability, such as exposures to lead, cigarette smoke, and industrial air pollution. They point to new evidence suggesting that chemicals found in commonly used plastics may have subtle but serious effects on child development, and that many disabilities spring from the complex interplay of environmental risk factors and genetic susceptibility. Rauch and Lanphear make a case for turning our attention to societal or population-level interventions that would rely less on medical and genetic technology and more on policies and regulations that would reduce children's exposure to ubiquitous environmental risks. Examples include required testing of new chemicals for developmental toxicity before they are put on the market; zoning regulations that separate residential communities from industrial areas; and restrictions on advertising of unhealthy products, such as tobacco, alcohol, and junk foods, to children. Rauch and Lanphear outline and assess the effectiveness of interventions that could be adopted, and suggest what a healthy modern community might look like. Such interventions, they acknowledge, are likely to be highly controversial, require both long-term investments and shifts in societal thinking, and produce less well-defined outcomes than individual medical treatments. But in the long run, the authors contend, such interventions could prevent many of the disabilities that now afflict millions of children and adults.     

Causes of lead toxicity in a Nigerian city.

BACKGROUND: Up to 70% of young Nigerian children have been reported to have blood lead concentrations > or =10 microg/dl. AIMS: To better elucidate risk factors for lead toxicity among Nigerian families with children at risk for lead toxicity. METHODS: Two geographic wards in Jos, Nigeria were selected for study, one previously reported to have a high mean blood lead level (37 (SD 13) microg/dl) and one with a lower mean blood lead level (17 (SD 10) microg/dl) in young children. Data pertaining to potential risk factors for lead exposure were collected from children and adults in 34 households. RESULTS: The mean (SD) blood lead concentration of 275 subjects, aged 3 weeks to 90 years, was 8.7 (5.7) microg/dl (range 1-34 microg/dl); 92 (34%) had concentrations > or =10 microg/dl. In multivariate analysis, an age of 5 years and under, flaking house paint, residence near a gasoline seller, male gender, increasing maternal and paternal education, and use of a lead ore eye cosmetic were independently associated with greater blood lead concentration. Vehicle ownership was associated with reduced lead concentration. Compared with the low-lead ward, residence in the high-lead ward remained significantly associated with greater lead values, indicating that additional factors likely contribute to lead exposure. CONCLUSION: Although the cause of increased lead levels in Jos appears to be multi-factorial, several remediable sources contribute to lead exposure in Nigeria.