Although the global ban on leaded gasoline has markedly reduced lead poisoning, many other environmental sources of lead exposure, such as paint, pipes, mines, and recycling sites remain. Existing ...methods to identify these sources are either costly or unreliable. We report here a new, sensitive, and inexpensive lead detection method that relies on the formation of a perovskite semiconductor. The method only requires spraying the material of interest with methylammonium bromide and observing whether photoluminesence occurs under UV light to indicate the presence of lead. The method detects as little as 1.0 ng/mm2 of lead by the naked eye and 50 pg/mm2 using a digital photo camera. We exposed more than 50 different materials to our reagent and found no false negatives or false positives. The method readily detects lead in soil, paint, glazing, cables, glass, plastics, and dust and could be widely used for testing the environment and preventing lead poisoning.
SignificanceConsiderable effort is expended to protect today's children from lead exposure, but there is little evidence on the harms past lead exposures continue to hold for yesterday's children, ...who are victims of what we term legacy lead exposures. We estimate that over 170 million Americans alive today were exposed to high-lead levels in early childhood, several million of whom were exposed to five-plus times the current reference level. Our estimates allow future work to plan for the health needs of these Americans and to inform estimation of the true contributions of lead exposure to population health. We estimate population-level effects on IQ loss and find that lead is responsible for the loss of 824,097,690 IQ points as of 2015.
During the past 45 years, exposure to lead has declined dramatically in the United States. This sustained decline is measured by blood and environmental lead levels and achieved through control of ...lead sources, emission reductions, federal regulations, and applied public health efforts.
Explore regulatory factors that contributed to the decrease in exposure to lead among the US population since 1970.
We present historical information about the control of lead sources and the reduction of emissions through regulatory and selected applied public health efforts, which have contributed to decreases in lead exposure in the United States. Sources of lead exposure, exposure pathways, blood lead measurements, and special populations at risk are described.
From 1976-1980 to 2015-2016, the geometric mean blood lead level (BLL) of the US population aged 1 to 74 years dropped from 12.8 to 0.82 μg/dL, a decline of 93.6%. Yet, an estimated 500 000 children aged 1 to 5 years have BLLs at or above the blood lead reference value of 5 μg/dL established by the Centers for Disease Control and Prevention. Low levels of exposure can lead to adverse health effects. There is no safe level of lead exposure, and child BLLs less than 10 μg/dL are known to adversely affect IQ and behavior. When the exposure source is known, approximately 95% of BLLs of 25 μg/dL or higher are work-related among US adults. Despite much progress in reducing exposure to lead in the United States, there are challenges to eliminating exposure.
There are future challenges, particularly from the inequitable distribution of lead hazards among some communities. Maintaining federal, state, and local capacity to identify and respond to populations at high risk can help eliminate lead exposure as a public health problem. The results of this review show that the use of strong evidence-based programs and practices, as well as regulatory authority, can help control or eliminate lead hazards before children and adults are exposed.
Lead causes a broad range of adverse effects in humans and animals. The objective was to evaluate the potency of lactobacilli to bind lead in vitro and the protective effects of a selected ...Lactobacillus plantarum CCFM8661 against lead-induced toxicity in mice. Nine strains of bacteria were used to investigate their binding abilities of lead in vitro, and L. plantarum CCFM8661 was selected for animal experiments because of its excellent lead binding capacity. Both living and dead L. plantarum CCFM8661 were used to treat 90 male Kunming mice during or after the exposure to 1 g/L lead acetate in drinking water. The results showed oral administration of both living and dead L. plantarum CCFM8661 offered a significant protective effect against lead toxicity by recovering blood δ-aminolevulinic acid dehydratase activity, decreasing the lead levels in blood and tissues, and preventing alterations in the levels of glutathione, glutathione peroxidase, malondialdehyde, superoxide dismutase, and reactive oxygen species caused by lead exposure. Moreover, L. plantarum CCFM8661 was more effective when administered consistently during the entire lead exposure, not after the exposure. Our results suggest that L. plantarum CCFM8661 has the potency to provide a dietary strategy against lead toxicity.
To evaluate trends in children's blood lead levels and the extent of blood lead testing of children at risk for lead poisoning from national surveys conducted during a 16-year period in the United ...States.
Data for children aged 1 to 5 years from the National Health and Nutrition Examination Survey III Phase I, 1988-1991, and Phase II, 1991-1994 were compared to data from the survey period 1999-2004.
The prevalence of elevated blood lead levels, >/=10 microg/dL, among children decreased from 8.6% in 1988-1991 to 1.4% in 1999-2004, which is an 84% decline. From 1988-1991 and 1999-2004, children's geometric mean blood lead levels declined in non-Hispanic black (5.2-2.8 microg/dL), Mexican American (3.9-1.9 microg/dL), and non-Hispanic white children (3.1 microg/dL to 1.7 microg/dL). However, levels continue to be highest among non-Hispanic black children relative to Mexican American and non-Hispanic white children. Blood lead levels were distributed as follows: 14.0% were <1.0 microg/dL, 55.0% were 1.0 to <2.5 microg/dL, 23.6% were 2.5 to <5 microg/dL, 4.5% were 5 to <7.5 microg/dL, 1.5% were 7.5 to <10 microg/dL, and 1.4% were >/=10 microg/dL. Multivariable analysis indicated that residence in older housing, poverty, age, and being non-Hispanic black are still major risk factors for higher lead levels. Blood lead testing of Medicaid-enrolled children increased to 41.9% from 19.2% in 1988-1991. Only 43.0% of children with elevated blood lead levels had previously been tested.
Children's blood lead levels continue to decline in the United States, even in historically high-risk groups for lead poisoning. To maintain progress made and eliminate remaining disparities, efforts must continue to test children at high risk for lead poisoning, and identify and control sources of lead. Coordinated prevention strategies at national, state, and local levels will help achieve the goal of elimination of elevated blood lead levels.
•We model chronic ingestion of environmental lead and cadmium in axenic mice.•We addressed the role of the microbiota in heavy-metal dissemination in organs.•We delineate the direct impact of the ...non-absorbed heavy metals on gut homeostasis.•We measure transport- and oxidative-gene expression in intestine.•It enlightens risk assessment of heavy metals in intestinal disease's susceptibility.
Environmental exposure to pollutants such as heavy metal(s) is responsible for various altered physiological functions which are detrimental for health. The gut microbiota is critical for intestinal homeostasis but its role on xenobiotic handling is not fully understood, especially when continuous sub-chronic exposure is addressed. We first confirmed the essential role of the intestinal microbiome to limit heavy metal body burden by using germ-free mice following 6-weeks oral exposure. Significant increases of cadmium and lead absorption and dissemination in blood and target organs were measured in germ-free mice when compared with conventional specific pathogen free (SPF) mice. Besides the “barrier” function of the luminal microbiota, this may involve specific host-genes such as metallothioneins, which are differentially expressed in the gastrointestinal tract of each group of mice. Considering genes relevant for divalent metal transporters and oxidative pathways, significant differences in basal gene expression were measured between control and germ-free mice. Moreover, the magnitude of induction of these genes upon stimulation by heavy metals varied greatly depending on the dose and type of metal as well as the microbial status of the animal. Collectively, these data illustrate the complex host-microbes interplay occurring with environmental pollutants inside the gut.
This review evaluates the sources of lead exposure worldwide. Studies from searches relating to sources of lead exposure in various countries within different regional zones were reviewed. Results ...indicated that in Nigeria, exposure sources include electronic waste, paint and batteries. In Mexico exposure sources include glazed ceramics, lead contaminated utensils and lead contaminated water, for India lead sources include cosmetics and traditional medicines. Sources of lead exposure in China include e-waste, traditional medicines and industrial emissions. In France, exposure sources included lead paint from older homes, imported ceramics and cosmetics and industrial emissions. Australia’s exposure sources include paint, dust, imported toys and traditional medicines. Finally, in the United States exposure sources included paint, the industrial legacy of lead exposure and batteries. In high-income countries (HICs) the legacy of lead exposure keeps populations continuously exposed. In lower- and middle-income countries (LMICs), in addition to the legacy of lead exposure, lack of regulations or the inability to enforce regulations keeps populations exposed. In all, evidence suggests that lead exposure remains an issue of public health significance in both HIC and LMIC.
Lead, a systemic toxicant affecting virtually every organ system, primarily affects the central nervous system, particularly the developing brain. Consequently, children are at a greater risk than ...adults of suffering from the neurotoxic effects of lead. To date, no safe lead-exposure threshold has been identified. The ability of lead to pass through the blood-brain barrier is due in large part to its ability to substitute for calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum can lead to a variety of neurologic disorders. At the molecular level, lead interferes with the regulatory action of calcium on cell functions and disrupts many intracellular biological activities. Experimental studies have also shown that lead exposure may have genotoxic effects, especially in the brain, bone marrow, liver, and lung cells. Knowledge of the neurotoxicology of lead has advanced in recent decades due to new information on its toxic mechanisms and cellular specificity. This paper presents an overview, updated to January 2009, of the neurotoxic effects of lead with regard to children, adults, and experimental animals at both cellular and molecular levels, and discusses the biomarkers of lead exposure that are useful for risk assessment in the field of environmental health.
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