Lead paint

Abstract: Lead poisoning is a serious hazard for children and causes significant biological and neurologic damage linked to cognitive and behavioral impairment (Bellinger 2008a, 2008b). The level of lead exposure has fallen dramatically over the past 30 years because the lead content has been reduced in gasoline, household paint, food canning, industrial emissions, water lead, and other sources, and because public health and housing initiatives have targeted the problem. According to the National Health and Nutritional Examination Survey (NHANES), a population survey administered by the Centers for Disease Control and Prevention (CDC), the geometric mean for blood lead levels (BLLs) for children 1–5 years of age fell from 14.9 μg/dL in 1976 to 1.7 μg/dL in 2006 (CDC 2007b). The number of children 1–5 years of age with BLLs at least 10 μg/dL has fallen from an estimated 13.5 million to 174,000 over the same period (NHANES 2003–2006). Although the 1- to 5-year age grouping is useful for comparison over time, I focus on a cohort of children ≤ 6 years of age in which there are an estimated 194,000 children with BLLs at least 10 μg/dL. Recent research has indicated that significant neurologic damage to children occurs even at very low levels of exposure (Bellinger 2008a, 2008b; Chen et al. 2007; Lanphear et al. 2005). Preventing these levels of exposure in young children will require controlling a significant and persistent cause of lead poisoning: lead paint used in housing before its ban in 1978. Although pre-1950 house paint has the largest concentration of lead-based paint hazards, house paint produced in 1950–1978 also contains substantial lead content. Poor, urban minorities disproportionately reside in housing units containing lead-based paint hazards, creating significant inequity in health and neurologic outcomes by ethnicity and socioeconomic status (CDC 2004). Because the costs of lead paint abatement are nontrivial and the removal must be done on a unit-by-unit basis (rather than imposed at an industry level), there must be substantial commitment to further reduce lead poisoning among vulnerable children. A growing body of literature has detailed the economic costs and risks of lead poisoning, including several analyses summarizing these costs and setting them against the estimated costs of lead paint hazard control. However, recent research has broadened still the scope of our understanding of the societal costs of lead poisoning. For example, new studies have begun to analyze the correlation of lead poisoning with crime rates and their associated costs, as well as linking early lead exposure to adult-onset health problems. In this article I aim to comprehensively address the costs and benefits of household lead hazard control vis-a-vis new discoveries in the medical, psychological, and economic literature. I focus on children ≤ 6 years of age, because lead exposure is the highest for this age group, and this is the period when lead exposure produces the most significant damage. In this analysis, I constructed an upper and lower bound on the cost-effectiveness of strategies to reduce lead exposure. The reasoning behind this methodology is that there is no single estimate that accurately reflects either the costs or benefits of lead hazard control. On the costs side, the actual expense of reducing lead paint hazards in affected homes varies with the extent of interventions required. On the benefits side, the number of children with lead exposure ranges from those reported in state child blood lead surveillance data to those determined from weighted estimates of national surveys. Although several factors could make one extreme or another more credible, it is likely that the truth lies within this interval.

Abstract: 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.

Abstract: The U.S. Department of Health and Human Services’ (DHHS) Healthy People 2010 initiative has set a national goal of eliminating blood lead (PbB) levels ≥ 10 μg/dL among children 1–5 years of age by 2010 (DHHS 2000). PbB used to define unsafe levels of exposure for children have decreased over the past few decades as additional evidence has demonstrated newly recognized adverse health effects, even at relatively low exposures [Canfield et al. 2003; Center for Disease Control and Prevention (CDC) 1991; Lanphear et al. 2005]. Childhood lead poisoning prevention efforts are sometimes called a victory in light of the dramatic reductions in population PbB. However, the magnitude of ongoing exposures, the remaining large stores of lead sources (particularly paint in older housing), and the length of time it has taken to address such exposures show that much remains to be done if a true, lasting victory is to be achieved (Jacobs et al. 2002; Lanphear 2007; Levin et al. 2008). We present new data on dust lead (PbD) loading and childhood PbB from the National Health and Nutrition Examination Survey (NHANES) 1999–2004 and examine their implications. The most important source of lead exposure for children today is from lead paint as it deteriorates or is disturbed and subsequently contaminates settled residential dust and soil (Lanphear et al. 1998; Reissman et al. 2002). Another important source of lead in dust and soil is the estimated 5.9 million tons of gasoline lead emitted from motor vehicles before its removal in the mid-1980s (Mielke 1999). Normal hand-to-mouth activity exposes young children to lead in the residential environment (Bornschein et al. 1987; Lanphear et al. 1998). In 1999 and 2001, respectively, the U.S. Department of Housing and Urban Development (HUD) and the U.S. Environmental Protection Agency (EPA) established a PbD standard for the home environment of 40 μg/ft2, along with similar standards for windowsill PbD (250 μg/ft2) and lead in soil [400 parts per million (ppm) in play areas]. The previous guidance from U.S. EPA was 100 μg/ft2 for floor PbD (U.S. EPA 1995). Prior studies have firmly established the robust correlation of settled PbD on both floors and windowsills with children’s PbB (Davies et al. 1990; Lanphear et al. 1998; Wilson et al. 2007). However, analysis of exposure pathways shows that floor PbD has a direct effect on children’s PbB, with sill PbD having an indirect effect as mediated by floor PbD (HUD 2004). Until recently, nationally representative data for PbD and PbB (CDC 2005; Jacobs et al. 2002) were collected only in separate surveys. But between 1999 and 2004, NHANES interviewers collected PbD wipe samples and housing-related questionnaire data relevant to lead exposure from the homes of children 1–5 years of age. Blood samples from these children were collected at NHANES mobile examination centers and were analyzed for lead and other parameters. We examined the relationship between PbB in children and PbD on floors and window-sills and estimated PbB across the range of floor PbD in this nationally representative cross-sectional sample of children 1–5 years of age. This marks the first time that nationally representative data on environmental and biologic measurements for lead have been obtained in a single integrated survey. A companion article in this issue presents the predictors of residential PbD (Gaitens et al 2009).

Abstract: Lead's toxicity has been recognized since antiquity, and certain themes recur during the history of its understanding. Warnings have been frequently pronounced, and frequently followed by statements that these warnings were exagerated. Childhood lead poisoning was first discovered in Brisbane, Australia in 1894. The cause, lead on the rails of the porches,was demonstrated by J.L. Gibson, and promptly derided by the business and medical communities. The first lead paint prevention act was passed in Australia in 1920. In the United States, it was believed that if a lead-poisoned child did not die, they recovered with no residua