Source: https://wiki.mnceh.org/index.php?title=Neurotoxicity:_Lead&diff=237&oldid=236
Timestamp: 2020-01-23 14:33:43
Document Index: 627068386

Matched Legal Cases: ['art 201', '§ 197', '§ 701', '§ 52', '§ 144', '§ 44']

(→‎Lead Screening)
Since 1991, the blood lead concentration of concern in children has been 10 µg/dL (micrograms per deciliter) as determined by the Centers for Disease Control and Prevention (CDC) (Levin ''et al''. 2008). However, subsequent studies have shown that blood lead levels as low as 2 µg/dL are associated with adverse effects, and therefore the CDC recommends abatement of ''any ''lead sources in the home (Levin ''et al''. 2008). Ultimately, it is critical to control all potential sources of childhood lead exposure, as discussed above, because a child’s exposure to lead is cumulative. This section summarizes current Michigan policies related to childhood lead poisoning, and provides recommendations for improving these policies to minimize childhood exposure to lead and to improve mitigation strategies.
=== Lead Screening ===
## In Michigan, only children enrolled in the special supplemental food program for women, infants, and children (WIC) or Medicaid are statutorily required to be tested for elevated lead levels. Children enrolled in Medicaid are required to receive a screening blood lead test at 12 and 24 months of age, and children between the ages of 36 and 72 months must receive a blood lead test if they have not been previously screened. The MDCH recommends that children enrolled in WIC be tested at 12 and 24 months of age (children enrolled in WIC are required under law to be tested, however there isn’t an age requirement in the provision, hence the recommendation).
5 Environmental Protection Agency (EPA) May 1985 Lead EPA Journal: “Lead Poisoning:
6 A Historical Perspective” by Jack Lewis
Childhood lead exposure may occur via ingestion or inhalation. Ingestion of lead-based paint or of contaminated soils, dust, foods or drinking water may result in elevated exposures. Inhalation of contaminated air may result in lead exposure, particularly for children living near emission sources such as waste incinerators (Levin et al. 2008). While direct ingestion of lead-based paint is the exposure route that receives the most attention during abatement and screening processes, recent data suggests that more than 30% of children with elevated blood lead levels do not have direct exposure to a lead paint source (Levin et al. 2008). These data suggest that other exposure routes and additional sources in the environment may be significant contributors to childhood lead poisoning. A child’s cumulative exposure to all sources of lead, which individually may be considered “safe,” may collectively put a child’s neurological system at risk (Weil 2007). A child’s cumulative exposure may come from the combined exposure to lead in paint chips, soil, air, household dust, jewelry, and toys (Weil 2007; Charneyet al. 1983). Both current and past maternal exposures contribute to lead levels in a mother’s breastmilk, and even low concentrations of lead in breast milk can influence a baby’s blood lead level (Levin et al. 2008). An unborn child can also be exposed to lead in utero. Fetal exposure can occur as a result of a mother’s current exposure to lead during pregnancy. Lead concentrations in fetal tissues are proportional to the mother’s blood lead levels during pregnancy (Goyer and Clarkston 2001). Furthermore, lead stored in the mother’s bones (from past exposures) can be mobilized during pregnancy, thus resulting in potentially significant exposure to the developing fetus (Huet al. 2006). There are several characteristics unique to young children that make them particularly vulnerable to exposure to lead in the environment. Children engage in frequent hand-to-mouth behavior that begins almost immediately after birth; this behavior is common until around age 3 or 4 years (Goyer, Clarkston 2001). Furthermore, children are low to the ground, so they can more easily ingest or inhale toxicants that are in the soil, on the floor, or even in house dust (Hu 2007; Schettler 2009). Additionally, the developing nervous system is more vulnerable to lead exposure than a mature nervous system (Needleman 2004). These characteristics, coupled with the fact that young children absorb lead more efficiently than adults and older children (Levin et al. 2008; Goyer, Clarkston 2001; Needleman 2004), make young children particularly vulnerable to lead exposure, and make minimizing early life exposures a top priority in reducing the overall effect of lead on the population. Exposure can be reduced by simple exposure-reducing behaviors and practices. One study in homes with lead-contaminated dust had the homes extensively cleaned and the children residing in them engaged in frequent hand washing showed that blood lead levels can drop significantly after one year given these exposure-reducing practices (Charneyet al. 1983). Other factors influencing the likelihood of a child’s exposure to lead include income level, age of housing, location of residence, country of origin, parental occupation, time of year/season, nutrition (such as iron, calcium, and zinc status), and the presence of tobacco smoke in the child’s environment(Levin et al. 2008; Goyer, Clarkston 2001). Many of these factors are interrelated, which can lead to disproportionate exposure in some population subgroups.
Children’s blood lead levels have continuously declined in the U.S. since the phase-out of lead-based gasoline (Schettler 2005). In fact, the decrease in average child blood lead concentration in the U.S. closely follows the decline in total lead used per year in gasoline (Figure 1). Figure 1. Decline in average blood lead levels in U.S. children and in total lead used per year in gasoline for years 1974-1992 (adapted from U.S. EPA 1999). Despite this substantial decline in average blood lead levels (BLL) in the U.S. due to decreases in atmospheric emissions, childhood lead poisoning remains a significant public health problem in the U.S., particularly for certain groups. It has been estimated that the cognitive impacts of lead poisoning (decreased IQ, productivity, and life time earnings) cost more than $43 billion each year in the U.S., although childhood lead poisoning is entirely preventable (Landriganet al. 2002). A recent report by the Michigan Network for Children’s Environmental Health estimated the annual cost in Michigan as a result of childhood lead exposure to be $4.85 billion(range: $3.2 to 4.85 billion) (Glaser et al. 2010). Furthermore, Gould (2009) estimated that, for every dollar spent on lead paint hazard control nationally, the returns would range from $17-$221; these returns would come from reductions in costs associated with health care, crime, and special education, as well as from increased future tax revenue. As such, there are both direct (ie. health care), and indirect costs associated with lead exposure in children. Special education serves as one example of an indirect cost associated with lead poisoning. For instance, an increased prevalence of elevated blood lead levels has been observed in special education classes relative to non-special education classes at Detroit Public Schools (Tarr et al., 2009). Due to a need for specialists to teach children in special education classes, the cost of educating special needs students can be quite a bit higher than that of educating other students (Gould 2009). In 2006, the state-specific costs of special education in Michigan were approximately $12,000/child/year amounting to $2.7 billion/year in Michigan (14.4% of children in the Michigan public school system were in special education) (Weil 2007). As previously stated, certain age groups are particularly vulnerable to lead exposure. This vulnerability is demonstrated through data on childhood blood lead levels in the U.S. For example, the 2001-2002 National Health and Nutrition Examination Survey (NHANES), conducted by the Centers for Disease Control (CDC), estimated that 1.7% of all children in the U.S. between the ages of 1 and 5 have blood-lead levels above the 10 g/dl (10 micrograms of lead per 1 deciliter of blood), the threshold set by the CDC (CDC 2007).[1] This percentage is a decrease from the NHANES III (phase 2, 1991-1994), which reported that 4.4% of children had BLL above 10 g/dl (Pirkle et al. 1998). The 2001-2002 NHANES also reported that younger children (age 1-5) had higher mean blood lead levels than children aged 6-11 years, who had higher levels than those 12-19 years (CDC 2005). Childhood lead exposure in the U.S. is also dependent on age of housing and family income. Results from a study conducted in all 50 states between 1998 and 2000 suggest that although the estimated number of housing units in the U.S. with lead-based paint has decreased, 35% of low-income housing still had lead-based paint hazards (Jacobs et al. 2002). This study also conferred that dust lead levels and soil lead levels may contribute to overall exposure, as 16% of all houses had dust lead levels above current guidelines, and 7% of houses had soil lead levels exceeding recommended levels (Jacobs et al. 2002). Additionally, blood lead levels vary by race and ethnicity (Levin et al. 2008). For example, blood lead levels are typically higher in the U.S. for black, non-Hispanic children than for Mexican American or white children (Figure 2) (CDC 2005). Much of this disparity is attributed to a larger percentage of children residing in lower-income, pre-1970’s housing with lead paint (CDC 1992). Additionally, the use of certain herbal remedies, cosmetics, or folk medicines among some ethnicities may potentially influence blood lead levels, as may refugee status (Levin et al. 2008). In fact, according to the CDC, blood lead levels were elevated in 45% of refugee children shortly after resettlement. One hypothesis for this is that this is due to a higher prevalence of iron deficiency in refugee children, as lead absorption rates are higher among iron-deficient children (Levin et al. 2008). Authors of other studies on elevated blood lead levels in refugee children hypothesize that leaded gasoline in home countries (such as those in sub-Saharan Africa, where leaded gasoline was phased out as late as 2006), resettlement into old housing stock, and use of traditional home remedies containing lead may be other factors in elevated blood lead levels in refugee children (Eisenberg et al., 2011; Plotinsky et al. 2008; Ritchey et al., 2011). Figure 2. Percentage of children in three NHANES survey periods with blood lead levels greater than 10 µg/dl, by race/ethnicity (CDC 2005).
According to the Michigan Department of Community Health’s 2007 Critical Health Indicators report, lead poisoning in Michigan follows national trends in that cases tend to be concentrated in more urban areas with older housing units (MDCH 2007). Although children living in the city of Detroit are particularly at risk, roughly half of Michigan’s zip codes are identified as being high risk. High risk areas are identified by the percentage of pre-1950s housing, as children can be at risk for lead poisoning due to deteriorating paint and/or renovations of these older homes (MDCH 2007). While legislation prohibiting lead from interior surfaces did not take effect until 1978, many structures built or renovated between 1960 and 1978 had already voluntarily remediated and/or non lead-based paint was selected; as such, pre-1950s housing carries a higher risk of leading to lead poisoning (Jabobset al. 2002). While lead paint particles remain the primary sources of exposure (Nadakavukaren 2000), Michigan’s children are potentially exposed to lead from a variety of other sources, including the many contaminated sites throughout the state. According to Michigan DEQ’s Part 201 Site List, out of 3,257 polluted sites in Michigan, 623 sites are reported to be contaminated with lead (MDEQ 2008). Furthermore, in the 2005 Michigan Toxic Chemical Release Inventory summary report, 320 facilities in Michigan released lead or lead compounds into the environment (MDEQ 2005). The 2005 Michigan Toxic Chemical Release Inventory (updated in 2007) indicated that more than 34,700 pounds of lead and lead compounds were released into the air (MDEQ 2005). It also indicated that over 2,000 pounds were released into the state’s water sources and nearly 280,000 pounds of lead were released/disposed of on land in 2006 (Figure 3).[2] In total, approximately 3,671,057 pounds of lead and lead compounds were released in Michigan during 2005 (MDEQ 2005). In the same year, the U.S. released 18,434,233 pounds of lead (EPA 2005). Figure 3: Reported release (lbs/year) of lead and lead compounds into Michigan’s environment in 2005 as summarized by Michigan Toxic Chemical Release Inventory (TRI) (Source: MDEQ 2005).
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Michigan ranks 6th worst in the nation in the percentage of lead poisoned children (MCLPPCC2007). In efforts to improve this statistic, the Childhood Lead Poisoning Prevention Program, through the Michigan Department of Community Health, works to coordinate lead poisoning surveillance and prevention for Michigan’s children. Under this program, children under the age of 6 and pregnant women are targeted for lead poisoning prevention. Many of the statistics provided in this section are compiled through this program. In 2008, 35.0% of Michigan children between the ages of 1 and 2 years (of a total population group of 253,207 children), and 20.1% of children under the age of 6 (of a total population group of 764,176 children) were tested for blood lead. Of those children tested, 9.8% had blood lead levels (BLL) greater than 5 µg/dl (5 micrograms of lead per deciliter of blood), and 1.1% of children had BLL greater than 10 µg/dl (MDCH 2008a). These percentages held irrespective of age strata (Figure 4). Figure 4. Stratified blood lead levels greater than 5 µg/dl (micrograms of lead per deciliter of blood) in Michigan children screened for lead (Source: MDCH 2008a).
===== Blood Lead Levels ===== Ages 1 and 2 Years Age < 6 Years
Number % * ===== Number ===== % *
BLL ≥5 µg/dl 8,865 10.0 15,018 9.8
BLL ≥10 µg/dl 984 1.1 1,686 1.1
Stratified BLLs
BLL 10-14 µg/dl 545 0.6 1,024 0.6
BLL 15-19 µg/dl 216 0.2 362 0.2
BLL 20-44 µg/dl 176 0.2 277 0.2
BLL ≥45 µg/dl 17 <0.1 23 <0.1
* Refers to percent of children tested
A notable success story lies in the lowering of children’s blood lead levels in response to public health interventions. In 2005, just 3 years prior to the above data, 17.2% of Michigan children tested (under the age of 6) had blood lead levels (BLL) greater than 5 µg/dl, and 2.4% (compared to 1.1%) of children had BLL greater than 10 µg/dl. Similar to national trends (Figure 1), the percentage of children with elevated blood lead levels has decreased in the state of Michigan during the past decade (Figure 5) – while rates of testing have increased in most, but not all, areas. Figure 5. Trends in elevated blood lead levels in Michigan children under age 6 tested from 1998 to 2008. Notes: Each line reflects the portion of all children who tested at that level and above. EBLL = Elevated Blood Lead Levels. (MDCH 2010). In 2005, the Michigan Department of Community Health (MDCH) projected that the number of children screened, and the number of children with elevated blood lead levels (defined as ≥10 µg/dl), would decline rapidly over the next several years (Figure 6). The 2006 MDCH report revealed that while the number of children with elevated blood levels decreased even further than their projection (1.6% of children tested had elevated BLLs compared to the 2% projection), the number of children that were tested fell short of the agency’s goal (MDCH 2006). Since 2004, the numbers of children tested have not met MDCH’s goal of a 10% annual increase (Figure 6). Figure 7 shows the number of children (less than 6 years of age) who received blood lead testing in Michigan, broken down by children who were Medicaid-enrolled or not Medicaid-enrolled. Although much of the testing is covered by insurance, significant state budget cuts and Medicaid reimbursement cuts will further impact the state’s ability to raise public awareness about the importance of testing and the ability of children on Medicaid to get tested. For example, in Kent County, Michigan, there was a 26% decrease in lead testing from 2004 to 2008 (Paul Haan - personal communication with the Ecology Center, 2009). Figure 6. Elevated blood lead levels (EBLL) (≥10 µg/dl) in Michigan children less than 6 years old in numbers and as a percentage of children tested. Data from 2001-2005, and projected data for years 2006-2010 (MDCH 2005). Figure 7. Number of children under six years of age tested for blood lead levels, 1998-2009. (MDCH 2010) Figure 8 indicates the extent of childhood lead poisoning among children age 6 and younger in the city of Detroit from 1998-2004. The percentage of children with elevated blood lead levels (EBLL, referring to levels ≥10 µg/dl) in Detroit, 18.7%, was well above the U.S. average of 7.6% in 1998 (CDC 2000).[4] This is consistent with other findings that children in urban areas face a disproportionate risk of lead poisoning. The proportion of children with EBLL among those tested decreased from 18.7% in 1998 to 6% in 2004 (Figure 8). Yet, Detroit children have consistently been at higher risk for EBLL over the years, and in 2011 the majority of lead poisoned children in the state were in the Detroit metropolitan area (Figures 9 & 10). In 2004, for instance, 2.5% of children under the age of six had EBLLs throughout the state, while 6% had EBLLs in Detroit. Of children under the age of six tested in Michigan in 2008, 1.1% had EBLLs (levels ≥10 µg/dl). However, of fourteen communities considered to be of particular risk, children in ten of them were above the Michigan average (MDCH 2008b). Figure 8. Extent of lead poisoning in the City of Detroit, 1998-2004.Total number of children age 6 and younger tested for lead and the number found with blood lead levels (BLL) of 10µg/dL (micrograms of lead per deciliter of blood) or above (EPA 2007).
Figure 9. Lead Poisoning in Detroit Compared with Michigan statewide, 1998-2004. Percent of children age 6 and younger tested for lead with blood lead levels of 10 µg/dL (micrograms of lead per deciliter of blood) or above (Sources of Data: MDCH 2005 and EPA 2007). Note: the Detroit Data includes children age 6, while the statewide data does not. Figure 10: Map of elevated blood lead levels among children less than six years of age in Michigan. (MDCH 2009) Despite declining numbers of children with elevated blood lead levels, childhood lead exposure is still a public health concern in Michigan. Exposure to lead during childhood places both a burden on a child’s health and development, and a social and economic burden on the state. It has been estimated that the education and human services necessary to address social and learning problems associated with lead exposure in Michigan present a lifetime cost of over $45,000 per lead-poisoned child (MCLPPCC 2007). By comparison, it costs approximately $600-700 to assess a Michigan residence for lead in the commercial market, with the average cost of abatement being roughly $9,000 per residence (MCLPPCC 2007). In 2007, the Michigan Childhood Lead Poisoning Prevention and Control Commission estimated that over 1.3 million occupied housing units in the state of Michigan contained lead paint hazards. The low costs of lead assessment and abatement in residences, relative to the high cost of lead poisoning, indicates that the state should consider prioritizing these measures as a means of reducing childhood lead exposures. Currently, several other states have programs in place which offer grants, loans, or tax credits in order to incentivize lead abatement in residences (ALM GL ch. 111, § 197E, § 701.337 R.S.Mo., N.J. Stat. § 52:27D-437.4, Minn. Stat. § 144.9512, R.I. Gen. Laws § 44-30.3-1).
Children under the age of 6 are at highest risk of lead poisoning because their bodies are not fully developed. Developing nervous systems, both during gestation and infancy, do not have an adequate blood brain barrier, and therefore lead can easily pass into the brain (ATSDR 2005).Lead affects the nervous system through several mechanisms, each of which can be critical to a developing brain. Specifically, lead can impair cellular signaling, which can lead to changes in neuronal circuitry (Goyer and Clarkson 2001). Lead alters neuron cell structure and neurotransmitter levels in the brain (acetylcholine, dopamine, glutamate) (Goyer and Clarkson 2001). Lead can also inhibit NMDA (glutamate) receptors in the brain (GBPSR 2000). Furthermore, lead can disrupt calcium homeostasis and impair calcium intake (ATSDR 2005; Goyer and Clarkson 2001). Calcium is critical to nerve signal transmission, so these interferences with calcium can result in a variety of negative impacts, including a decrease in available energy necessary for brain functioning and disruption of signaling necessary for cell communications (Goyer and Clarkson 2001). Lead poisoning can cause permanent and irreversible damage to the nervous system. Its effects include hearing and vision loss, reductions in cognitive development and attention span, hyperactivity, aggressive behavior, loss of IQ, learning disabilities, developmental delay, coma and even death (EPA COI 2007; MCLPPCC 2007). Many human and animal studies have directly linked elevated lead body burden with neurological impacts, and there is even some evidence that these impacts may begin to materialize in utero. An unborn child can be exposed prenatally to lead from the mother’s gestational exposures and from mobilization of stored blood lead during pregnancy (Hu et al. 2006). The timing of lead exposure during pregnancy may influence health outcomes later in life. A recent study reported that fetal exposure during the first trimester (higher maternal blood lead levels) may result in a lower Mental Development Index (MDI) at 24 months of age (Hu et al. 2006). Additionally, there is evidence linking children’s lead body burden with several different indicators of neurological impacts. For example, in a study conducted in Boston, MA, elevated blood lead levels were correlated with behavioral changes in children, such as distractibility, frustration, attention deficit, and impulsivity(Tuthill 1996). Other studies have shown correlation with aggressive and destructive behavior (GBPSR 2000). Figure 10 (below) demonstrates a dose-dependent association between lead body burden in children and behavioral traits possibly associated with ADHD. The first graph in Figure 10 is extracted from an often-cited study conducted in 1979, in which teacher-evaluated student behavior was correlated with dentine lead levels (Needleman et al. 1979). The graph shows a dose-response relationship between dentine lead levels and percent of children exhibiting the behaviors of interest (Figure 11). The second graph is adapted from a similar study conducted in 1984 (Yule et al. 1984), and also demonstrates an association between childhood lead body burden and decreased classroom performance. Figure 11. Association between student lead body burden and teacher ratings. The bars represent the percent of students in each lead category considered by their teachers to have the corresponding challenges. Graphics adapted from: Needleman et al. 1979 and Yule W, et al. 1984. Recent studies have similarly indicated that subtle behavioral effects may be linked to lead exposure. A 2008 study in Syracuse, NY found elevated childhood blood lead levels (>20 μg/dl) to be associated with repeat teen pregnanciesas well as tobacco use (Lane et al. 2008). The authors explain that lead poisoning can delay cognitive development as well as executive functioning in young women. These results indicate that lead poisoning may have a long-lasting impact on children’s functioning, development, and behavior. Another study confirmed that lead can have long lasting effects on behavior by showing that early-life exposure to lead is associated with adult criminal behavior. That long-term study found that increased prenatal and postnatal blood lead concentrations are associated with higher rates of total arrests and/or arrests for offenses involving violence (Wright et al. 2008).Another study correlated preschool lead exposure with criminal behavior 20 years later (the peak age for index crime rates). This study was also able to correlate the high levels of lead in the air in larger cities with higher crime rates for the years following their peak air lead levels (Nevin 2007).
Environmental Protection Agency (EPA) May 1985 Lead EPA Journal: “Lead Poisoning:
A Historical Perspective” by Jack Lewis
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