Lead Poisoning: Still a Common Problem in Chicago

Helen J. Binns, MD, MPH

aSpring 2001

Chicago can claim  a few laudable firsts: the largest public library and the tallest building in the United States. However, Chicago is among the top competitors for a “first” that is disturbing and should alarm those who provide health care here: the most lead-poisoned children of any city in the United States. Last year a Minneapolis public health worker jokingly commented to me that the major risk for lead poisoning in Minneapolis is moving from Chicago! I wouldn’t be surprised if this were actually true. In 1998, according to the Chicago Department of Public Health 101,671 Chicago children (an estimated 33% of Chicago children less than or equal to 6 years of age) had a blood lead test (Figure 1). Among those tested, 20% had a level greater than or equal to 10 µg/dL and 3.3% had a level greater than or equal to 20 µg/dL. There were 149 children with a blood lead level greater than or equal to 45 µg/dL. The Chicago Department of Health has developed maps that indicate the neighborhoods with the highest rates (Figure 2). Neighborhoods with the highest rates are generally in the west and south areas of the city. Further information on lead screening and lead poisoning rates for Chicago community areas are available at www.chicagolead.org.

Figure 1 Percent of children who received a blood lead test, Chicago, 1998. Data from Chicago Department of Public Health. Available at www.chicagolead.org.

Figure 2 Percent of children with blood lead levels >=10 µg/dL for Chicago, 1998. Data from Chicago Department of Public Health. Available at www.chicagolead.org.

WHY IS CHICAGO A LEADER IN LEAD POISONING?

First, Chicago homes are old; 59% of Chicago housing stock was built before 1950.[1] Paints with high lead content were used for window systems, door systems and porches, surfaces which are subject to weathering and friction. Some lead-based paint is found in 88% of privately owned, occupied homes built before 1940, 92% of homes built between 1940 and 1959, and 76% of homes built between 1960 and 1979.[2] Many of Chicago’s previously stately homes have experienced years of deferred maintenance. According to the Chicago Department of Planning & Development’s Housing Inventory, 1.7% of Chicago homes built before 1978 are dilapidated, 4.6% need major repair, and 21.2% need minor repair. However, in some neighborhoods the majority of homes need repairs.

Particular components within the home may be the greatest contributor to lead exposure. Paints with the highest lead content were used for window systems, door systems and porches, surfaces which are subject to weathering and friction. Friction or impact to these surfaces creates lead-containing dust, a major vehicle for childhood lead poisoning. A national study found greatest concentrations of lead-containing dust in window wells, followed by window sills, then interior floors at average levels of 14,350, 258, and 19 µg lead/ft², respectively.[3] Children playing at windows can be exposed to very high levels of lead dust by normal hand-to-mouth activity. In my own clinical experience, children with the highest lead levels nearly always have identifiable lead hazards within the home interior or at the windows. The EPA recently published new federal standards for lead in dust, lowering the level needed to achieve clearance to 40 µg lead/ft²on floors, and 250 µg/ft2 on window sills.[4]

Figure 3 Relationship of dust lead loading and soil/exterior lead to blood lead level. Adapted from Lanphear et al.7

Second, Chicago also likely has high levels of lead in soil. Urban areas, especially within close proximity to busy streets, were subject to the deposition of lead from automobile exhaust from 1928 through the late 1970s, the years when leaded gasoline was used. Additionally, although the highest amount of leaded paint falls to the drip line area during exterior home repainting, it can also travel quite widely within a neighborhood.[5] Lead in soil does not decay or wash away. For example, paint scraping done 50 years ago, before vinyl siding was placed on a home, probably left unacceptably high levels of lead in soil at the building drip line. Although there is no overall assessment of soil lead contamination for Chicago, our past tests of soil lead in one Chicago neighborhood showed concerning results.[6]

In that study the median soil lead level in the residential area tested was 1773 parts per million (ppm). Soil lead measurements showed spatial relationships with higher points, possibly due to paint contamination, proximity to a busy street, and past home industry. Recent EPA regulations set standards for lead in soil.[4] Children’s play areas should have lead at < 400 ppm. An acceptable average for bare soil areas in other parts of a yard has been set at 1200 ppm. To date, soil excavation is the only known means to reduce children’s exposure to lead in soil. We are in the midst of a HUD-funded research project, the Safer Yards Project, which will examine lower-cost methods of reducing soil lead exposure.

Research data suggest that the highest rates of lead poisoning are in areas where children are exposed to both interior and exterior lead (Figure 3).[7] For example, in areas where both interior and exterior lead are high (55 µg/ft² and 2000 ppm, respectively), 45% of children would be expected to have a blood lead level (BLL) of greater than or equal to 10 µg/dL. In contrast, in areas when the sole impact is from high interior lead, only 23% of children would be expected to have an elevated blood lead level.

Finally, lead poisoning rates are high for children living in poverty. According to the 1990 U.S. Census, 36% of Chicago children live below the poverty level. Among children participating in the NHANES III 1991–94, children on Medicaid were 3 times more likely than those not on Medicaid to have an elevated BLL.[8] Of children 1–5 years old, those on Medicaid accounted for 60% of those with BLLs greater than or equal to 10 µg/dL and 83% of those with BLLs greater than or equal to 15 µg/dL, but only 20% of this group of children received a screening blood lead test.[8]

WHAT BLOOD LEAD LEVEL IS CONSIDERED “SAFE”?

With lead, none is better than any. There is no physiologic need for lead. However, it is quite pervasive in our environment, so almost everybody has a measurable level. A recent MMWR report says that the average US child’s BLL is now down to 2 µg/dL.[9] Lead has no threshold for effects, and lasting negative developmental and behavioral effects can occur even at levels lower than 10 µg/dL.[10,11] Evaluating safe lead levels is difficult because many studies on effects of lead used a control population with BLLs we would now consider to be high. More study is needed on development and behavioral outcomes for blood lead ranging from 0–15 µg/dL.

A child’s brain is likely to be more sensitive to lead during the fastest period of development, before or around age 2 years.[10] Additionally, it is likely that damage done by lead is not reversible. Therefore, prevention and screening steps, which accomplish lowered lead exposure and identification of rising blood lead levels at early stages, are key to reducing the negative impact of lead on a child’s cognitive abilities and behavior.

WHEN SHOULD CHILDREN BE TESTED?

In September 1999, the Chicago Department of Public Health established new lead screening guidelines for the city to accomplish early identification. The new guidelines call for blood lead screening “at least 3 times before age 3” (at 9, 15, and 24 months or at 6, 12, 18, and 24 months) and again at age 3 years. Unless risk factors change, older children with past low levels do not need additional blood lead testing. Analysis of Chicago lead data has shown that reliance on a single low BLL at age 1 year is not sufficient. In a Chicago cohort, 39% of the children with blood lead < 10 µg/dL when tested at approximately 1 year of age were retested at age greater than or equal to 2 years. Among those tested, 21% had elevated BLLs at the later screening.[12] This is an expected change, given that children’s activity and thus exposures (locomotion, play activities, oral behaviors) change greatly over that period. Between ages 2 and 3, children play outdoors more than younger infants; hence the need to check for blood lead elevation at age 3 years.

SOMETIMES TESTING MAY BE INDICATED, UNRELATED TO CHILD AGE OR NEW EXPOSURES

Because of high environmental exposure to lead, infants and children adopted from China should have a blood lead test as a standard screening measure.[13] Infants from Cambodia, Russia, and Central and South America may also be at increased risk.[13]

Children with developmental problems tend to have persistent hand-to-mouth behaviors, and thus might have persistent or rising lead levels at older ages than expected. These children should continue regular testing until oral behaviors cease or levels are persistently low.

LEAD POISONING IS NOT CONFINED TO THE CITY OF CHICAGO

Although suburban rates are lower than in Chicago, instances of lead poisoning are found in all suburban areas. The housing stock in some Chicago suburbs is quite old (e.g., Oak Park, 77% built before 1950; Cicero, 69% built before 1950; Evanston, 63% built before 1950).[1] Blood lead screening rates are quite low in these areas and rate of elevated blood lead among those screened is high. Thus, it is likely that many suburban children with high lead levels are not being identified.

Older farm homes in rural areas also have potential for lead exposure. In North Carolina the risk of lead poisoning is higher among children living in rural areas than in urban areas.[14] I have seen several children from area farming communities with elevated BLLs. On inspection, one farm home had elevated levels of lead in the expected places (windows, walls, and exterior) and also had paint with high lead content on the playroom floor! Past spillage of leaded gasoline near storage tanks at farms also presents another source of potential exposure.

PUBLIC HEALTH PROGRAMS ARE ABLE PARTNERS

Lead programs in the Chicago and Cook County Departments of Public Health respond rapidly to evaluate children’s homes when elevated BLLs are found. Both programs have improved their service delivery every year. Chicago recently added “collateral inspection” to their activities; i.e., if one child in the building has an elevated level, all units with children in that building will undergo inspection.

Home inspection plays a key role in decreasing child exposure to lead. Inspectors identify lead hazards and educate parents and landlords on hazard locations and steps to immediately reduce child exposure to the identified hazards. Additionally, inspectors may assist the property owner to develop a lead hazard reduction plan and gain training on safe methods of repair.

By state law, all blood lead results and children’s address information must be reported by testing laboratories to the state health department. However, in actual practice, some laboratories have only partial address information, or reporting is delayed or nonexistent, which slows down responses for home evaluations. Direct requests to health departments for home inspections may speed the process by circumventing the traditional reporting system. Guidelines for requesting home inspections are: (1) infants with any elevated blood lead level, (2) children aged 6 and younger with a BLL greater than or equal to 20 µg/dL, and (3) BLL persistently at 15–19 µg/dL (2 tests at least 6 months apart). Requests to inspect homes with Chicago addresses should be directed to the Chicago Department of Health at 312-747-LEAD. For homes with Cook County addresses (other than within the city) call 708-492-2035. Other counties report to their local health department. A reporting form for Chicago addresses, which can be completed and faxed in, is available at www.chicagolead.org.

Both Chicago and Cook County Health Departments have HUD money and programs to provide repair of lead hazards for low-income homeowners in targeted areas. However, the funds currently available will address only a small part of the problem. The Cook County Board is in the process of developing a program to use $14 million freed from the Torren’s Fund to provide funding for lead abatement in Cook County.

STEPS TO LOWER LEAD EXPOSURE

Safe repair of lead hazards and regular monitoring for paint deterioration are the only sure ways to lower a child’s exposure to lead on a reliable basis. Some steps parents can take to lower their child’s exposure to lead include (1) identifying areas in the home likely to have older, deteriorated lead paint (especially windows) or higher loads of dust (porches, basements); (2) creating barriers to prevent children from touching those areas; and (3) practicing regular cleaning to lower lead dust on floors, window sills, and wells. Another often unrecognized hazard is lead dust trapped in old carpets. Older carpets in homes with lead paint may have lead-containing dust, which vacuuming does not remove. This lead-containing dust goes from carpet to hand to mouth. Washable floors, cleaned regularly, are preferred.

Downloadable handouts for parents to assist identification of likely exposure sites for lead in their home and steps to reduce exposure are available in English and Spanish at www.chicagolead.org. When parents are sufficiently concerned to sustain these actions (e.g., if their child’s blood lead level is rising), these steps help reduce lead exposure. Similar measures used as a test of lead poisoning prevention in a high-risk area did not prevent rises in blood lead over the first 2 years of life.[15,16] Developing parental motivation to sustain these actions may be key.

Many families do not know when their home was built, so they do not realize the risk. Parents can check their home’s age by address using Chicago or Cook County Tax Assessment records on the website provided by the Center for Neighborhood Technology, www.newschicago.org.

Sources of lead are many, too numerous to delineate here. Two sources of lead have recently come to my attention. The first of these is candle wicks; about 10% of metallic candle wicks contain lead, which is readily absorbed on burning. There is no reliable way to tell whether a metallic wick contains lead or not. For a child, a 45-minute exposure would exceed the recommended daily limit for lead inhalation.[17] A second source, lead weights used to balance automobile tires, contributes to roadside lead dust. These weights may come loose, dislodge onto the roadside, and can be easily crushed to a fine powder.[18] These sources are not likely major factors in Chicago’s lead problem, but I’m wondering when we’ll finally recognize that the long-lasting effects of lead overshadow short-term gain and find alternative products with less toxicity.

ADEQUATE IRON AND CALCIUM INTAKE LOWERS LEAD ABSORPTION

Parents aiming at prevention should ensure that their children have sufficient body stores of iron and ingest an adequate amount of dietary calcium daily. Lead is known to interfere with red blood cell production, but this effect is seen only at BLLs of around 40 µg/dL or higher. However, low iron stores promote lead absorption. Therefore, children with iron deficiency exposed to lead are more likely to be hit with a double whammy—the lasting negative effects on cognitive development due to iron deficiency in infancy, and the lasting negative effects due to lead.[19,20] More than half of US children 1–2 years old have a daily iron intake below the recommended amount.[21]

The relationships between lead and calcium absorption have been well studied. Insufficient daily calcium intake promotes lead absorption. This effect is seen in both calcium-replete and calcium-deficient states. Too much calcium is not beneficial, however. Besides the fact that cow’s milk is very low in iron, excess calcium inhibits iron absorption from other sources. The daily calcium requirement is usually met by 2 servings of dairy at age 2 years (milk or yogurt are best sources) and 3 servings at age 3 years. If milk is not an option, calcium-fortified juices provide an equal amount of calcium per serving as milk, but they lack the benefits of protein and phosphorus, which milk provides.

Lead in water is a low-level source of exposure and is highly overrated compared to the risks of paint. However, no lead is better that any, and it is easy to lower lead concentration in water. The main source for lead in water is lead solder within the home itself. Turning on faucets for about 2 minutes every morning flushes standing water from the pipes, which has had longer opportunity to absorb lead. Also, cold water leaches lead more slowly than warm water, so always use cold water. Many families have water filters, which effectively lower lead in water. Others drink bottled water. While there are no mandated standards for lead content in bottled water, most likely it is low. However, most bottled waters lack fluoride. Some exceptions are bottled water intended for infant use and, on special request, from a few companies that provide home delivery.

SHOULD A YOUNG WOMAN PLANNING TO GET PREGNANT BE CONCERNED ABOUT HER BLOOD LEAD LEVEL?

Women of reproductive age have low BLLs compared to the rest of the population.[22] According to 1988–91 NHANES data, the mean BLL for US women ages 20–29 is approximately 2 µg/dL. However, women with higher BLLs as children will likely have lead stores above average into young adulthood, because the half-life of lead in bone is very long. Lead transfers from mother to fetus during pregnancy and through breast milk. The mother’s BLL is highest in the third trimester and during lactation, when increased bone activity in the mother mobilizes lead stored in bone.[23] However, adequate calcium intake during both pregnancy and lactation significantly decreases the amount of lead mobilized and thus transferred to the baby in those periods.[24,25] Breast-feeding has many other beneficial effects, and it should be encouraged unless the mother’s lead level is quite high. Pregnant women should also avoid eating nonfood items (dirt, clay, pottery, etc.) which may contain lead; pica behaviors are common in some cultures and regions. Of course, pregnant women should not be exposed to home renovation activities.

Studies of child outcomes related to prenatal lead exposure have found some associations with developmental tests at young ages, but later developmental tests in those same cohorts show more significant associations with childhood exposures than with prenatal exposures. A recent study suggests that low-level prenatal lead exposure may have a more lasting impact.[26] Further study of the prenatal exposure effect is underway in a Mexico City cohort examining the relationship of child cognitive outcomes to maternal lead stores measured in bone.

Finally, lead is only one effect on a child’s development. A mother’s lead level that is higher than adult US norms may not be something she can change quickly. Other factors which significantly affect a child’s cognitive development include: breast-feeding; not smoking; family stability; a healthy home environment that promotes a child’s cognitive development; mother’s and father’s IQ and educational levels; alcohol or drugs during pregnancy; and parenting skills.

CONCLUSION

Lead is a major environmental toxin and pervasive in our environment. Lead is the best studied of environmental toxins, but may be competing soon for a place along other emerging toxic exposures. Recent publications explore the impact of methylmercury (found in ocean fish), PCBs (which contaminate the Great Lakes), pesticides, and other compounds that affect the endocrine or neurologic systems with even minute exposures. The lessons we’ve learned from lead should sensitize us to be cautious about environmental releases. In the case of lead, and likely other pollutants also, we need to stop using children as “the canary in the coal mine,” the age-old indicator of toxic release.

REFERENCES

1. 1990 U.S. Census.

2. U.S. Environmental Protection Agency, Office of Pollution Prevention and Toxics. April 1995. Report on the national survey of lead based paint in housing—base report. EPA 747-R-003.

3. Evaluation of the HUD Lead-Based Paint Hazard Control Grant Program Interim Report, 1998.

4. U.S. Federal Register. 2001;66:1206–1240.

5. Gulson BL, Davis JJ, Bawden-Smith J. Paint as a source of recontamination of houses in urban environments and its role in maintaining elevated blood leads in children. Sci Total Environment. 1995;164:221–235.

6. Shinn NJ, Bing-Canar J, Cailas M, Peneff N, Binns HJ. Determination of spatial continuity of soil lead levels in an urban residential neighborhood. Environ Res. 2000;82:46–52.

7. Lanphear BP, Matte TD, Rogers J, et al. The contribution of lead- contaminated house dust and residential soil to children’s blood lead levels. A pooled analysis of 12 epidemiologic studies. Environ Res.1998;79:51–68.

8. U.S. General Accounting Office. Medicaid: elevated blood lead levels in children. Washington, DC: US General Accounting Office, 1998; GAO publication no. GAO/HEHS 98–78.

9. Centers for Disease Control. Blood lead levels in young children—United States and selected states, 1996–1999. MMWR. 2000;49:1133–34.

10. Bellinger DC, Stiles KM, Needleman HL. Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study. Pediatrics 1992;90:855–61 and Pediatrics (letter) 1993;91:855–56.

11. Schwartz J. Low-level lead exposure and children’s IQ: a meta-analysis and search for a threshold. Environ Res. 1994;65:42–55.

12. Centers for Disease Control and Prevention. Recommendations for blood lead screening of young children enrolled in Medicaid: targeting a group at high risk—United States. MMWR.2000;49(RR-14):5.

13. Centers for Disease Control. Elevated blood lead levels among internationally adopted children—United States, 1998. MMWR. 2000;49:97–100.

14. Norman EH, Bordley WC, Hertz-Picciotto I, Newton DA. Rural-urban blood lead differences in North Carolina children. Pediatrics. 1994;94:60–61.

15. Lanphear BP, Howard C, Eberly S, et al. Primary prevention of childhood lead exposure: a randomized trial of dust control. Pediatrics. 1999;103:772–777.

16. Lanphear BP, Winter NL, Apetz L, Eberly S, Weitzman M. A randomized trial of the effect of dust control on children’s blood lead levels. Pediatrics. 1996; 35–40.

17. Sobel HL, Lurie P, Wolfe SM. Lead exposure from candles (letter). JAMA. 2000;284:180.

18. Root RA. Lead Loading of urban streets by motor vehicle wheel weights. Environ Health Perspect. 2000;108:937–940.

19. Lozoff B, Jimenez E, Hagen J, Mollen E, Wolf A. Poorer behavioral and developmental outcome more than 10 years after treatment for iron deficiency in infancy. Pediatrics. 2000;105:E51.

20. Wasserman G, Graziano JH, Factor-Litvah P, et al. Independent effects of lead exposure and iron deficiency anemia on developmental outcome at age 2 years. J Pediatr. 1992;121:695–703.

21. Alaimo K, McDowell, MA, Briefel RR, et al. Dietary intake of vitamins, minerals, and fiber of persons ages 2 months and over in the United States: Third National Health and Nutrition Examination Survey, phase 1, 1988–91. NCHS Advance Data. 1994;258:1–26.

22. Brody DJ., Pirkle JL, Kramer RA, et al. Blood lead levels in the US population: phase 1 of the Third National Health and Nutrition Examination Survey (NHANES III, 1988 to 1991). JAMA. 1994:272:277–283.

23. Gulson BL, Jameson CW, Mahaffey KR, Mizon KJ, Korsch MJ, Vimpani G. Pregnancy increases mobilization of lead from maternal skeleton. J Lab Clin Med. 1997;130:51–62.

24. Farias P, Borja-Aburto VH, Rios C, Hertz-Picciotto I, Rojas-Lopez M, Chavez-Ayala R. Blood lead levels in pregnant women of high and low socioeconomic status in Mexico City. Environ Health Perspect.1996;104:1070–1074.

25. Hernandez-Avila M, Gonzalez-Cossio T, Palazuelos E, et al. Dietary and environmental determinants of blood and bone lead levels in lactating postpartum women living in Mexico City. Environ Health Perspect. 1996;104:1076–1082.

26. Wasserman GA, Liu X, Popovac D, et al. The Yugoslavia Prospective Lead Study: contributions of prenatal and postnatal lead exposure to early intelligence. Neurotoxicol Teratol. 2000;22:811–818.

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