Blood Lead and Pediatric Asthma

Abstract

To the Editor: Lead activates signaling proteins in the immune system, is associated with increased IgE,1 and has been hypothesized to be a risk factor for asthma.2,3 To test this hypothesis, we conducted a retrospective cohort study of 1297 children with a venous blood lead test between 18 and 24 months and continuous Medicaid coverage (at least 335 days per year) through age 9. Blood lead data were abstracted from the Missouri Childhood Lead Poisoning Prevention Program, and asthma diagnosis was obtained from inpatient, outpatient, and prescription claims data in the Missouri Medicaid database. An incident case of asthma was defined as one occurring between a child’s 3rd and 9th birthday, with diagnosis based on the definition for persistent asthma established by the National Committee for Quality Assurance Healthcare Effectiveness Data and Information Set. Individual and neighborhood-level covariates were considered in multivariable logistic regression models. Individual-level covariates included sex, race, poverty, chronic lead exposure (three or more blood measures ≥5 µg/dL), and rhinitis. Census block-level variables included urbanization, housing age, neighborhood deprivation, per-capita income, and degree of racial isolation. Multilevel analysis was conducted to account for clustering in this two-level structure. General estimating equations were used to account for intraclass correlation. The majority of children were black, male, and from very low-income households. Approximately 62% had blood lead levels at or above 5 µg/dL and 23% above 10 µg/dL. The mean per-capita income for all block groups was $15,016. The average proportion of older housing per block group was 45%; 23% of block groups were categorized as impoverished (e Tables 1 and 2, https://links.lww.com/EDE/A667). Asthma was diagnosed in 20% of children. Of those, 59% had blood lead levels ≥5 µg/dL, and 21% were ≥10 µg/dL. In multivariable analysis, the main predictors of asthma were male sex (adjusted odds ratio =1.6; 95% confidence interval [CI] = 1.2–2.1), black race (2.1; 1.4–3.1), and a diagnosis of rhinitis (5.8; 3.8–8.8). Blood lead ≥10 µg/dL was not associated with asthma (0.91; 95% CI: 0.55–1.48), nor was chronic lead exposure (0.95; 0.58–1.55) (Table). Stratification of analysis by race (black and white) showed no effect modification. Given the shared risks for both asthma and lead exposure, we also examined the extent to which neighborhood factors are consistently associated with both asthma and blood lead levels. The results of multilevel modeling indicate that individual rather than neighborhood factors drive asthma risk, whereas neighborhood factors are significantly associated with elevated lead.TABLE: Adjusted Relationship Between Blood Lead Level ≥10 µg/dL and Asthma Multilevel Logistic RegressionThe majority of asthmatics had elevated blood lead. This is consistent with findings from the health disparities literature that impoverished children are at risk for multiple pediatric environmental health conditions.4 Lead exposure—defined as blood lead levels ≥5 µg/dL, ≥10 µg/dL, or chronic exposure—was not, however, associated in our study with the risk of developing asthma, using multilevel models adjusting for individual- and neighborhood-level covariates. Other studies have found an association between blood lead and asthma. This inconsistency could be due to the cross-sectional design of most previous studies and the use of prevalent asthma cases.3,5–8 We found that factors associated with elevated blood lead were substantially different from those associated with incident asthma. Even though a majority of asthmatics had elevated blood lead levels, blood lead was not itself a risk factor for development of asthma. ACKNOWLEDGMENTS We thank the Missouri Department of Social Services for assistance in accessing and using the Medicaid data. Felicia A. Rabito Department of Epidemiology Tulane University School of Public Health and Tropical Medicine New Orleans, LA [email protected] Libby Horter Elizabeth C. Langlois Department of Global Environmental Health Sciences Center for Applied Environmental Public Health Tulane University School of Public Health and Tropical Medicine New Orleans, LA John C. Carlson Department of Pediatrics Tulane University School of Medicine New Orleans, LA LuAnn E. White Department of Global Environmental Health Sciences Center for Applied Environmental Public Health Tulane University School of Public Health and Tropical Medicine New Orleans, LA Kris Schwartz Patricia Osman Bureau of Environmental Epidemiology Missouri Department of Health and Senior Services Jefferson City, MO Janet C. Rice Department of Biostatistics and Bioinformatics Tulane University School of Public Health and Tropical Medicine New Orleans, LA