There is no safe detectable level of lead (Pb) in the blood of young children. In the United States, predominantly African-American Black children are exposed to more Pb and present with the highest mean blood lead levels (BLLs). However, racial disparity has not been fully examined within risk factors for early childhood Pb exposure. Therefore, we conducted secondary analysis of blood Pb determinations for 2841 US children at ages 1-5 years with citizenship examined by the cross-sectional 1999 to 2010 National Health and Nutrition Examination Survey (NHANES). The primary measures were racial disparities for continuous BLLs or an elevated BLL (EBLL) ≥5 µg/dL in selected risk factors between non-Hispanic Black children (n = 608) and both non-Hispanic White (n = 1208) or Hispanic (n = 1025) children. Selected risk factors included indoor household smoking, low income or poverty, older housing built before 1978 or 1950, low primary guardian education <12th grade/general education diploma (GED), or younger age between 1 and 3 years. Data were analyzed using a regression model corrected for risk factors and other confounding variables. Overall, Black children had an adjusted +0.83 µg/dL blood Pb (95% CI 0.65 to 1.00, p < 0.001) and a 2.8 times higher odds of having an EBLL ≥5 µg/dL (95% CI 1.9 to 3.9, p < 0.001). When stratified by risk factor group, Black children had an adjusted 0.73 to 1.41 µg/dL more blood Pb (p < 0.001 respectively) and a 1.8 to 5.6 times higher odds of having an EBLL ≥5 µg/dL (p ≤ 0.05 respectively) for every selected risk factor that was tested. For Black children nationwide, one in four residing in pre-1950 housing and one in six living in poverty presented with an EBLL ≥5 µg/dL. In conclusion, significant nationwide racial disparity in blood Pb outcomes persist for predominantly African-American Black children even after correcting for risk factors and other variables. This racial disparity further persists within housing, socio-economic, and age-related risk factors of blood Pb outcomes that are much more severe for Black children.
Kawasaki disease (KD) is a systemic vasculitis primarily affecting children < 5 years old. Genes significantly associated with KD mostly involve cardiovascular, immune, and inflammatory responses. Recent studies have observed stronger associations for KD risk with multiple genes compared to individual genes. Therefore, we investigated whether gene combinations influenced KD susceptibility or coronary artery lesion (CAL) formation. We examined 384 single-nucleotide polymorphisms (SNPs) for 159 immune-related candidate genes in DNA samples from KD patients with CAL (n = 73), KD patients without CAL (n = 153), and cohort controls (n = 575). Individual SNPs were first assessed by univariate analysis (UVA) and multivariate analysis (MVA). We used multifactor dimensionality reduction (MDR) to examine individual SNPs in one-, two-, and three-locus best fit models. UVA identified 53 individual SNPs that were significantly associated with KD risk or CAL formation (p < 0.10), while 35 individual SNPs were significantly associated using MVA (p ≤ 0.05). Significant associations in MDR analysis were only observed for the two-locus models after permutation testing (p ≤ 0.05). In logistic regression, combined possession of PDE2A (rs341058) and CYFIP2 (rs767007) significantly increased KD susceptibility (OR = 3.54; p = 4.14 x 10−7), while combinations of LOC100133214 (rs2517892) and IL2RA (rs3118470) significantly increased the risk of CAL in KD patients (OR = 5.35; p = 7.46 x 10−5). Our results suggest varying gene-gene associations respectively predispose individuals to KD risk or its complications of CAL.
A superantigen or autoimmunity has been hypothesized to be the main cause of the Kawasaki's Disease but the etiology is unknown. Medical literature, epidemiological findings, and some case reports have suggested that mercury may play a pathogenic role. Several patients with Kawasaki's Disease have presented with elevated urine mercury levels compared to matched controls. Most symptoms and diagnostic criteria which are seen in children with acrodynia, known to be caused by mercury, are similar to those seen in Kawasaki's Disease. Genetic depletion of glutathione S-transferase , a susceptibility marker for Kawasaki's Disease, is known to be also a risk factor for acrodynia and may also increase susceptibility to mercury . Coinciding with the largest increase (1985-1990) of thimerosal (49.6% ethyl mercury) in vaccines, routinely given to infants in the U.S. by 6 months of age (from 75microg to 187.5microg), the rates of Kawasaki's Disease increased ten times, and, later (1985-1997), by 20 times. Since 1990 88 cases of patients developing Kawasaki's Disease some days after vaccination have been reported to the Centers of Disease Control (CDC) including 19% manifesting symptoms the same day. The presented pathogenetic model may lead to new preventive- and therapeutic strategies for Kawasaki's disease.
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