Joint Exposure to Chemical and Nonchemical Neurodevelopmental Stressors in U.S. Women of Reproductive Age in NHANES

Abstract

Lead (Pb) and methyl mercury (MeHg) are well established neurodevelopmental toxicants (NDTs), but joint exposure to chemical and nonchemical (e.g., maternal stress) stressors has rarely been considered. We characterized exposure to Pb, MeHg and a measure of physiological dysregulation associated with chronic stress and examined race/ethnicity as a predictor of joint NDT exposure. Using data from the 2003−2004 NHANES, potential chronic stress exposure was estimated using allostatic load (AL), a quantitative measure of physiological dysregulation. A Hazard Index was calculated for joint exposure to Pb and MeHg (HINDT). Logistic regression was used to assess the relationship between an indicator of elevated joint NDT exposures (HINDT > 1) and race/ethnicity. The multivariate model was stratified by AL groups to examine effect measure modification. African American (adjusted odds ratio [OR] [95% confidence interval] = 2.2 [1.4, 3.3]) and Mexican American (1.4 [0.7, 2.6]) women were more likely to have an HINDT > 1 compared to Caucasian women. Chronic stress was identified as an effect measure modifier with the largest ORs among women with high AL scores (African Americans = 4.3 [2.0, 9.5]; Mexican Americans = 4.2 [1.3, 14.1]). Chronic stress was found to modify the association between elevated joint NDT exposure and race/ethnicity, highlighting the importance of evaluating chemical and nonchemical stressor exposures leading to a common endpoint.

Concurrent Fetal Exposure to Multiple Environmental Chemicals along the U.S.—Mexico Border: An Exploratory Study in Brownsville, Texas

“…While the health implications of low-level fetal exposure to a complicated combination of OC pesticides, PCBs, and PAHs is legitimate cause for concern, the aggregate effects are largely unknown [ 1 , 2 , 3 , 4 , 21 , 22 , 23 ]. Measurements of exposures have tended to focus on individual chemicals or chemical classes [ 21 , 22 , 23 , 25 ], and understanding of biological mechanisms underlying disease processes is limited [ 27 , 28 , 29 , 30 , 31 , 32 , 33 ]. Nevertheless, maternal exposures and related cross-placental transport remain a public health priority because the developing fetus is acutely sensitive to xenobiotic chemicals during certain time windows of vulnerability when seemingly insignificant amounts of exogenous substances can cause serious adverse effects on the fetus and/or on the course of subsequent development [ 1 , 2 , 3 , 4 , 21 , 24 , 27 , 28 , 31 , 32 , 33 ].…”

“…Biological markers in umbilical cord blood are typically used to establish fetal exposure concentrations, with the vast majority of published studies reporting data for either a single chemical or chemical class [ 2 , 21 , 22 , 23 ]. However, there is ample evidence that the fetus is exposed routinely to a complex and constantly changing mixture of chemicals, including neurotoxicants, carcinogens, and endocrine disrupters [ 24 , 25 , 26 , 27 ], which may result in cumulative effects that are greater than the sum of individual toxicities [ 28 , 29 , 30 , 31 , 32 , 33 , 34 ].…”

Multifactorial Origin of Neurodevelopmental Disorders: Approaches to Understanding Complex Etiologies

“…Both epidemiological and experimental studies have explored hypotheses on the interaction between allostatic load and neurotoxicant exposure during development suggesting common target physiological systems and pathways for both toxicants and stress. In a very recent study conducted on the US cohort of women in reproductive age enrolled inside the National Health and Nutrition Examination Survey (NHANES) program, chronic stress was found to modify the association between elevated lead/methylmercury exposure and race/ethnicity [ 198 ], highlighting the importance of evaluating chemical and nonchemical stressor exposures. Previous studies had showed controversial relationships between higher environmental chemicals’ exposure and lower social economic status, suggesting that more epidemiological research is needed to clarify which variables (chemical and nonchemical) are really involved in the potential interaction between chronic stress and chemical hazard [ 199 , 200 ].…”

Cumulative Risk and Impact Modeling on Environmental Chemical and Social Stressors

“…Urban children exposed to violence had higher risks of developing asthma in the presence of traffic-related air pollution [14]. Social stressors, measured by indicators such as poverty and race/ethnicity, have been often included as one of the key effect modifiers in environmental health research to address disparities [15–22]. Social stressors such as educational attainment level and population density were examined previously as well [20].…”