Disparities in Toxic Chemical Exposures and Associated Neurodevelopmental Outcomes: A Scoping Review and Systematic Evidence Map of the Epidemiological Literature.

BACKGROUND: Children are routinely exposed to chemicals known or suspected of harming brain development. Targeting Environmental Neuro-Development Risks (Project TENDR), an alliance of >50 leading scientists, health professionals, and advocates, is working to protect children from these toxic chemicals and pollutants, especially the disproportionate exposures experienced by children from families with low incomes and families of color. OBJECTIVE: This scoping review was initiated to map existing literature on disparities in neurodevelopmental outcomes for U.S. children from population groups who have been historically economically/socially marginalized and exposed to seven exemplar neurotoxicants: combustion-related air pollution (AP), lead (Pb), mercury (Hg), organophosphate pesticides (OPs), phthalates (Phth), polybrominated diphenyl ethers (PBDEs), and polychlorinated biphenyls (PCBs). METHODS: Systematic literature searches for the seven exemplar chemicals, informed by the Population, Exposure, Comparator, Outcome (PECO) framework, were conducted through 18 November 2022, using PubMed, CINAHL Plus (EBSCO), GreenFILE (EBSCO), and Web of Science sources. We examined these studies regarding authors' conceptualization and operationalization of race, ethnicity, and other indicators of sociodemographic and socioeconomic disadvantage; whether studies presented data on exposure and outcome disparities and the patterns of those disparities; and the evidence of effect modification by or interaction with race and ethnicity. RESULTS: Two hundred twelve individual studies met the search criteria and were reviewed, resulting in 218 studies or investigations being included in this review. AP and Pb were the most commonly studied exposures. The most frequently identified neurodevelopmental outcomes were cognitive and behavioral/psychological. Approximately a third (74 studies) reported investigations of interactions or effect modification with 69% (51 of 74 studies) reporting the presence of interactions or effect modification. However, less than half of the studies presented data on disparities in the outcome or the exposure, and fewer conducted formal tests of heterogeneity. Ninety-two percent of the 165 articles that examined race and ethnicity did not provide an explanation of their constructs for these variables, creating an incomplete picture. DISCUSSION: As a whole, the studies we reviewed indicated a complex story about how racial and ethnic minority and low-income children may be disproportionately harmed by exposures to neurotoxicants, and this has implications for targeting interventions, policy change, and other necessary investments to eliminate these health disparities. We provide recommendations on improving environmental epidemiological studies on environmental health disparities. To achieve environmental justice and health equity, we recommend concomitant strategies to eradicate both neurotoxic chemical exposures and systems that perpetuate social inequities. https://doi.org/10.1289/EHP11750.

Healthy Air, Healthy Brains: Advancing Air Pollution Policy to Protect Children's Health.

Evidence is growing on the adverse neurodevelopmental effects of exposure to combustion-related air pollution. Project TENDR (Targeting Environmental Neurodevelopmental Risks), a unique collaboration of leading scientists, health professionals, and children's and environmental health advocates, has identified combustion-related air pollutants as critical targets for action to protect healthy brain development. We present policy recommendations for maintaining and strengthening federal environmental health protections, advancing state and local actions, and supporting scientific research to inform effective strategies for reducing children's exposures to combustion-related air pollution. Such actions not only would improve children's neurological development but also would have the important co-benefit of climate change mitigation and further improvements in other health conditions.

Traffic, air pollution, minority and socio-economic status: addressing inequities in exposure and risk.

Higher levels of nearby traffic increase exposure to air pollution and adversely affect health outcomes. Populations with lower socio-economic status (SES) are particularly vulnerable to stressors like air pollution. We investigated cumulative exposures and risks from traffic and from MNRiskS-modeled air pollution in multiple source categories across demographic groups. Exposures and risks, especially from on-road sources, were higher than the mean for minorities and low SES populations and lower than the mean for white and high SES populations. Owning multiple vehicles and driving alone were linked to lower household exposures and risks. Those not owning a vehicle and walking or using transit had higher household exposures and risks. These results confirm for our study location that populations on the lower end of the socio-economic spectrum and minorities are disproportionately exposed to traffic and air pollution and at higher risk for adverse health outcomes. A major source of disparities appears to be the transportation infrastructure. Those outside the urban core had lower risks but drove more, while those living nearer the urban core tended to drive less but had higher exposures and risks from on-road sources. We suggest policy considerations for addressing these inequities.

Validation of a novel air toxic risk model with air monitoring.

Three modeling systems were used to estimate human health risks from air pollution: two versions of MNRiskS (for Minnesota Risk Screening), and the USEPA National Air Toxics Assessment (NATA). MNRiskS is a unique cumulative risk modeling system used to assess risks from multiple air toxics, sources, and pathways on a local to a state-wide scale. In addition, ambient outdoor air monitoring data were available for estimation of risks and comparison with the modeled estimates of air concentrations. Highest air concentrations and estimated risks were generally found in the Minneapolis-St. Paul metropolitan area and lowest risks in undeveloped rural areas. Emissions from mobile and area (nonpoint) sources created greater estimated risks than emissions from point sources. Highest cancer risks were via ingestion pathway exposures to dioxins and related compounds. Diesel particles, acrolein, and formaldehyde created the highest estimated inhalation health impacts. Model-estimated air concentrations were generally highest for NATA and lowest for the AERMOD version of MNRiskS. This validation study showed reasonable agreement between available measurements and model predictions, although results varied among pollutants, and predictions were often lower than measurements. The results increased confidence in identifying pollutants, pathways, geographic areas, sources, and receptors of potential concern, and thus provide a basis for informing pollution reduction strategies and focusing efforts on specific pollutants (diesel particles, acrolein, and formaldehyde), geographic areas (urban centers), and source categories (nonpoint sources). The results heighten concerns about risks from food chain exposures to dioxins and PAHs. Risk estimates were sensitive to variations in methodologies for treating emissions, dispersion, deposition, exposure, and toxicity.

Cumulative risk assessment and environmental equity in air permitting: interpretation, methods, community participation and implementation of a unique statute.

In 2008, the statute authorizing the Minnesota Pollution Control Agency (MPCA) to issue air permits was amended to include a unique requirement to analyze and consider "cumulative levels and effects of past and current environmental pollution from all sources on the environment and residents of the geographic area within which the facility's emissions are likely to be deposited." Data describing the Statute Area suggest it is challenged by environmental and socioeconomic concerns, i.e., concerns which are often described by the phrase 'environmental equity'. With input from diverse stakeholders, the MPCA developed a methodology for implementing a cumulative levels and effects analysis when issuing air permits in the designated geographic area. A Process Document was created defining explicit steps a project proposer must complete in the analysis. An accompanying Reference Document compiles all available environmental health data relevant to the Statute Area that could be identified. The final cumulative levels and effects methodology is organized by health endpoint and identifies hazard, exposure and health indices that require further evaluation. The resulting assessment is summarized and presented to decision makers for consideration in the regulatory permitting process. We present a description of the methodology followed by a case study summary of the first air permit processed through the "cumulative levels and effects analysis".

Mercury speciation, reactivity, and bioavailability in a highly contaminated estuary, Berry's Creek, New Jersey Meadowlands.

Speciation and reactivity of mercury were examined in Berry's Creek estuary downstream of a highly mercury-contaminated U.S. EPA Superfund site during the summers of 2002 and 2003. Surface water samples from Berry's Creek estuary, its confluence with the Hackensack River, and upstream of that confluence were analyzed for total (THg), particulate (PHgT), and dissolved (DHg) mercury, total and particulate monomethylmercury (MeHg), dissolved gaseous mercury (DGM), and bacterial merA gene and transcript abundances. Surface water concentrations of THg in Berry's Creek estuary (210-6800 pM) are among the highest in North America. A downstream gradient of Hg contamination is a permanent feature of Berry's Creek estuary, and the upper estuary appears to be a perennial source of Hg to the lower estuary and the Hackensack River. MeHg concentrations in Berry's Creek surface waters ranged from 2 to 14 pM, with the highest concentrations occurring at a midestuary site 2 km downstream of the tide gate. The suspended particle phase dominated Hg and MeHg speciation throughout this system, accounting for > 90% of THg in Berry's Creek estuary and 35-94% of THg in the Hackensack River. Concentrations of DGM in Berry's Creek estuary (0.1-1.0 pM) are similar to levels of DGM in other much less contaminated estuaries (0.04-0.75 pM). In addition, expression levels of the bacterial mercuric reductase gene, merA, a gene of the inorganic Hg(II)-regulated, mercury resistance (mer) operon, were low throughout Berry's Creek estuary. Thus, despite very high concentrations of mercury in Berry's Creek estuary, relatively low concentrations of DGM and merA gene expression levels indicate limited bioavailability of inorganic Hg in the estuary's surface waters. A system-wide limitation on the bioavailability of inorganic Hg, together with bacterial demethylation activity, may account for observed MeHg concentrations that, although elevated, are lower than expected given the concentrations of THg in this estuary.

Role of the bacterial organomercury lyase (MerB) in controlling methylmercury accumulation in mercury-contaminated natural waters.

The curious phenomenon of similar levels of methylmercury (MeHg) accumulation in fish from contaminated and pristine environments may be explained by the observation that the proportion of total mercury (HgT) present as MeHg is inversely related to HgT in natural waters. We hypothesize that this "MeHg accumulation paradox" is explained by the quantitative induction of bacterial enzymes that are encoded by the mercury resistance (mer) operon, organomercury lyase (MerB), and mercuric reductase (MerA) by inorganic Hg (Hg[II]). We tested this hypothesis in two ecosystems in New Jersey: Berry's Creek in the Meadowlands (ML) and Pine Barren (PB) lakes. Across all sites, an inverse correlation (r2 = 0.80) between the concentration of HgT (ML, 113-4220 ng L(-1); PB, 0.3-5.4 ng L(-1)) and the proportion of HgT as MeHg (MeHg in ML and PB ranged from 0.08 to 1.6 and from 0.03 to 0.34 ng L(-1), respectively) was observed. The planktonic microbial community in Meadowlands surface waters exhibited adaptation to mercury, the presence of mer genes and mRNA transcripts, and high rates of reductive demethylation (k(deg) = 0.19 day(-1)). In contrast, the microbial community of PB was not adapted to mercury and demonstrated low rates of oxidative demethylation (k(deg) = 0.01 day(-1)). These results strongly support our hypothesis and show that the degradation of MeHg by mer-encoded enzymes by the water column microbiota of contaminated environments can significantly affect the amount of MeHg that is available for entry into the aquatic food web.