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Aims To evaluate the safety of irrigation water sources based on phenotypic antimicrobial resistance (AMR) in Enterococcus spp., a potential environmental reservoir for AMR determinants. Methods and Results Eleven sites representing fresh and brackish water rivers, ponds and reclaimed water, were sampled over 2 years. Samples (n = 333) yielded 198 unique isolates of Ent. faecalis and Ent. faecium which were tested for antimicrobial susceptibility by microbroth dilution. Species distribution was influenced by water type and season. Enterococcus faecalis was more likely found in freshwater rivers and in summer, and Ent. faecium in reclaimed water and in spring. Only 11% of isolates were pansusceptible, while 48.5% and 26.3% were single (SDR) and multidrug resistant (MDR), respectively. MDR was more likely detected in Ent. faecium than Ent. faecalis. Winter isolates were more likely than summer isolates to exhibit MDR than SDR. Conclusions Enterococcus faecalis and Ent. faecium in surface and reclaimed water exhibited diverse phenotypic AMR and a low-level resistance to clinically important antimicrobials such as ampicillin, vancomycin and linezolid. Significance and Impact of the Study Single and multidrug resistance in E. faecalis and E. faecium varied by season but not water type. Antimicrobial resistance prevalence can assist decisions on the safety of irrigation water sources for fresh produce crops.

The emergence of low-cost air quality sensors as viable tools for the monitoring of air quality at population and individual levels necessitates the evaluation of these instruments. The Flow air quality tracker, a product of Plume Labs, is one such sensor. To evaluate these sensors, we assessed 34 of them in a controlled laboratory setting by exposing them to PM

A concrete block plant located in Bladensburg, Maryland, wants to expand to include a concrete batching plant on the same property. This expansion could further degrade air quality and impact the h...

A concrete block plant located in Bladensburg, Maryland, wants to expand to include a concrete batching plant on the same property. This expansion could further degrade air quality and impact the h...

Toxic chemicals — “toxicants” — have been studied and regulated as single entities, and, carcinogens aside, almost all toxicants, single or mixed and however altered, have been thought harmless in very low doses or very weak concentrations. Yet much work in recent decades has shown that toxicants can injure wildlife, laboratory animals, and humans following exposures previously expected to be harmless. Additional work has shown that toxicants can act not only individually and cumulatively but also collectively and even synergistically and that they affect disadvantaged communities inordinately — and therefore, as argued by reformers, unjustly. As late as December 2016, the last full month before the inauguration of a president promising to rescind major environmental regulations, the United States federal environmental-health establishment, as led by the Environmental Protection Agency (EPA), had not developed coherent strategies to mitigate such risks, to alert the public to their plausibility, or to advise leadership in government and industry about their implications. To understand why, we examined archival materials, reviewed online databases, read internal industry communications, and interviewed experts. We confirmed that external constraints, statutory and judicial, had been in place prior to EPA’s earliest interest in mixture toxicity, but we found no overt effort, certainly no successful effort, to loosen those constraints. We also found internal constraints: concerns that fully committing to the study of complex mixtures involving numerous toxicants would lead to methodological drift within the toxicological community and that trying to act on insights from such study could lead only to regulatory futility. Interaction of these constraints, external and internal, shielded the EPA by circumscribing its responsibilities and by impeding movement toward paradigmatic adjustment, but it also perpetuated scientifically dubious policies, such as those limiting the evaluation of commercial chemical formulations, including pesticide formulations, to only those ingredients said by their manufacturers to be active. In this context, regulators’ disregard of synergism contrasted irreconcilably with biocide manufacturers’ understanding that synergism enhanced lethality and patentability. In the end, an effective national response to mixture toxicity, cumulative risk, and environmental injustice did not emerge. In parallel, though, the National Institute of Environmental Health Sciences, which was less constrained, pursued with scientific investigation what the EPA had not pursued with regulatory action.

PURPOSE OF REVIEW We identified 24 publications from January 2010 until September 2018 in the peer-reviewed literature addressing the relationship of long-term air pollution exposures and type 2 diabetes-related morbidity and mortality among adults. We examine key methodological issues, synthesize findings, and address study strengths and limitations. We also discuss biological mechanisms, policy implications, and future research needed to address existing knowledge gaps. RECENT FINDINGS In general, the studies included in this review employed rigorous methodology with large sample sizes, appropriate study designs to maximize available cohort study or administrative data sources, and exposure modeling that accounted for spatial patterns in air pollution levels. Overall, studies suggested increased risks of type 2 diabetes-related morbidity and mortality among adults associated with increased exposures; however, findings were not uniformly positive nor statistically significant. SUMMARY Current research is particularly limited regarding the biological mechanisms involved and the relationship between ozone and diabetes. Additionally, more research is needed to distinguish clearly the effects of nitrogen oxides from those of other pollutants and to identify potential subpopulations with greater susceptibility for certain pollutant exposures. A better understanding of the potential link between long-term ambient air pollution exposures and type 2 diabetes may provide opportunities for the reduction of health risks and inform future interventions for environmental protection and diabetes management.

Background: The twin pandemics of COVID-19 and systemic racism during 2020 have forced a conversation across many segments of our society, including the environmental health sciences (EHS) research community. We have seen the proliferation of statements of solidarity with the Black Lives Matter movement and commitments to fight racism and health inequities from academia, nonprofit organizations, governmental agencies, and private corporations. Actions must now arise from these promises. As public health and EHS scientists, we must examine the systems that produce and perpetuate inequities in exposure to environmental pollutants and associated health effects. Objectives: We outline five recommendations the EHS research community can implement to confront racism and move our science forward for eliminating racial inequities in environmental health. Discussion: Race is best considered a political label that promotes inequality. Thus, we should be wary of equating race with biology. Further, EHS researchers should seriously consider racism as a plausible explanation of racial disparities in health and consider structural racism as a factor in environmental health risk/impact assessments, as well as multiple explanations for racial differences in environmental exposures and health outcomes. Last, the EHS research community should develop metrics to measure racism and a set of guidelines on the use and interpretation of race and ethnicity within the environmental sciences. Numerous guidelines exist in other disciplines that can serve as models. By taking action on each of these recommendations, we can make significant progress toward eliminating racial disparities. https://doi.org/10.1289/EHP8186

Little progress has been made to advance U.S. federal policy responses to growing scientific findings about cumulative environmental health impacts and risks, which also show that many low income and racial and ethnic minority populations bear a disproportionate share of multiple environmental burdens. Recent scholarship points to a “standard narrative” by which policy makers rationalize their slow efforts on environmental justice because of perceived lack of data and analytical tools. Using a social constructivist approach, ethnographic research methods, and content analysis, we examined the social context of policy challenges related to cumulative risks and impacts in the state of Maryland between 2014 and 2016. We identified three frames about cumulative impacts as a health issue through which conflicts over such policy reforms materialize and are sustained: (a) perceptions of evidence, (b) interpretations of social justice, and (c) expectations of authoritative bodies. Our findings illustrate that policy impasse over cumulative impacts is highly dependent on how policy-relevant actors come to frame issues around legislating cumulative impacts, rather than the “standard narrative” of external constraints. Frame analysis may provide us with more robust understandings of policy processes to address cumulative risks and impacts and the social forces that create health policy change.

Background: The combined effects of multiple environmental toxicants and social stressor exposures are widely recognized as important public health problems contributing to health inequities. However cumulative environmental health risks and impacts have received little attention from U.S. policy makers at state and federal levels to develop comprehensive strategies to reduce these exposures, mitigate cumulative risks, and prevent harm. An area for which the inherent limitations of current approaches to cumulative environmental health risks are well illustrated is children’s neurodevelopment, which exhibits dynamic complexity of multiple interdependent and causally linked factors and intergenerational effects. Objectives: We delineate how a complex systems approach, specifically system dynamics, can address shortcomings in environmental health risk assessment regarding exposures to multiple chemical and nonchemical stressors and reshape associated public policies. Discussion: Systems modeling assists in the goal of solving problems by improving the “mental models” we use to make decisions, including regulatory and policy decisions. In the context of disparities in children’s cumulative exposure to neurodevelopmental stressors, we describe potential policy insights about the structure and behavior of the system and the types of system dynamics modeling that would be appropriate, from visual depiction (i.e., informal maps) to formal quantitative simulation models. A systems dynamics framework provides not only a language but also a set of methodological tools that can more easily operationalize existing multidisciplinary scientific evidence and conceptual frameworks on cumulative risks. Thus, we can arrive at more accurate diagnostic tools for children’s’ environmental health inequities that take into consideration the broader social and economic environment in which children live, grow, play, and learn. https://doi.org/10.1289/EHP7333

Background Given policy regulations restricting bisphenol A (BPA) in food-related products, and consumer concerns about adverse health effects, newer bisphenols such as bisphenol F (BPF) and bisphenol S (BPS) have been developed. Exposure to BPA has been linked to dietary behaviors and poor health outcomes. Objectives We sought to examine how the Healthy Eating Index (HEI) and its 13 subgroups, the healthy American diet, the Mediterranean diet, the vegetarian diet, and other dietary quality behaviors are related to BPA and the newer substitutes in a representative sample of US adults. Methods Dietary intakes from the NHANES were used to determine dietary scores. Osmolality-adjusted urinary BPA (n = 6418) and BPF and BPS (n = 2520) concentrations were tested for their association with dietary intake in models that adjusted for sociodemographics. Results Compared with low scores, high scores for total HEI and the American, Mediterranean, and vegetarian diets were associated with lower odds of high BPA concentration (OR: 0.65, 0.60, 0.59, and 0.60, respectively). Of the HEI subgroups, lower BPA concentration was associated with high total fruit (OR: 0.61; 99.95% CI: 0.42, 0.89), whole fruit (OR: 0.59; 99.95% CI: 0.41, 0.86), and whole grain (OR: 0.68; 99.95% CI: 0.40, 0.94) intake, when compared with low intakes. Compared with low intakes, high intakes of plain and tap water were associated with lower odds of high BPA concentration (OR: 0.65; 99.95% CI: 0.47, 0.91 and OR: 0.70; 99.95% CI: 0.50, 0.99, respectively). A perception of high, compared with low, dietary quality was also associated with lower odds of high BPA concentration (OR: 0.72; 99.95% CI: 0.53, 0.98). Conclusions Healthier dietary quality and several HEI subgroups were related to lower urinary BPA concentrations; no significant (P ≤ 0.0005) findings were observed for BPF and BPS. The association between bisphenol substitutes and dietary quality should continue to be monitored as bisphenol substitutes continue to increase in the food system.

Background Numerous international studies have examined cross-sectional correlates of food insecurity (FI) among postsecondary education students. Research is needed to synthesize the findings of this work to support vulnerable students. Objective To systematically review peer-reviewed and gray literature to assess the prevalence of FI on postsecondary education institutions, as well as factors related to FI among students and suggested/practiced solutions. Design Systematic literature review. Medline, Web of Science, and PsycINFO databases were searched for peer-reviewed literature for FI research; a Google search (Google Inc) was conducted to obtain gray literature on FI among postsecondary education students. Participants/setting Undergraduate and graduate students at postsecondary institutions of higher education. Main outcome measures Measures included prevalence of FI; sociodemographic, health, and academic factors related to FI; and solutions to address FI on postsecondary institutions. Results Seventeen peer-reviewed studies and 41 sources of gray literature were identified (out of 11,476 titles). All studies were cross-sectional. Rates of FI were high among students, with average rates across the gray and peer-reviewed literature of 35% and 42%, respectively. FI was consistently associated with financial independence, poor health, and adverse academic outcomes. Suggested solutions to address food security among postsecondary institutions addressed all areas of the socioecologic model, but the solutions most practiced included those in the intrapersonal, interpersonal, and institutional levels. Conclusions FI is a major public health problem among postsecondary education students. Studies are needed to assess the long-term influence of FI among this vulnerable population. More research is needed on the effectiveness of FI interventions.

Emerging adulthood (ages 18-25 years) is a key turning point in the life course characterized by particularly poor eating behaviors (e.g., low in fruits and vegetables, and high in fast food) and weight gain. Emerging adults are also prime consumers of personal care and other consumer products that may result in differential exposures to environmental contaminants, such as Bisphenol A (BPA), compared to adults aged 26+ years. This is of concern given BPA has been associated with adverse health outcomes such as obesity, metabolic disorders, miscarriage, infertility and breast cancer. However, no research has examined exposure to BPA among emerging adults.To assess trends of exposure to urinary BPA among a representative sample of emerging adults compared to adults aged 26+ years. Secondarily, we aimed to identify differential associations between BPA concentrations and sociodemographic characteristics and BMI by age group.This study uses National Health and Examination Surveys (NHANES) over 2003-2014 to test differences in BPA concentrations comparing emerging adults to adults aged 26+ years. Generalized linear models predicting log BPA by age group and sex, race/ethnicity, education, income, and food security status, and generalized linear models predicting BMI by log BPA, both age group and age as a continuous variable, sex, race/ethnicity, education, income, and food security status were conducted. Interactions with age group (i.e., age group x sex) were examined for the mutually adjusted models. All models controlled for survey year, month, and time of day, and were run with, and without, an adjustment for urinary creatinine.In models adjusted, and not adjusted, for urinary creatinine, emerging adults had a higher log BPA concentration than adults aged 26+ years (β=0.153, p=0.004; β=0.544, p0.001), and a significantly steeper decline in BPA concentration between 2003-2004 and 2013-2014 than adults aged 26+ years (ß=-0.051, p=0.002; ß=-0.071, p=0.001). Males' log BPA concentration were lower than that for females when urinary creatinine was included in the model, and higher when urinary creatinine was excluded from the model (ß=-0.188, p0.001; β=0.203, p0.001). Higher income was significantly associated with lower log BPA concentration (ß=-0.220, p0.001; ß=-0.166, p0.001). A significant interaction between emerging adult age group and food security status was observed, which was associated with higher BPA exposures. Log BPA concentration was associated with BMI only when urinary creatinine was excluded from the models (urinary creatinine included: β=0.031, p=0.747; β=0.022, p=0.815, urinary creatinine excluded: β=0.528, p0.001; β=0.552, p0.001).Findings indicate that emerging adults had higher BPA exposures than adults aged 26+ years in 2003-2004, and that emerging adults' exposure level has decreased faster than that of adults aged 26+ years. There were suggestions that the BPA concentration of emerging adults in 2013-2014 was lower than that for adults aged 26+ years, and that BPA exposure is associated with higher BMI. Our results highlight the need for additional research to identify the sources and routes of exposure to BPA and BPA replacements among emerging adults and to better characterize the variability in exposure. Intervention studies are needed to assist emerging adults in limiting their exposure to BPA, and potentially also the BPA alternatives.

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.

Background Neonicotinoids are a class of systemic insecticides widely used on food crops globally. These pesticides may be found in “off-target” food items and persist in the environment. Despite the potential for extensive human exposure, there are limited studies regarding the prevalence of neonicotinoid residues in foods sold and consumed in the United States. Methods Residue data for seven neonicotinoid pesticides collected between 1999 and 2015 by the US Department of Agriculture’s Pesticide Data Program (PDP) were collated and summarized by year across various food commodities, including fruit, vegetable, meat, dairy, grain, honey, and baby food, as well as water to qualitatively describe and examine trends in contamination frequency and residue concentrations. Results The highest detection frequencies (DFs) for neonicotinoids by year on all commodities were generally below 20%. Average DFs over the entire study period, 1999–2015, for domestic and imported commodities were similar at 4.5%. For all the samples (both domestic and imported) imidacloprid was the neonicotinoid with the highest overall detection frequency at 12.0%. However, higher DFs were observed for specific food commodity-neonicotinoid combinations such as: cherries (45.9%), apples (29.5%), pears (24.1%) and strawberries (21.3%) for acetamiprid; and cauliflower (57.5%), celery (20.9%), cherries (26.3%), cilantro (30.6%), grapes (28.9%), collard greens (24.9%), kale (31.4%), lettuce (45.6%), potatoes (31.2%) and spinach (38.7%) for imidacloprid. Neonicotinoids were also detected in organic commodities, (DF

Cumulative risk assessment (CRA) has been proposed as a means of evaluating possible additive and synergistic effects of multiple chemical, physical and social stressors on human health, with the goal of informing policy and decision-making, and protecting public health. Routine application of CRA to environmental regulatory and policy decision making, however, has been limited due to a perceived lack of appropriate quantitative approaches for assessing combined effects of chemical and nonchemical exposures. Seven research projects, which represented a variety of disciplines, including population health science, laboratory science, social sciences, geography, statistics and mathematics, were funded by the US Environmental Protection Agency (EPA) to help address this knowledge gap. We synthesize key insights from these unique studies to determine the implications for CRA practice and priorities for further research. Our analyses of these seven projects demonstrate that the necessary analytical methods to support CRA are available but are ultimately context-dependent. These projects collectively provided advancements for CRA in the areas of community engagement, characterization of exposures to nonchemical stressors, and assessment of health effects associated with joint exposures to chemical and psychosocial stressors.

We examined community perspectives and experiences with fracking in Doddridge County, West Virginia, USA as part of a larger assessment to investigate the potential health impacts associated with fracking in neighboring Maryland, USA. In November 2013, we held two focus groups with community residents who had been impacted by fracking operations and conducted field observations in the impacted areas. Employing grounded theory, we conducted qualitative analysis to explore emergent themes related to direct and indirect health impacts of fracking. Three components of experience were identified, including (a) meanings of place and identity, (b) transforming relationships, and (c) perceptions of environmental and health impacts. Our findings indicate that fracking contributes to a disruption in residents' sense of place and social identity, generating widespread social stress. Although community residents acknowledged the potential for economic growth brought about by fracking, rapid transformations in meanings of place and social identity influenced residents' perceptions of environmental and health impacts. Our findings suggest that in order to have a more complete understanding of the health impacts of fracking, future work must consider the complex linkages between social disruption, environmental impacts, and health outcomes through critical engagements with communities undergoing energy development.

It is widely recognized that Americans are exposed daily to multiple chemical compounds in our air, food, water, and consumer products, and that many low income and racial and ethnic minority popul...

Formally evaluating how specific policy measures influence environmental justice is challenging, especially in the context of regulatory analyses in which quantitative comparisons are the norm. However, there is a large literature on developing and applying quantitative measures of health inequality in other settings, and these measures may be applicable to environmental regulatory analyses. In this paper, we provide information to assist policy decision makers in determining the viability of using measures of health inequality in the context of environmental regulatory analyses. We conclude that quantification of the distribution of inequalities in health outcomes across social groups of concern, considering both within-group and between-group comparisons, would be consistent with both the structure of regulatory analysis and the core definition of environmental justice. Appropriate application of inequality indicators requires thorough characterization of the baseline distribution of exposures and risks, leveraging data generally available within regulatory analyses. Multiple inequality indicators may be applicable to regulatory analyses, and the choice among indicators should be based on explicit value judgments regarding the dimensions of environmental justice of greatest interest.

Studies have documented cumulative health effects of chemical and nonchemical exposures, particularly chronic environmental and social stressors. Environmental justice groups have advocated for community participation in research that assesses how these interactions contribute to health disparities experienced by low-income and communities of color. In 2009, the U.S. Environmental Protection Agency issued a request for research applications (RFA), “Understanding the Role of Nonchemical Stressors and Developing Analytic Methods for Cumulative Risk Assessments.” Seven research projects were funded to help address this knowledge gap. Each engaged with communities in different ways. We describe the community engagement approaches of the seven research projects, which ranged from outreach through shared leadership/participatory. We then assess the experiences of these programs with respect to the community engagement goals of the RFA. We present insights from these community engagement efforts, including how the grants helped to build or enhance the capacity of community organizations in addition to contributing to the research projects. Our analysis of project proposals, annual grantee reports, and participant observation of these seven projects suggests guidelines for the development of future funding mechanisms and for conducting community-engaged research on cumulative risk involving environmental and social stressors including: 1) providing for flexibility in the mode of community engagement; 2) addressing conflict between research timing and engagement needs, 3) developing approaches for communicating about the uniquely sensitive issues of nonchemical stressors and social risks; and 4) encouraging the evaluation of community engagement efforts.

© 2016, Public Health Services, US Dept of Health and Human Services. All rights reserved. Children in America today are at an unacceptably high risk of developing neurodevelopmental disorders that affect the brain and nervous system including autism, attention deficit hyperactivity disorder, intellectual disabilities, and other learning and behavioral disabilities. These are complex disorders with multiple causes—genetic, social, and environmental. The contribution of toxic chemicals to these disorders can be prevented. Approach: Leading scientific and medical experts, along with children’s health advocates, came together in 2015 under the auspices of Project TENDR: Targeting Environmental Neuro-Developmental Risks to issue a call to action to reduce widespread exposures to chemicals that interfere with fetal and children’s brain development. Based on the available scientific evidence, the TENDR authors have identified prime examples of toxic chemicals and pollutants that increase children’s risks for neurodevelopmental disorders. These include chemicals that are used extensively in consumer products and that have become widespread in the environment. Some are chemicals to which children and pregnant women are regularly exposed, and they are detected in the bodies of virtually all Americans in national surveys conducted by the U.S. Centers for Disease Control and Prevention. The vast majority of chemicals in industrial and consumer products undergo almost no testing for developmental neurotoxicity or other health effects. Conclusion: Based on these findings, we assert that the current system in the United States for evaluating scientific evidence and making health-based decisions about environmental chemicals is fundamentally broken. To help reduce the unacceptably high prevalence of neurodevelopmental disorders in our children, we must eliminate or significantly reduce exposures to chemicals that contribute to these conditions. We must adopt a new framework for assessing chemicals that have the potential to disrupt brain development and prevent the use of those that may pose a risk. This consensus statement lays the foundation for developing recommendations to monitor, assess, and reduce exposures to neurotoxic chemicals. These measures are urgently needed if we are to protect healthy brain development so that current and future generations can reach their fullest potential.

The recent growth of unconventional natural gas development and production (UNGDP) has outpaced research on the potential health impacts associated with the process. The Maryland Marcellus Shale Public Health Study was conducted to inform the Maryland Marcellus Shale Safe Drilling Initiative Advisory Commission, State legislators and the Governor about potential public health impacts associated with UNGDP so they could make an informed decision that considers the health and well-being of Marylanders. In this paper, we describe an impact assessment and hazard ranking methodology we used to assess the potential public health impacts for eight hazards associated with the UNGDP process. The hazard ranking included seven metrics: 1) presence of vulnerable populations (e.g. children under the age of 5, individuals over the age of 65, surface owners), 2) duration of exposure, 3) frequency of exposure, 4) likelihood of health effects, 5) magnitude/severity of health effects, 6) geographic extent, and 7) effectiveness of setbacks. Overall public health concern was determined by a color-coded ranking system (low, moderately high, and high) that was generated based on the overall sum of the scores for each hazard. We provide three illustrative examples of applying our methodology for air quality and health care infrastructure which were ranked as high concern and for water quality which was ranked moderately high concern. The hazard ranking was a valuable tool that allowed us to systematically evaluate each of the hazards and provide recommendations to minimize the hazards.

While many federal agencies are undertaking environmental justice-related activities to respond to Executive Order 12898 issued by President Clinton in 1994: “Federal Actions to Address Environmental Justice in Minority Populations and Low-Income Populations,” there is a lack of guidance on how to assess disproportionate human health or environmental effects of agency programs, policies, and actions on minority and low-income populations. Meanwhile, many state governments are now developing their own strategies for identifying disproportionate environmental health impacts and addressing environmental justice concerns. The purpose of this study is to review the diversity of state-level approaches and methodologies for conducting disproportionate environmental health impact evaluations as part of their environmental justice programs and initiatives. We found state approaches to these assessments, often called “environmental justice analyses” range from simple qualitative evaluations of demographic ...

Conventionally, in its decision-making, the U.S. EPA has evaluated the effects and risks associated with a single pollutant in a single exposure medium. In reality, people are exposed to mixtures of pollutants or to the same pollutant through a variety of media, including the air, water, and food. It is now more recognized than before that environmental exposure to pollutants occurs via multiple exposure routes and pathways, including inhalation, ingestion, and dermal absorption. Moreover, chemical, biologic, radiologic, physical, and psychologic stressors are all acknowledged as affecting human health. Although many EPA offices attempt to consider cumulative risk assessment and cumulative effects in various ways, there is no Agency-wide policy for considering these risks and the effects of exposure to these risks when making environmental decisions. This article examines how U.S. courts might assess EPA’s general authority and discretion to use cumulative risk assessment as the basis for developing data in support of environmental decision-making, and how courts might assess the validity of a cumulative risk assessment methodology itself.

In March 2010, the Environmental Protection Agency (EPA) collaborated with government and nongovernmental organizations to host a groundbreaking symposium, “Strengthening Environmental Justice Research and Decision Making: A Symposium on the Science of Disproportionate Environmental Health Impacts.” The symposium provided a forum for discourse on the state of scientific knowledge about factors identified by EPA that may contribute to higher burdens of environmental exposure or risk in racial/ethnic minorities and low-income populations. Also featured were discussions on how environmental justice considerations may be integrated into EPA's analytical and decision-making frameworks and on research needs for advancing the integration of environmental justice into environmental policymaking. We summarize key discussions and conclusions from the symposium and briefly introduce the articles in this issue.

One's place of birth is a major determinant of his or her exposure to environmental toxicants. By understanding biological burdens of long half-life toxicants by race and nativity we can better understand geographic variation in toxicant distribution. We used the National Health and Nutrition Examination Survey (1999–2006) biomonitoring data to examine differences in blood and urine levels of long half-life environmental toxicants of foreign-born relative to US-born people by race/ethnicity. We log transformed blood and urine measures of 51 environmental toxicants. We then used “seemingly unrelated regression,” a robust technique for making multiple comparisons across a group of variables with correlated error terms, to examine differences in blood and urine toxicants by nativity and race. We found that, compared to native-born Americans, the foreign-born are generally more likely to be exposed to metals (p < 0.001) and organochlorine pesticides (p < 0.001), but less likely to be exposed to dioxin-like compounds (p < 0.001) or polyflourinated compounds (p < 0.001). While levels of toxicants varied greatly by region of birth, US-born participants had consistently higher levels of dioxin-like compounds and polyflourinated compounds.

We focus on the disproportionate exposures to environmental contaminants and associated health outcomes with regards to Asian Americans and Pacific Islanders (APIAs). We review several env...

In 1994, the National Institute of Environmental Health Sciences (NIEHS) initiated a program to address communication gaps between community residents, researchers and health care providers in the context of disproportionate environmental exposures. Over 13 years, together with the Environmental Protection Agency and National Institute for Occupational Health and Safety, NIEHS funded 54 environmental justice projects. Here we examine the methods used and outcomes produced based on data gathered from summaries submitted for annual grantees' meetings. Data highlight how projects fulfilled program objectives of improving community awareness and capacity and the positive public health and public policy outcomes achieved. Our findings underscore the importance of community participation in developing effective, culturally sensitive interventions and emphasize the importance of systematic program planning and evaluation.

Biomonitoring is a valuable tool for identifying exposures to chemicals that pose potential harm to human health. However, to date there has been little published on ways to evaluate the relative public health significance of biomonitoring data for different chemicals and even less on cumulative assessment of multiple chemicals. The objectives of our study are to develop a methodology for a health risk interpretation of biomonitoring data and to apply it using NHANES 1999−2002 body burden data for organophosphorus (OP) pesticides. OP pesticides present a particularly challenging case given the nonspecificity of many metabolites monitored through NHANES. We back-calculate OP pesticide exposures from urinary metabolite data and compare cumulative dose estimates with available toxicity information for a common mechanism of action (brain cholinesterase inhibition) using data from U.S. EPA. Our results suggest that approximately 40% of children in the United States may have had insufficient margins of exposure...

In 1997 President Clinton signed Executive Order (EO) 13045, Protection of Children from Environmental Health Risks and Safety Risks (Clinton 1997). This order directs each federal agency to “make it a high priority to identify and assess environmental health risks and safety risks that may disproportionately affect children” and to “ensure that its policies, programs, activities, and standards address disproportionate risks to children that result from environmental health risks or safety risks” (Clinton 1997). That same year, the U.S. Environmental Protection Agency (EPA) created the Office of Children’s Health Protection to support its implementation of the Executive Order and its National Agenda to Protect Children’s Health from Environmental Threats (U.S. EPA 1996). Finally, U.S. EPA created the Children’s Health Protection Advisory Committee (CHPAC) in 1997, which is an independent body that advises U.S. EPA on regulations, research, and communication issues relevant to children. These actions were taken in direct response to the growing body of scientific knowledge that demonstrated that children may suffer disproportionately from environmental health and safety risks [National Research Council (NRC) 1993, 1994]. Disproportionate risks to or impacts on children may occur when children are more sensitive to, are more likely to be exposed to, or are likely to be exposed to higher levels of a particular pollutant or agent being considered in the rulemaking than adults are (U.S. EPA 2006c). Although EO 13045 has been pointed to as a model policy because it specifically addresses children and directs federal agencies to deliberately consider disproportionate risks to children (Fischer 2007), others say that the impact of EO has waned over the years (Carlson 2005; Spady 2006). The U.S. EPA recently marked the tenth anniversary of EO 13045, and CHPAC concluded that children’s environmental health considerations are still not explicitly addressed in U.S. EPA decisions, policies, and programs and urged renewed commitment to EO 13045 (Johnson 2007; Marty 2007). In this article we review U.S. EPA regulatory actions to evaluate applicability of EO 13045 and consideration of children’s health issues in U.S. EPA rulemakings.

Objectives. We systematically reviewed the Environmental Protection Agency, National Center for Environmental Research’s (NCER’s) requests for applications (RFAs) and identified strategies that NCER and other funders can take to bolster community engagement. Methods. We queried NCER’s publically available online archive of funding opportunities from fiscal years 1997 to 2013. From an initial list of 211 RFAs that met our inclusion criteria, 33 discussed or incorporated elements of community engagement. We examined these RFAs along 6 dimensions and the degree of alignments between them. Results. We found changes over time in the number of RFAs that included community engagement, variations in how community engagement is defined and expected, inconsistencies between application requirements and peer review criteria, and the inclusion of mechanisms supporting community engagement in research. Conclusions. The results inform a systematic approach to developing RFAs that support community engagement in research.

On May 24-25, 2005 in Ann Arbor, Michigan, the US Environmental Protection Agency, the National Institute of Environmental Health Sciences, and the University of Michigan sponsored a technical workshop on the topic of connecting social and environmental factors to measure and track environmental health disparities. The workshop was designed to develop a transdisciplinary scientific foundation for exploring the conceptual issues, data needs, and policy applications associated with social and environmental factors used to measure and track racial, ethnic, and class disparities in environmental health. Papers, presentations, and discussions focused on the use of multilevel analysis to study environmental health disparities, the development of an organizing framework for evaluating health disparities, the development of indicators, and the generation of community-based participatory approaches for indicator development and use. Group exercises were conducted to identify preliminary lists of priority health outcomes and potential indicators and to discuss policy implications and next steps. Three critical issues that stem from the workshop were: (a) stronger funding support is needed for community-based participatory research in environmental health disparities, (b) race/ethnicity and socioeconomic position need to be included in environmental health surveillance and research, and (c) models to elucidate the interrelations between social, physical, and built environments should continue to be developed and empirically tested.

Regulatory interventions are the first line of action used by the U.S. Environmental Protection Agency to fulfill its mission to protect the environment and health. Although the agency has prioritized the integration of environmental justice into its activities, uncertainty remains in how these considerations will be incorporated into its regulatory decision-making processes. In this article, we examine the emerging practice of Health Impact Assessment and argue for its use within the regulatory assessment paradigm to help answer policy-relevant environmental justice questions. Through the use of a health lens, Health Impact Assessments can lead to a better characterization of the potential impacts and benefits of a rule by introducing novel assessments of potentially significant health effects that would otherwise be excluded, revealing whether the rule is likely to exacerbate inequities or create new ones. This article proposes a framework to overcome analytic barriers in achieving a more comprehensive, equity-focused regulatory analysis.

Background: The Pediatric Environmental Health Specialty Units (PEHSU's) were created in 1998 by US EPA and ATSDR. In the early 1990's, two widespread incidents occurred in which environmental toxi...

Author(s): Shenassa, Edmond D; Rossen, Lauren M; Cohen, Jonathan; Morello-Frosch, Rachel; Payne-Sturges, Devon C | Abstract: IntroductionPrior studies have found considerable racial and ethnic disparities in secondhand smoke (SHS) exposure. Although a number of individual-level determinants of this disparity have been identified, contextual determinants of racial and ethnic disparities in SHS exposure remain unexamined. The objective of this study was to examine disparities in serum cotinine in relation to area-level income inequality among 14 649 children from the National Health and Nutrition Examination Survey.MethodsWe fit log-normal regression models to examine disparities in serum cotinine in relation to Metropolitan Statistical Areas level income inequality among 14 649 nonsmoking children aged 3-15 from the National Health and Nutrition Examination Survey (1999-2012).ResultNon-Hispanic black children had significantly lower serum cotinine than non-Hispanic white children (-0.26; 95% CI: -0.38, -0.15) in low income inequality areas, but this difference was attenuated in areas with high income inequality (0.01; 95% CI: -0.16, 0.18). Serum cotinine declined for non-Hispanic white and Mexican American children with increasing income inequality. Serum cotinine did not change as a function of the level of income inequality among non-Hispanic black children.ConclusionsWe have found evidence of differential associations between SHS exposure and income inequality by race and ethnicity. Further examination of environments which engender SHS exposure among children across various racial/ethnic subgroups can foster a better understanding of how area-level income inequality relates to health outcomes such as levels of SHS exposure and how those associations differ by race/ethnicity.ImplicationsIn the United States, the association between children's risk of SHS exposure and income inequality is modified by race/ethnicity in a manner that is inconsistent with theories of income inequality. In overall analysis this association appears to be as predicted by theory. However, race-specific analyses reveal that higher levels of income inequality are associated with lower levels of SHS exposure among white children, while levels of SHS exposure among non-Hispanic black children are largely invariant to area-level income inequality. Future examination of the link between income inequality and smoking-related health outcomes should consider differential associations across racial and ethnic subpopulations.

Background The United States (US) presidential Executive Order No. 12898 mandates each Federal agency to make achieving Environmental Justice (EJ) part of its mission by identifying and addressing,...

Healthy People 2010 [US Department of Health and Human Services, 2004. Healthy People 2010. Available: http://www.healthypeople.gov/Publications/ [accessed May 22, 2004]] has established as a top priority the elimination of health disparities. Current research suggests that characteristics of the social, physical and built environment contribute to these disparities. In order to track progress and to assess the potential contributions of the various components of the "environment," tools specific to environmental health disparities are required. In this paper, we discuss one potential tool, a set of candidate measures that may be used to track disparities in outcomes, as well as measures that may be used analytically to assess potential causal pathways. Several other reports on health and environmental measures have been produced, including the Environmental Protection Agency's (EPA) America's Children and the Environment. However, there has not been a comprehensive discussion about environmental measures that focus on racial, ethnic and socioeconomic disparities in health. Therefore, we focus on measures specific to historically disadvantaged populations. Based on a conceptual framework that views health disparities as partially driven by differential access to resources and exposures to hazards, we group the measures into four categories: social processes, environmental contaminants/exposures, bodyburdens of environmental contaminants, and health outcomes. We provide a few examples to illustrate each category, including residential segregation, PM(2.5) exposures, blood mercury concentrations, and asthma morbidity and mortality. These measures and categories are derived from a review of environmental health disparities from several disciplines. As a next step in a long-term effort to better understand the relationship between social disadvantage, environment, and health disparities, we hope that the proposed measures and literature review serve as a foundation for future monitoring of environmental health disparities. These efforts may aid community organizations, local agencies, scientists and policy makers in allocating resources and developing interventions.

Although it is often acknowledged that social and environmental factors interact to produce racial and ethnic environmental health disparities, it is still unclear how this occurs. Despite continued controversy, the environmental justice movement has provided some insight by suggesting that disadvantaged communities face greater likelihood of exposure to ambient hazards. The exposure–disease paradigm has long suggested that differential “vulnerability” may modify the effects of toxicants on biological systems. However, relatively little work has been done to specify whether racial and ethnic minorities may have greater vulnerability than do majority populations and, further, what these vulnerabilities may be. We suggest that psychosocial stress may be the vulnerability factor that links social conditions with environmental hazards. Psychosocial stress can lead to acute and chronic changes in the functioning of body systems (e.g., immune) and also lead directly to illness. In this article we present a multidisciplinary framework integrating these ideas. We also argue that residential segregation leads to differential experiences of community stress, exposure to pollutants, and access to community resources. When not counterbalanced by resources, stressors may lead to heightened vulnerability to environmental hazards.

Human exposure research has consistently shown that, for most volatile organic compounds (VOCs), personal exposures are vastly different from outdoor air concentrations. Therefore, risk estimates based on ambient measurements may over- or underestimate risk, leading to ineffective or inefficient management strategies. In the present study we examine the extent of exposure misclassification and its impact on risk for exposure estimated by the U.S. Environmental Protection Agency (U.S. EPA) Assessment System for Population Exposure Nationwide (ASPEN) model relative to monitoring results from a community-based exposure assessment conducted in Baltimore, Maryland (USA). This study is the first direct comparison of the ASPEN model (as used by the U.S. EPA for the Cumulative Exposure Project and subsequently the National-Scale Air Toxics Assessment) and human exposure data to estimate health risks. A random sampling strategy was used to recruit 33 nonsmoking adult community residents. Passive air sampling badges were used to assess 3-day time-weighted-average personal exposure as well as outdoor and indoor residential concentrations of VOCs for each study participant. In general, personal exposures were greater than indoor VOC concentrations, which were greater than outdoor VOC concentrations. Public health risks due to actual personal exposures were estimated. In comparing measured personal exposures and indoor and outdoor VOC concentrations with ASPEN model estimates for ambient concentrations, our data suggest that ASPEN was reasonably accurate as a surrogate for personal exposures (measured exposures of community residents) for VOCs emitted primarily from mobile sources or VOCs that occur as global "background" source pollutant with no indoor source contributions. Otherwise, the ASPEN model estimates were generally lower than measured personal exposures and the estimated health risks. ASPEN's lower exposures resulted in proportional underestimation of cumulative cancer risk when pollutant exposures were combined to estimate cumulative risk. Median cumulative lifetime cancer risk based on personal exposures was 3-fold greater than estimates based on ASPEN-modeled concentrations. These findings demonstrate the significance of indoor exposure sources and the importance of indoor and/or personal monitoring for accurate assessment of risk. Environmental health policies may not be sufficient in reducing exposures and risks if they are based solely on modeled ambient VOC concentrations. Results from our study underscore the need for a coordinated multimedia approach to exposure assessment for setting public health policy.

a Columbia University, Mailman School of Public Health, 600 West 168th Street, 6th Floor, New York, NY, 10032, USA b United States Environmental Protection Agency, National Center for Environmental Research, Office of Research and Development, Ariel Rios Building MC 8723P, 1200 Pennsylvania Ave. NW, Washington, DC 20460, USA c University of California, Los Angeles, School of Public Health, Department of Community Health Sciences, USA

In late 1998, the Maryland Department of the Environment, the agency responsible for maintaining the statewide childhood blood lead surveillance system, published a report1 indicating that (1) the city of Baltimore had the highest percentage of children with elevated blood lead levels and lead poisoning in Maryland and (2) prevalence rates of elevated blood lead levels and lead poisoning were, respectively, 7 and 16.5 times higher in Baltimore than in the United States as a whole (Table 1 ▶). Given these alarming statistics, the Childhood Lead Poisoning Prevention Program of the Baltimore City Health Department conducted a close examination of the Department of the Environment's data analyses. TABLE 1— Childhood Blood Lead Surveillance in Maryland: Summary Results From the Maryland Department of the Environment 1997 Annual Report During our review, we discovered major shortcomings in the structure and maintenance of the state blood lead database and in the department's data quality and analyses. These problems included lack of unique identifiers and a flawed approach to handling incomplete address information. Therefore, the ability to accurately track and interpret lead poisoning trends and screening rates over time and to relate blood lead surveillance data to the Department of the Environment's other lead poisoning databases was severely limited. We shared our findings regarding Maryland's blood lead surveillance system with other local environmental health directors who had similar concerns. Subsequently, we drafted recommendations for improving the state's childhood blood lead surveillance system and presented them to the Department of the Environment and the Maryland Department of Health and Mental Hygiene. Our recommendations included the following: Development and enforcement of the use of standardized laboratory report forms to be submitted to the Department of the Environment; Implementation of a relational database and improvement of quality control measures at the Department of the Environment; Creation of an electronic link for blood lead data transmission between the Department of the Environment, the Department of Health and Mental Hygiene, and local health departments; Improvement of the Department of the Environment's annual report through inclusion of (1) elevated blood lead level and blood lead poisoning incidence and prevalence rates, (2) demographic data, and (3) state and local blood lead concentration distributions. We learned 2 important lessons from our experience. First, the sharing of concerns about childhood lead poisoning surveillance among local environmental health directors and the joint presentation of recommendations to the state confirmed local public health as a critical link in environmental health. Second, our evaluation of lead surveillance in Maryland signaled a need to examine other lead programs. Lead exposure surveillance is often touted as a success story at the national level and as a model for the development of tracking mechanisms for other environmentally related surveillance efforts. However, current childhood blood lead surveillance practices at the state and local levels may not be as effective in regard to providing accurate, meaningful information to those who need it. Because there are no mandated federal guidelines for state blood lead surveillance systems and data collection methods, and because blood lead reporting levels vary among states, meaningful data analysis is limited. Surveillance is increasingly recognized as a crucial component of successful environmental health practice. As a result, this may be an opportune time not only to consider new areas for environmental health tracking but also to reevaluate and improve existing surveillance programs, including those focusing on blood lead poisoning.