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Across the United States, thousands of people, most of them in low-income or minority communities, live next to heavily polluting industrial sites. Many of them reach a point at which they say \"Enough is enough.\" After living for years with poisoned air and water, contaminated soil, and pollution-related health problems, they start to take action--organizing, speaking up, documenting the effects of pollution on their neighborhoods. In Sacrifice Zones, Steve Lerner tells the stories of twelve communities, from Brooklyn to Pensacola, that rose up to fight the industries and military bases causing disproportionately high levels of chemical pollution. He calls these low-income neighborhoods \"sacrifice zones.\" And he argues that residents of these sacrifice zones, tainted with chemical pollutants, need additional regulatory protections. Sacrifice Zones goes beyond the disheartening statistics and gives us the voices of the residents themselves, offering compelling portraits of accidental activists who have become grassroots leaders in the struggle for environmental justice and details the successful tactics they have used on the fenceline with heavy industry.

Systematic-review methodologies provide objectivity and transparency to the process of collecting and synthesizing scientific evidence in reaching conclusions on specific research questions. There is increasing interest in applying these procedures to address environmental health questions. The goal was to develop a systematic-review framework to address environmental health questions by extending approaches developed for clinical medicine to handle the breadth of data relevant to environmental health sciences (e.g., human, animal, and mechanistic studies). The Office of Health Assessment and Translation (OHAT) adapted guidance from authorities on systematic-review and sought advice during development of the OHAT Approach through consultation with technical experts in systematic review and human health assessments, as well as scientific advisory groups and the public. The method was refined by considering expert and public comments and through application to case studies. Here we present a seven-step framework for systematic review and evidence integration for reaching hazard identification conclusions: 1) problem formulation and protocol development, 2) search for and select studies for inclusion, 3) extract data from studies, 4) assess the quality or risk of bias of individual studies, 5) rate the confidence in the body of evidence, 6) translate the confidence ratings into levels of evidence, and 7) integrate the information from different evidence streams (human, animal, and \"other relevant data\" including mechanistic or in vitro studies) to develop hazard identification conclusions. The principles of systematic review can be successfully applied to environmental health questions to provide greater objectivity and transparency to the process of developing conclusions.

Autism spectrum disorder (ASD) is a developmental disorder with increasing prevalence worldwide, yet has unclear etiology. We explored the association between maternal exposure to particulate matter (PM) air pollution and odds of ASD in her child. We conducted a nested case-control study of participants in the Nurses' Health Study II (NHS II), a prospective cohort of 116,430 U.S. female nurses recruited in 1989, followed by biennial mailed questionnaires. Subjects were NHS II participants' children born 1990-2002 with ASD (n = 245), and children without ASD (n = 1,522) randomly selected using frequency matching for birth years. Diagnosis of ASD was based on maternal report, which was validated against the Autism Diagnostic Interview-Revised in a subset. Monthly averages of PM with diameters ≤ 2.5 μm (PM2.5) and 2.5-10 μm (PM10-2.5) were predicted from a spatiotemporal model for the continental United States and linked to residential addresses. PM2.5 exposure during pregnancy was associated with increased odds of ASD, with an adjusted odds ratio (OR) for ASD per interquartile range (IQR) higher PM2.5 (4.42 μg/m3) of 1.57 (95% CI: 1.22, 2.03) among women with the same address before and after pregnancy (160 cases, 986 controls). Associations with PM2.5 exposure 9 months before or after the pregnancy were weaker in independent models and null when all three time periods were included, whereas the association with the 9 months of pregnancy remained (OR = 1.63; 95% CI: 1.08, 2.47). The association between ASD and PM2.5 was stronger for exposure during the third trimester (OR = 1.42 per IQR increase in PM2.5; 95% CI: 1.09, 1.86) than during the first two trimesters (ORs = 1.06 and 1.00) when mutually adjusted. There was little association between PM10-2.5 and ASD. Higher maternal exposure to PM2.5 during pregnancy, particularly the third trimester, was associated with greater odds of a child having ASD.

There are several suspected environmental risk factors for non-Hodgkin lymphoma (NHL). The associations between NHL and environmental chemical exposures have typically been evaluated for individual chemicals (i.e., one-by-one). We determined the association between a mixture of 27 correlated chemicals measured in house dust and NHL risk. We conducted a population-based case-control study of NHL in four National Cancer Institute-Surveillance, Epidemiology, and End Results centers--Detroit, Michigan; Iowa; Los Angeles County, California; and Seattle, Washington--from 1998 to 2000. We used weighted quantile sum (WQS) regression to model the association of a mixture of chemicals and risk of NHL. The WQS index was a sum of weighted quartiles for 5 polychlorinated biphenyls (PCBs), 7 polycyclic aromatic hydrocarbons (PAHs), and 15 pesticides. We estimated chemical mixture weights and effects for study sites combined and for each site individually, and also for histologic subtypes of NHL. The WQS index was statistically significantly associated with NHL overall [odds ratio (OR) = 1.30; 95% CI: 1.08, 1.56; p = 0.006; for one quartile increase] and in the study sites of Detroit (OR = 1.71; 95% CI: 1.02, 2.92; p = 0.045), Los Angeles (OR = 1.44; 95% CI: 1.00, 2.08; p = 0.049), and Iowa (OR = 1.76; 95% CI: 1.23, 2.53; p = 0.002). The index was marginally statistically significant in Seattle (OR = 1.39; 95% CI: 0.97, 1.99; p = 0.071). The most highly weighted chemicals for predicting risk overall were PCB congener 180 and propoxur. Highly weighted chemicals varied by study site; PCBs were more highly weighted in Detroit, and pesticides were more highly weighted in Iowa. An index of chemical mixtures was significantly associated with NHL. Our results show the importance of evaluating chemical mixtures when studying cancer risk.

Background: There is increasing recognition of the importance of early environmental exposures in the development of childhood asthma. Outdoor air pollution is a recognized asthma trigger, but it is unclear whether exposure influences incident disease. We investigated the effect of exposure to ambient air pollution in utero and during the first year of life on risk of subsequent asthma diagnosis in a population-based nested case—control study. Methods: We assessed all children born in southwestern British Columbia in 1999 and 2000 (n = 37,401) for incidence of asthma diagnosis up to 3-4 years of age using outpatient and hospitalization records. Asthma cases were age- and sex-matched to five randomly chosen controls from the eligible cohort. We estimated each individual's exposure to ambient air pollution for the gestational period and first year of life using high-resolution pollution surfaces derived from regulatory monitoring data as well as land use regression models adjusted for temporal variation. We used logistic regression analyses to estimate effects of carbon monoxide, nitric oxide, nitrogen dioxide, particulate matter ≤ 10 μm and ≤ 2.5 μm in aerodynamic diameter (PM₁₀ and ${\\rm PM}_{2.5}$), ozone, sulfur dioxide, black carbon, woodsmoke, and proximity to roads and point sources on asthma diagnosis. Results: A total of 3,482 children (9%) were classified as asthma cases. We observed a statistically significantly increased risk of asthma diagnosis with increased early life exposure to CO, NO, NO₂, PM₁₀, SO₂, and black carbon and proximity to point sources. Traffic-related pollutants were associated with the highest risks: adjusted odds ratio = 1.08 (95% confidence interval, 1.04-1.12) for a 10-μg/m³ increase of NO, 1.12 (1.07-1.17) for a 10-μg/m³ increase in NO₂, and 1.10 (1.06-1.13) for a 100-μg/m³ increase in CO. These data support the hypothesis that early childhood exposure to air pollutants plays a role in development of asthma.

Groundwater nitrate pollution is a serious threat to human health in many regions of the world. The present study was performed to assess the nitrate contamination in groundwater in the region of Nirmal province, South India, where people purely depend on groundwater for drinking purposes. The associated human health risks for different age groups (male, female, and children) also were evaluated based on the United States Environmental Protection Agency model. Results indicate that nitrate concentration in groundwater is in the range of 0.8–130 mg/L with a mean of 36.51 mg/L. Furthermore, 26.47% of groundwater samples exceeded the WHO drinking water guidelines for NO3− in the study region. The contribution of oral ingestion is very higher than the dermal contact in the total hazard quotient or noncarcinogenic health risk. The total hazard quotient values ranged from 0.02 to 3.13 for adult males, 0.02 to 3.70 for adult females, and 0.03 to 4.32 for children. The health risk assessment highlights that children are more exposed to the noncarcinogenic health risks of nitrate than adult females and males in the study region. Therefore, specific groundwater quality measures should be formulated to address the health risk problems for children in the study region.

Chronic obstructive pulmonary disease (COPD) is a heterogeneous pulmonary disease affecting 16 million Americans. Individuals with COPD are susceptible to environmental disturbances including heat and cold waves that can exacerbate disease symptoms. Our objective was to estimate heat and cold wave-associated mortality risks within a population diagnosed with a chronic respiratory disease. We collected individual level data with geocoded residential addresses from the Veterans Health Administration on 377,545 deceased patients with COPD (2016 to 2021). A time stratified case-crossover study was designed to estimate the incidence rate ratios (IRR) of heat and cold wave mortality risks using conditional logistic regression models examining lagged effects up to 7 d. Attributable risks (AR) were calculated for the lag day with the strongest association for heat and cold waves, respectively. Effect modification by age, gender, race, and ethnicity was also explored. Heat waves had the strongest effect on all-cause mortality at lag day 0 [IRR: 1.04; 95% confidence interval (CI): 1.02, 1.06] with attenuated effects by lag day 1. The AR at lag day 0 was 651 (95% CI: 326, 975) per 100,000 veterans. The effect of cold waves steadily increased from lag day 2 and plateaued at lag day 4 (IRR: 1.04; 95% CI: 1.02, 1.07) with declining but still elevated effects over the remaining 7-d lag period. The AR at lag day 4 was 687 (95% CI: 344, 1,200) per 100,000 veterans. Differences in risk were also detected upon stratification by gender and race. Our study demonstrated harmful associations between heat and cold waves among a high-risk population of veterans with COPD using individual level health data. Future research should emphasize using individual level data to better estimate the associations between extreme weather events and health outcomes for high-risk populations with chronic medical conditions. https://doi.org/10.1289/EHP13176.

The frequency and destructiveness of hurricanes and related extreme weather events (e.g., cyclones, severe storms) have been increasing due to climate change. A growing body of evidence suggests that victims of hurricanes have increased incidence of cardiovascular disease (CVD), likely due to increased stressors around time of the hurricane and in their aftermath. The objective was to systematically examine the evidence of the association between hurricanes (and related extreme weather events) and adverse CVD outcomes with the goal of understanding the gaps in the literature. A comprehensive literature search of population-level and cohort studies focused on CVD outcomes (i.e., myocardial infarction, stroke, and heart failure) related to hurricanes, cyclones, and severe storms was performed in the following databases from inception to December 2021: Ovid MEDLINE, Ovid EMBASE, Web of Science, and The Cochrane Library. Studies retrieved were then screened for eligibility against predefined inclusion/exclusion criteria. Studies were then qualitatively synthesized based on the time frame of the CVD outcomes studied and special populations that were studied. Gaps in the literature were identified based on this synthesis. Of the 1,103 citations identified, 48 met our overall inclusion criteria. We identified articles describing the relationship between CVD and extreme weather, primarily hurricanes, based on data from the United States (42), Taiwan (3), Japan (2), and France (1). Outcomes included CVD and myocardial infarction-related hospitalizations (30 studies) and CVVD-related mortality (7 studies). Most studies used a retrospective study design, including one case-control study, 39 cohort studies, and 4 time-series studies. Although we identified a number of papers that reported evaluations of extreme weather events and short-term adverse CVD outcomes, there were important gaps in the literature. These gaps included ) a lack of rigorous long-term evaluation of hurricane exposure, ) lack of investigation of hurricane exposure on vulnerable populations regarding issues related to environmental justice, ) absence of research on the exposure of multiple hurricanes on populations, and ) absence of an exploration of mechanisms leading to worsened CVD outcomes. Future research should attempt to fill these gaps, thus providing an important evidence base for future disaster-related policy. https://doi.org/10.1289/EHP11252.

Background: Previous studies of DDT and breast cancer assessed exposure later in life when the breast may not have been vulnerable, after most DDT had been eliminated, and after DDT had been banned. Objectives: We investigated whether DDT exposure in young women during the period of peak DDT use predicts breast cancer. Methods: We conducted a prospective, nested case-control study with a median time to diagnosis of 17 years using blood samples obtained from young women during 1959-1967. Subjects were members of the Child Health and Development Studies, Oakland, California, who provided blood samples 1-3 days after giving birth (mean age, 26 years). Cases (n = 129) developed breast cancer before the age of 50 years. Controls (n = 129) were matched to cases on birth year. Serum was assayed for p,p'-DDT, the active ingredient of DDT; o,p'-DDT, a low concentration contaminant; and p,p'-DDE, the most abundant p,p'-DDT metabolite. Results: High levels of serum p,p'-DDT predicted a statistically significant 5-fold increased risk of breast cancer among women who were born after 1931. These women were under 14 years of age in 1945, when DDT came into widespread use, and mostly under 20 years as DDT use peaked. Women who were not exposed to p,p'-DDT before 14 years of age showed no association between p,p'-DDT and breast cancer (p = 0.02 for difference by age). Conclusions: Exposure to p,p'-DDT early in life may increase breast cancer risk. Many U.S. women heavily exposed to DDT in childhood have not yet reached 50 years of age. The public health significance of DDT exposure in early life may be large.

Objectives: The National Environmental Policy Act and related state laws require many public agencies to analyze and disclose potentially significant environmental effects of agency actions, including effects on human health. In this paper we review the purpose and procedures of environmental impact assessment (EIA), existing regulatory requirements for health effects analysis, and potential barriers to and opportunities for improving integration of human health concerns within the EIA process. Data sources: We use statutes, regulations, guidelines, court opinions, and empirical research on EIA along with recent case examples of integrated health impact assessment (HIA)/EIA at both the state and federal level. Data synthesis: We extract lessons and recommendations for integrated HIA/EIA practice from both existing practices as well as case studies. Conclusions: The case studies demonstrate the adequacy, scope, and power of existing statutory requirements for health analysis within EIA. The following support the success of integrated HIA/EIA: a proponent recognizing EIA as an available regulatory strategy for public health; the openness of the agency conducting the EIA; involvement of public health institutions; and complementary objectives among community stakeholders and health practitioners. We recommend greater collaboration among institutions responsible for EIA, public health institutions, and affected stakeholders along with guidance, resources, and training for integrated HIA/EIA practice.