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BACKGROUND: Reduced fetal growth increases the risk for adverse health outcomes. Growing evidence suggests that metal exposures contribute to reduced fetal growth, but little is known about the effects of complex metal mixtures. OBJECTIVES: We investigated the impact of a complex mixture of metals on birth weight for gestational age (BW for GA) in the Maternal and Developmental Risks from Environmental and Social Stressors study, a predominately lower-income Hispanic pregnancy cohort in Los Angeles, California. METHODS: Cadmium (Cd), cobalt (Co), mercury (Hg), nickel (Ni), molybdenum (Mo), lead (Pb), antimony (Sb), tin (Sn), and thallium (Tl) were measured by inductively coupled plasma mass spectrometry (ICP-MS) in maternal urine samples collected in early pregnancy (median GA: 13.1 wk). Speciated urinary arsenic (As) (inorganic+monomethyl+dimethyl As) was measured by high-performance liquid chromatography coupled to ICPMS. Primary analyses focused on a mixture of seven metals that have previously been associated individually with fetal growth (i.e., As, Cd, Co, Hg, Ni, Pb, Tl) (푛 = 262). In exploratory analyses, we additionally examined three metals that have been less studied in relation to fetal growth (i.e., Mo, Sb, Sn). Covariate-adjusted Bayesian kernel machine regression was used to investigate metal mixture associations with BW for GA 푧-scores. RESULTS: In primary analyses, Hg and Ni ranked highest as predictors of BW for GA. An inverse linear association was estimated for Hg, whereas a positive association was estimated for Ni at low-to-moderate concentrations. A potential interaction between Hg and Ni was also identified. In our exploratory analysis, Sb ranked highest as a predictor of BW for GA, followed by Hg and Ni. CONCLUSIONS: Our findings suggest that in this understudied population, Hg may reduce fetal growth, whereas Ni may promote fetal growth. We also identified Sb as a potential metal of concern for this population, which merits additional investigation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Abundant historical evidence demonstrates how environmental changes can affect social stability and, in turn, human health. A rapidly growing body of literature, largely from political science and economics, is examining the potential for and consequences associated with social instability related to current climate change. However, comparatively little of this research incorporates the effects on human health or the role of health systems in influencing the magnitude and types of instability that could occur. OBJECTIVE: The objective of this commentary is to articulate a conceptual framework incorporating health outcomes and health systems into theorized and observed linkages between climate change and social instability, illustrating in particular the health effects of natural resource shortages, infectious disease outbreaks, and migration. DISCUSSION: Although increasing evidence exists that climate change, health, and social instability are related, key questions remain about the pathways linking these factors, as well as the magnitude, causality, and directionality of relationships across spatial and temporal scales. Models seeking to explain and predict climate-related social unrest should incorporate the many linkages between climate change, human health, and social instability. Members of the environmental health research community should work closely with those in the political science and economics communities to help deepen understandings of climate-related stressors and shocks that affect instability and worsen health outcomes. [ABSTRACT FROM AUTHOR]

Background: Prior calculations of the burden of disease from toxic exposures have not included estimates of the burden from toxic waste sites due to the absence of exposure data. Objective: We developed a disability-adjusted life year (DALY)-based estimate of the disease burden attributable to toxic waste sites. We focused on three low- and middle-income countries (LMICs): India, Indonesia, and the Philippines. Methods: Sites were identified through the Blacksmith Institute's Toxic Sites Identification Program, a global effort to identify waste sites in LMICs. At least one of eight toxic chemicals was sampled in environmental media at each site, and the population at risk estimated. By combining estimates of disease incidence from these exposures with population data, we calculated the DALYs attributable to exposures at each site. Results: We estimated that in 2010, 8,629,750 persons were at risk of exposure to industrial pollutants at 373 toxic waste sites in the three countries, and that these exposures resulted in 828,722 DALYs, with a range of 814,934-1,557,121 DALYs, depending on the weighting factor used. This disease burden is comparable to estimated burdens for outdoor air pollution (1,448,612 DALYs) and malaria (725,000 DALYs) in these countries. Lead and hexavalent chromium collectively accounted for 99.2% of the total DALYs for the chemicals evaluated. Conclusions: Toxic waste sites are responsible for a significant burden of disease in LMICs. Although some factors, such as unidentified and unscreened sites, may cause our estimate to be an underestimate of the actual burden of disease, other factors, such as extrapolation of environmental sampling to the entire exposed population, may result in an overestimate of the burden of disease attributable to these sites. Toxic waste sites are a major, and heretofore underrecognized, global health problem. [ABSTRACT FROM AUTHOR]

Background: Air pollution exposure increases cardiovascular morbidity and mortality and is a major global public health concern. Objectives: We investigated the benefits of reducing personal exposure to urban air pollution in patients with coronary heart disease. Methods: In an open randomized crossover trial, 98 patients with coronary heart disease walked on a predefined route in central Beijing, China, under different conditions: once while using a highly efficient face mask, and once while not using the mask. Symptoms, exercise, personal air pollution exposure, blood pressure, heart rate, and 12-lead electrocardiography were monitored throughout the 24-hr study period. Results: Ambient air pollutants were dominated by fine and ultrafine particulate matter (PM) that was present at high levels [74 µg/m³ for PM2.5 (PM with aerodynamic diameter <2.5 µm)]. Consistent with traffic-derived sources, this PM contained organic carbon and polycyclic aromatic hydrocarbons and was highly oxidizing, generating large amounts of free radicals. The face mask was well tolerated, and its use was associated with decreased self-reported symptoms and reduced maximal ST segment depression (-142 vs. -156 µV, p = 0.046) over the 24-hr period. When the face mask was used during the prescribed walk, mean arterial pressure was lower (93 ± 10 vs. 96 ± 10 mmHg, p = 0.025) and heart rate variability increased (high-frequency power: 54 vs. 40 msec², p = 0.005; high-frequency normalized power: 23.5 vs. 20.5 msec, p = 0.001; root mean square successive differences: 16.7 vs. 14.8 msec, p = 0.007). However, mask use did not appear to influence heart rate or energy expenditure. Conclusions: Reducing personal exposure to air pollution using a highly efficient face mask appeared to reduce symptoms and improve a range of cardiovascular health measures in patients with coronary heart disease. Such interventions to reduce personal exposure to PM air pollution have the potential to reduce the incidence of cardiovascular events in this highly susceptible population. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent research highlights the promise of remotely sensed aerosol optical depth (AOD) as a proxy for ground-level particulate matter with aerodynamic diameter ≤ 2.5 μm (PM2.5.). Particular interest lies in estimating spatial heterogeneity using AOD, with important application to estimating pollution exposure for public health purposes. Given the correlations reported between AOD and PM2.5., it is tempting to interpret the spatial patterns in AOD as reflecting patterns in PM2.5.. OBJECTIVES: We evaluated the degree to which AOD can help predict long-term average PM2.5. concentrations for use in chronic health studies. METHODS: We calculated correlations of AOD and PM2.5. at various temporal aggregations in the eastern United States in 2004 and used statistical models to assess the relationship between AOD and PM2.5 and the potential for improving predictions of PM2.5. in a subregion, the mid-Atlantic. RESULTS: We found only limited spatial associations of AOD from three satellite retrievals with daily and yearly PM2.5.. The statistical modeling shows that monthly average AOD poorly reflects spatial patterns in PM2.5. because of systematic, spatially correlated discrepancies between AOD and PM2.5. Furthermore, when we included AOD as a predictor of monthly PM2.5. in a statistical prediction model, AOD provided little additional information in a model that already accounts for land use, emission sources, meteorology, and regional variability. CONCLUSIONS: These results suggest caution in using spatial variation in currently available AOD to stand in for spatial variation in ground-level PM2.5. in epidemiologic analyses and indicate that when PM2.5. monitoring is available, careful statistical modeling outperforms the use of AOD. [ABSTRACT FROM AUTHOR]

BACKGROUND: Chronic epidemiologic studies of particulate matter (PM) are limited by the lack of monitoring data, relying instead on citywide ambient concentrations to estimate exposures. This method ignores within-city spatial gradients and restricts studies to areas with nearby monitoring data. This lack of data is particularly restrictive for fine particles (PM with aerodynamic diameter < 2.5 µm; PM2.5) and coarse particles (PM with aerodynamic diameter 2.5--10 µm; PM10--2.5), for which monitoring is limited before 1999. To address these limitations, we developed spatiotemporal models to predict monthly outdoor PM2.5 and PM10--2.5 concentrations for the northeastern and midwestern United States. METHODS: For PM2.5, we developed models for two periods: 1988--1998 and 1999--2002. Both models included smooth spatial and regression terms of geographic information system--based and meteorologic predictors. To compensate for sparse monitoring data, the pre-1999 model also included predicted PM10 (PM with aerodynamic diameter < 10 µm) and extinction coefficients (km--1). PM10--2.5 levels were estimated as the difference in monthly predicted PM10 and PM2.5, with predicted PM10 from our previously developed PM10 model. RESULTS: Predictive performance for PM2.5 was strong (cross-validation R2 = 0.77 and 0.69 for post-1999 and pre-1999 PM2.5 models, respectively) with high precision (2.2 and 2.7 µg/m3, respectively). Models performed well irrespective of population density and season. Predictive performance for PM10--2.5 was weaker (cross-validation R2 = 0.39) with lower precision (5.5 µg/m3). PM10--2.5 levels exhibited greater local spatial variability than PM10 or PM2.5, suggesting that PM2.5 measurements at ambient monitoring sites are more representative for surrounding populations than for PM10 and especially PM10--2.5. CONCLUSIONS: We provide semiempirical models to predict spatially and temporally resolved long-term average outdoor concentrations of PM2.5 and PM10--2.5 for estimating exposures of populations living in the northeastern and midwestern United States. [ABSTRACT FROM AUTHOR]

Organotins, important environmental pollutants widely used in agricultural and industrial applications, accumulate in the food chain and induce imposex in several marine species as well as neurotoxic and immunotoxic effects in higher animals. Reduced birth weight and thymus involution, observed upon exposure to organotins, can also be caused by excessive glucocorticoid levels. We now demonstrate that organotins efficiently inhibit 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), converting active 11beta-hydroxyglucocorticoids into inactive 11-ketoglucocorticoids, but not 11beta-HSD1, which catalyzes the reverse reaction. Di- and tributyltin as well as di- and triphenyltin inhibited recombinant and endogenous 11beta-HSD2 in lysates and intact cells with IC50 values between 500 nM and 3 microM. Dithiothreitol protected 11beta-HSD2 from organotin-dependent inhibition, indicating that organotins act by binding to one or more cysteines. Mutational analysis and 3-D structural modeling revealed several important interactions of cysteines in 11beta-HSD2. Cys90, Cys228, and Cys264 were essential for enzymatic stability and catalytic activity, suggesting that disruption of such interactions by organotins leads to inhibition of 11beta-HSD2. Enhanced glucocorticoid concentrations due to disruption of 11beta-HSD2 function may contribute to the observed organotin-dependent toxicity in some glucocorticoid-sensitive tissues such as thymus and placenta. [ABSTRACT FROM AUTHOR]

The National Children's Study is considering a wide spectrum of airborne pollutants that are hypothesized to potentially influence pregnancy outcomes, neurodevelopment, asthma, atopy, immune development, obesity, and pubertal development. In this article we summarize six applicable exposure assessment lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research that may enhance the National Children's Study: a) Selecting individual study subjects with a wide range of pollution exposure profiles maximizes spatial-scale exposure contrasts for key pollutants of study interest. b) In studies with large sample sizes, long duration, and diverse outcomes and exposures, exposure assessment efforts should rely on modeling to provide estimates for the entire cohort, supported by subject-derived questionnaire data. c) Assessment of some exposures of interest requires individual measurements of exposures using snapshots of personal and microenvironmental exposures over short periods and/or in selected microenvironments. d) Understanding issues of spatial-temporal correlations of air pollutants, the surrogacy of specific pollutants for components of the complex mixture, and the exposure misclassification inherent in exposure estimates is critical in analysis and interpretation. e) 'Usual' temporal, spatial, and physical patterns of activity can be used as modifiers of the exposure/outcome relationships. f) Biomarkers of exposure are useful for evaluation of specific exposures that have multiple routes of exposure. If these lessons are applied, the National Children's Study offers a unique opportunity to assess the adverse effects of air pollution on interrelated health outcomes during the critical early life period. [ABSTRACT FROM AUTHOR]

As part of a multiyear birth-cohort study examining the roles of pre- and postnatal environmental exposures on developmental deficits and asthma among children, we measured personal exposures to polycyclic aromatic hydrocarbons (PAHs) among 348 pregnant women in northern Manhattan and the South Bronx, New York. Nonsmoking African-American or Dominican women were identified and recruited into the study. During the third trimester of pregnancy, each subject wore a personal air monitor for 48 hr to determine exposure levels to nine PAH compounds. In this study, we examined levels of exposures to PAHs and tested for associations with potential predictor variables collected from questionnaires addressing socioeconomic factors and day-to-day activities during pregnancy as well as activities and environmental exposures during the 48-hr monitoring period. Reliable personal monitoring data for women who did not smoke during the monitoring period were available for 344 of 348 subjects. Mean PAH concentrations ranged from 0.06 ng/m³ for dibenz[a,h]anthracene to 4.1 ng/m³ for pyrene; mean benzo[a]pyrene concentration was 0.50 ng/m³. As found in previous studies, concentrations of most PAHs were higher in winter than in summer. Multiple linear regression analysis revealed associations between personal PAH exposures and several questionnaire variables, including time spent outdoors, residential heating, and indoor burning of incense. This is the largest study to date characterizing personal exposures to PAHs, a ubiquitous class of carcinogenic air contaminants in urban environments, and is unique in its focus on pregnant minority women. [ABSTRACT FROM AUTHOR]

Summarizes experimental and carcinogenesis results that provide insights on the health consequences of worker exposure to natural and synthetic chemicals used in wood industries. Wood dust; Arsenic; Creosotes; Chromated-copper-arsenate; Pentachlorophenol; Formaldehyde.

Comments on the need for assessment of long-term effects of outdoor air pollution in the United States. Dependence of epidemiologic assessment on distribution exposure among participants; Use of geographic information system exposure data to coordinate geocodes of residential location; Advantages of aging cohorts for the study of respiratory and cardiovascular diseases.

Discusses health issues related to the use of iodine for water disinfection. Controversy about the maximum safe iodine dose and duration of use when iodine is ingested in excess of the recommended daily dietary amount; Danger of thyroid disorders, primarily hypothyroidism; Indication of a temporal dose-response relationship between iodine intake and thyroid function; Suggestion that iodine can be used safely for water disinfection if thyroid function is monitored.

A letter to the editor is presented in response to the article “Arsenic cancer risk confounder in southwest Taiwan data set,” Lamm et al. in the vol. 114, 2006 issue.

A response by Lao et al. to a letter to the editor about their article “GIS approaches for the estimation of residential-level ambient PM concentrations,” which appeared in the vol. 114, 2006 issue is presented.

Comments on the study conducted by John Gamble regarding the cause-effect and statistical association of cohort studies. Inconsistencies of the research; Reliance of the study on aggregate-level incidence; Inability of the study to address substantial ecological issues.

Background: Traffic-related air pollution (TRAP) is made up of complex mixtures of particulate matter, gases and volatile compounds. However, the effects of TRAP on the cardiopulmonary system in most animal studies have been tested using acute exposure to singular pollutants. The cardiopulmonary effects and molecular mechanisms in animals that are chronically exposed to unmodified air pollution as a whole have yet to be studied. Additionally, sex-dependent toxicity of TRAP exposure has rarely been evaluated. OBJECTIVES: This study sought to assess the cardiopulmonary effect of chronic exposure to unmodified, real-world TRAP in both female and male rats. Methods: Four-week-old male and female rats were exposed to TRAP or filtered air for 14 months in a novel facility drawing air from a major freeway tunnel system in Northern California. Inflammation and oxidative stress markers were examined in the lung, heart, spleen, and plasma, and TRAP deposits were quantified in the lungs of both male and female rats. RESULTS: Elemental analysis showed higher levels of eight elements in the female lungs and one element in the male lungs. Expression of genes related to fibrosis, aging, oxidative stress, and inflammation were higher in the rat hearts exposed to TRAP, with female rats being more susceptible than males. Enhanced collagen accumulation was found only in the TRAP-exposed female hearts. Plasma cytokine secretion was higher in both female and male rats, but inflammatory macrophages were higher only in TRAP-exposed male spleens. Discussion: Our results in rats suggest pathological consequences from chronic TRAP exposure, including sex differences indicating females may be more susceptible to TRAP-induced cardiac fibrosis. https://doi.org/10.1289/EHP7045, Introduction Epidemiological studies worldwide have shown that exposure to ambient air pollution is associated with significantly higher incidence of cardiovascular and respiratory diseases contributing to overall global mortality (Brook et [...]

The assessment of chemical mixtures is a complex topic for toxicologists, regulators, and the public. In this article the linkage between the science of toxicology and the needs of governmental [...]

Breast cancer is the most common cancer in women and the leading cause of cancer death among women 35-54 years of age. Rising incidence, increased risk among migrants to higher [...]

In this paper, we present national maps of relative rates of mortality associated with short-term exposure to particulate matter < 10 [micro]m in aerodynamic diameter (P[M.sub.10]). We report results for [...]

Background: In 2016, 23% of children (155 million) aged Objectives: We adopt a new perspective, assessing how climate change may affect child stunting via its impacts on two interacting socioeconomic drivers: incomes of the poorest 20% of populations (due to climate impacts on crop production, health, labor productivity, and disasters) and food prices. Methods: We developed a statistical model to project moderate and severe stunting in children aged Results: We estimated that in the absence of climate change, 110 million children aged 1 million under the poverty/high climate change scenario. The projected impact of climate change on stunting was greater in rural vs. urban areas under both socioeconomic scenarios. In countries with lower incomes and relatively high food prices, we projected that rising prices would tend to increase stunting, whereas in countries with higher incomes and relatively low food prices, rising prices would tend to decrease stunting. These findings suggest that food prices that provide decent incomes to farmers alongside high employment with living wages will reduce undernutrition and vulnerability to climate change. Conclusions: Shifting the focus from food production to interactions between incomes and food price provides new insights. Futures that protect health should consider not just availability, accessibility, and quality of food, but also the incomes generated by those producing the food., Introduction Despite being a focus of health and global development policy for decades, and notwithstanding significant progress in many countries, child undernutrition remains a major contributor to the global burden [...]

doi: 10.1289/ehp.10205R Szpiro et al. suggest that our findings Liao et al. (2006) do not adequately support using national-scale, log-normal ordinary kriging to estimate daily mean concentrations of PM10 (particulate [...]