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Prenatal exposures to endocrine-disrupting chemicals (EDCs) during critical developmental windows have been implicated in the etiologies of a wide array of adverse perinatal and pediatric outcomes. Epidemiological studies have concentrated on the health effects of individual chemicals, despite the understanding that EDCs act together via common mechanisms, that pregnant women are exposed to multiple EDCs simultaneously, and that substantial toxicological evidence of adverse developmental effects has been documented. There is a move toward multipollutant models in environmental epidemiology; however, there is no current consensus on appropriate statistical methods. We aimed to review the statistical methods used in these studies, to identify additional applicable methods, and to determine the strengths and weaknesses of each method for addressing the salient statistical and epidemiological challenges. We searched Embase, MEDLINE, and Web of Science for epidemiological studies of endocrine-sensitive outcomes in the children of mothers exposed to EDC mixtures during pregnancy and identified alternative statistical methods from the wider literature. We identified 74 studies and analyzed the methods used to estimate mixture health effects, identify important mixture components, account for nonmonotonicity in exposure–response relationships, assess interactions, and identify windows of exposure susceptibility. We identified both frequentist and Bayesian methods that are robust to multicollinearity, performing shrinkage, variable selection, dimension reduction, statistical learning, or smoothing, including methods that were not used by the studies included in our review. Compelling motivation exists for analyzing EDCs as mixtures, yet many studies make simplifying assumptions about EDC additivity, relative potency, and linearity, or overlook the potential for bias due to asymmetries in chemical persistence. We discuss the potential impacts of these choices and suggest alternative methods to improve analyses of prenatal exposure to EDC mixtures. https://doi.org/10.1289/EHP2207.

Stunting, a form of malnutrition characterized by impaired linear growth in the first two years of life, affects one quarter of children globally. While nutritional status remains the key cause of stunting, there is evidence that environmental risk factors are associated with stunting. The objective of this review is to explore the current literature and compile the environmental risk factors that have been associated with stunting. Further, we seek to discover which risk factors act independently of nutritional intake. A systematic search of the literature was performed using PubMed, EMBASE, Scopus, TOXNET, and CINAHL. A search of the grey literature was conducted. Papers were included in this review if they examined an association between childhood stunting and exposure to environmental risk factors. We included 71 reports in the final analysis. The included studies showed that foodborne mycotoxins, a lack of adequate sanitation, dirt floors in the home, poor quality cooking fuels, and inadequate local waste disposal are associated with an increased risk of childhood stunting. Access to safe water sources was studied in a large number of studies, but the results remain inconclusive due to inconsistent study findings. Limited studies were available for arsenic, mercury, and environmental tobacco, and thus their role in stunting remains inconclusive. The identified research did not control for nutritional intake. A causal model identified solid fuel use and foodborne mycotoxins as being environmental risk factors with the potential to have direct effects on childhood growth. A diverse range of environmental risk factors are, to varying degrees, associated with stunting, demonstrating the importance of considering how the environment interacts with nutrition. Health promotion activities may be more effective if they consider environmental factors alongside nutritional interventions.

[...]ambient air pollution, chemical pollution, and soil pollution—the forms of pollution produced by industry, mining, electricity generation, mechanised agriculture, and petroleum-powered vehicles—are all on the rise, with the most marked increases in rapidly developing and industrialising low-income and middle-income countries. Pollution mitigation and prevention can yield large net gains both for human health and the economy. [...]air quality improvements in the high-income countries have not only reduced deaths from cardiovascular and respiratory disease but have also yielded substantial economic gains. In addition to improving health in countries around the world (SDG 3), pollution control will help to alleviate poverty (SDG 1), improve access to clean water and improve sanitation (SDG 6), promote social justice (SDG 10), build sustainable cities and communities (SDG 11), and protect land and water (SDGs 14 and 15). Pollution control, in turn, will benefit from efforts to slow the pace of climate change (SDG 13) by transitioning to a sustainable, circular economy that relies on non-polluting renewable energy, on efficient industrial processes that produce little waste, and on transport systems that restrict use of private vehicles in cities, enhance public transport, and promote active travel.

Viral infections can worsen episodes of allergic sensitization to allergens, putting the affected individuals, often children, at risk for developing persistent asthma during adult life. Understanding how the mechanisms mediating the antiviral response and driving allergic inflammation caused by allergens interact is crucial. This will provide insights into when and what player or molecule to target for treatment and prevention of asthma in children at the early stages of the disease. Prospective birth cohort studies tracking asthma initiation and consolidation in community cohorts have identified viral infections occurring against a background of allergic sensitization to aeroallergens as a uniquely potent risk factor for the expression of acute severe asthma-like symptoms and for the ensuing development of asthma that can persist through childhood and into adulthood. A combination of recent experimental and human studies have suggested that underlying this bipartite process are a series of interactions between antiviral and atopic inflammatory pathways that are mediated by local activation of myeloid cell populations in the airway mucosa and the parallel programming and recruitment of their replacements from bone marrow. Targeting key components of these pathways at the appropriate stages of asthma provides new opportunities for the treatment of established asthma but, more crucially, for primary and secondary prevention of asthma during childhood.

Abstract Macrophages are dynamic cells that mature under the influence of signals from the local microenvironment into either classically (M1) or alternatively (M2) activated macrophages with specific functional and phenotypic properties. Although the phenotypic identification of M1 and M2 macrophages is well established in mice, this is less clear for human macrophages. In addition, the persistence and reversibility of polarized human phenotypes is not well established. Human peripheral blood monocytes were differentiated into uncommitted macrophages (M0) and then polarized to M1 and M2 phenotypes using LPS/IFN-γ and IL-4/IL-13, respectively. M1 and M2 were identified as CD64+CD80+ and CD11b+CD209+, respectively, by flow cytometry. Polarized M1 cells secreted IP-10, IFN-γ, IL-8, TNF-α, IL-1β, and RANTES, whereas M2 cells secreted IL-13, CCL17, and CCL18. Functionally, M2 cells were highly endocytic. In cytokine-deficient medium, the polarized macrophages reverted back to the M0 state within 12 days. If previously polarized macrophages were given the alternative polarizing stimulus after 6 days of resting in cytokine-deficient medium, a switch in polarization was seen (i.e., M1 macrophages switched to M2 and expressed CD11b+CD209+ and vice versa). In summary, we report phenotypic identification of human M1 and M2 macrophages, their functional characteristics, and their ability to be reprogrammed given the appropriate stimuli.

Electronic waste (e-waste) is produced in staggering quantities, estimated globally to be 41.8 million tonnes in 2014. Informal e-waste recycling is a source of much-needed income in many low- to middle-income countries. However, its handling and disposal in underdeveloped countries is often unsafe and leads to contaminated environments. Rudimentary and uncontrolled processing methods often result in substantial harmful chemical exposures among vulnerable populations, including women and children. E-waste hazards have not yet received the attention they deserve in research and public health agendas. We provide an overview of the scale and health risks. We review international efforts concerned with environmental hazards, especially affecting children, as a preface to presenting next steps in addressing health issues stemming from the global e-waste problem. The e-waste problem has been building for decades. Increased observation of adverse health effects from e-waste sites calls for protecting human health and the environment from e-waste contamination. Even if e-waste exposure intervention and prevention efforts are implemented, legacy contamination will remain, necessitating increased awareness of e-waste as a major environmental health threat. Global, national, and local levels efforts must aim to create safe recycling operations that consider broad security issues for people who rely on e-waste processing for survival. Paramount to these efforts is reducing pregnant women and children's e-waste exposures to mitigate harmful health effects. With human environmental health in mind, novel dismantling methods and remediation technologies and intervention practices are needed to protect communities. Heacock M, Kelly CB, Asante KA, Birnbaum LS, Bergman AL, Bruné MN, Buka I, Carpenter DO, Chen A, Huo X, Kamel M, Landrigan PJ, Magalini F, Diaz-Barriga F, Neira M, Omar M, Pascale A, Ruchirawat M, Sly L, Sly PD, Van den Berg M, Suk WA. 2016. E-waste and harm to vulnerable populations: a growing global problem. Environ Health Perspect 124:550-555; http://dx.doi.org/10.1289/ehp.1509699.

Background Evidence of the association of coal mining with health outcomes such as increased mortality and morbidity in the general population has been provided by epidemiological studies in the last 25 years. Given the diverse sources of data included to investigate different health outcomes in the exposed populations, the International Classification of Diseases (ICD) can be used as a single classification standard to compare the findings of studies conducted in different socioeconomic and geographic contexts. The ICD classifies diagnoses of diseases and other disorders as codes organized by categories and chapters. Objectives Identify the ICD codes found in studies of morbidity and/or mortality in populations resident or in proximity of coal mining and assess the methods of these studies conducting a systematic review. Methods A systematic database search of PubMed, EMBASE and Scopus following the PRISMA protocol was conducted to assess epidemiological studies from 1990 to 2016. The health outcomes were mapped to ICD codes and classified by studies of morbidity and/or mortality, and the categories and chapters of the ICD. Results Twenty-eight epidemiological studies with ecological design from the USA, Europe and China were included. The exposed populations had increased risk of mortality and/or morbidity by 78 ICD diagnosis categories and 9 groups of ICD categories in 10 chapters of the ICD: Neoplasms, diseases of the circulatory, respiratory and genitourinary systems, metabolic diseases, diseases of the eye and the skin, perinatal conditions, congenital and chromosomal abnormalities, and external causes of morbidity. Exposed populations had non-increased risk of 9 ICD diagnosis categories of diseases of the genitourinary system, and prostate cancer. Conclusions There is consistent evidence of the association of coal mining with a wide spectrum of diseases in populations resident or in proximity of the mining activities. The methods of the studies included in this review can be integrated with individual-level and longitudinal studies to provide further evidence of the exposure pathways linked to increased risk in the exposed populations.

The United Nations has declared that humans have a right to clean air. Despite this, many deaths and disability-adjusted life years are attributed to air pollution exposure each year. We face both challenges to air quality and opportunities to improve, but several areas need to be addressed with urgency. This paper summarises the recent research presented at the Pacific Basin Consortium for Environment and Health Symposium and focuses on three key areas of air pollution that are important to human health and require more research. Indoor spaces are commonly places of exposure to poor air quality and are difficult to monitor and regulate. Global climate change risks worsening air quality in a bi-directional fashion. The rising use of electric vehicles may offer opportunities to improve air quality, but it also presents new challenges. Government policies and initiatives could lead to improved air and environmental justice. Several populations, such as older people and children, face increased harm from air pollution and should become priority groups for action.

Perioperative respiratory adverse events in children are one of the major causes of morbidity and mortality during paediatric anaesthesia. We aimed to identify associations between family history, anaesthesia management, and occurrence of perioperative respiratory adverse events. We prospectively included all children who had general anaesthesia for surgical or medical interventions, elective or urgent procedures at Princess Margaret Hospital for Children, Perth, Australia, from Feb 1, 2007, to Jan 31, 2008. On the day of surgery, anaesthetists in charge of paediatric patients completed an adapted version of the International Study Group for Asthma and Allergies in Childhood questionnaire. We collected data on family medical history of asthma, atopy, allergy, upper respiratory tract infection, and passive smoking. Anaesthesia management and all perioperative respiratory adverse events were recorded. 9297 questionnaires were available for analysis. A positive respiratory history (nocturnal dry cough, wheezing during exercise, wheezing more than three times in the past 12 months, or a history of present or past eczema) was associated with an increased risk for bronchospasm (relative risk [RR] 8·46, 95% CI 6·18–11·59; p<0·0001), laryngospasm (4·13, 3·37–5·08; p<0·0001), and perioperative cough, desaturation, or airway obstruction (3·05, 2·76–3·37; p<0·0001). Upper respiratory tract infection was associated with an increased risk for perioperative respiratory adverse events only when symptoms were present (RR 2·05, 95% CI 1·82–2·31; p<0·0001) or less than 2 weeks before the procedure (2·34, 2·07–2·66; p<0·0001), whereas symptoms of upper respiratory tract infection 2–4 weeks before the procedure significantly lowered the incidence of perioperative respiratory adverse events (0·66, 0·53–0·81; p<0·0001). A history of at least two family members having asthma, atopy, or smoking increased the risk for perioperative respiratory adverse events (all p<0·0001). Risk was lower with intravenous induction compared with inhalational induction (all p<0·0001), inhalational compared with intravenous maintenance of anaesthesia (all p<0·0001), airway management by a specialist paediatric anaesthetist compared with a registrar (all p<0·0001), and use of face mask compared with tracheal intubation (all p<0·0001). Children at high risk for perioperative respiratory adverse events could be systematically identified at the preanaesthetic assessment and thus can benefit from a specifically targeted anaesthesia management. Department of Anaesthesia, Princess Margaret Hospital for Children, Swiss Foundation for Grants in Biology and Medicine, and the Voluntary Academic Society Basel.

Many studies have indicated the detrimental effect of ambient ozone to respiratory health in different countries. The levels of ozone in Hanoi, Vietnam are frequently above the WHO guideline but very few studies on the effects of ambient ozone on human health have been conducted in this location. This study aimed to examine the effects of ozone on hospital admission for respiratory diseases in Hanoi, by diseases, ages and seasons. Hospital admissions, air pollutants and meteorological data were collected from January 2010 to June 2014. We used generalized linear models and distributed lag linear model to assess the association. In addition to full year analysis, we conducted restricted analysis of the data for two summer (from June-August) and winter (from December-February) seasons and grouped hospital admissions by diseases and ages (all ages, children 0 to 5 years and elderly >65 years). The delayed effect of ozone was assessed using lags of up to 5 days. Ozone has a stronger effect on the risk of hospital admission for respiratory diseases and wheeze-associated disorders in the winter. For respiratory diseases, children were affected by ozone more than other age groups in both winter and summer. Each increase of 10 μg/m3 of ozone is associated with an increase of 6.2% risk of admission for respiratory disease among children in the winter and 1.2% in the summer. For wheeze-associated disorders, the elderly group seemed to be more affected by ozone in full year and winter but no significant association was found between ozone and admission for wheeze-associated diseases in any age group. Ozone is a risk factor for respiratory admission, especially amongst children under 5 years old in Hanoi, and ozone has a stronger effect in the winter than in the summer in this city.