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Objective: The National Children's Study is a long-term epidemiologic study of 100,000 children from 105 locations across the United States. It will require information on a large number of environmental variables to address its core hypotheses. The resources available to collect actual home and personal exposure samples are limited, with most of the home sampling completed on periodic visits and the personal sampling generally limited to biomonitoring. To fill major data gaps, extant data will be required for each study location. The Queens Vanguard Center has examined the extent of those needs and the types of data that are generally and possibly locally available.Data: In this review we identify three levels of data--national, state and county--and local data and information sets (levels 1--3, respectively), each with different degrees of availability and completeness, that can be used as a starting point for the extant data collection in each study location over time. We present an example on the use of this tiered approach, to tailor the data needs for Queens County and to provide general guidance for application to other NCS locations.Conclusions: Preexisting and continually evolving databases are available for use in the NCS to characterize exposure. The three levels of data we identified will be used to test a method for developing exposure indices for segments and homes during the pilot phase of NCS, as outlined in this article. [ABSTRACT FROM AUTHOR]

CONTEXT: Private wells that tap groundwater are largely exempt from federal drinking-water regulations, and in most states well water is not subject to much of the mandatory testing required of public water systems. Families that rely on private wells are thus at risk of exposure to a variety of unmeasured contaminants. CASE PRESENTATION: A family of seven--two adults and five children--residing in rural northwestern Connecticut discovered elevated concentrations of uranium in their drinking water, with levels measured at 866 and 1,160 microg/L, values well above the U.S. Environmental Protection Agency maximum contaminant level for uranium in public water supplies of 30 microg/L. The uranium was of natural origin, and the source of exposure was found to be a 500-foot well that tapped groundwater from the Brookfield Gneiss, a geologic formation known to contain uranium. Other nearby wells also had elevated uranium, arsenic, and radon levels, though concentrations varied widely. At least one 24-hr urine uranium level was elevated (> 1 microg/24 hr) in six of seven family members (range, 1.1-2.5 microg/24 hr). To assess possible renal injury, we measured urinary beta-2-microglobulin. Levels were elevated (> 120 microg/L) in five of seven family members, but after correction for creatine excretion, the beta-2-microglobulin excretion rate remained elevated (> 40 microg/mmol creatinine) only in the youngest child, a 3-year-old with a corrected level of 90 microg/mmol creatinine. Three months after cessation of well water consumption, this child's corrected beta-2-microglobulin level had fallen to 52 microg/mmol creatinine. SIGNIFICANCE: This case underscores the hazards of consuming groundwater from private wells. It documents the potential for significant residential exposure to naturally occurring uranium in well water. It highlights the special sensitivity of young children to residential environmental exposures, a reflection of the large amount of time they spend in their homes, the developmental immaturity of their kidneys and other organ systems, and the large volume of water they consume relative to body mass. [ABSTRACT FROM AUTHOR]

Prospective, multiyear epidemiologic studies have proven to be highly effective in discovering preventable risk factors for chronic disease. Investigations such as the Framingham Heart Study have produced blueprints for disease prevention and saved millions of lives and billions of dollars. To discover preventable environmental risk factors for disease in children, the US Congress directed the National Institute of Child Health and Human Development, through the Children's Health Act of 2000, to conduct the National Children's Study. The National Children's Study is hypothesis-driven and will seek information on environmental risks and individual susceptibility factors for asthma, birth defects, dyslexia, attention-deficit/hyperactivity disorder, autism, schizophrenia, and obesity, as well as for adverse birth outcomes. It will be conducted in a nationally representative, prospective cohort of 100,000 US-born children. Children will be followed from conception to 21 years of age. Environmental exposures (chemical, physical, biological, and psychosocial) will be assessed repeatedly during pregnancy and throughout childhood in children's homes, schools, and communities. Chemical assays will be performed by the Centers for Disease Control and Prevention, and banks of biological and environmental samples will be established for future analyses. Genetic material will be collected on each mother and child and banked to permit study of gene-environment interactions. Recruitment is scheduled to begin in 2007 at 7 Vanguard Sites and will extend to 105 sites across the United States. The National Children's Study will generate multiple satellite studies that explore methodologic issues, etiologic questions, and potential interventions. It will provide training for the next generation of researchers and practitioners in environmental pediatrics and will link to planned and ongoing prospective birth cohort studies in other nations. Data from the National Children's Study will guide development of a comprehensive blueprint for disease prevention in children. [ABSTRACT FROM AUTHOR]

Background: Postdisaster crisis interventions have been viewed by some as appropriate to enhance the mental health status of persons affected by large-scale traumatic events. However, studies and systematic reviews have challenged the effectiveness of these efforts.Objectives: The focus of this study was to examine the impact of brief mental health interventions received by employees at the worksite after the World Trade Center disaster (WTCD) among workers in New York City (NYC).Research Design: The data for the present study come from a prospective cohort study of 1121 employed adults interviewed by telephone in a household survey 1 year and 2 years after the WTCD. All study participants were living in NYC at the time of the attacks. For the current study, we used propensity scores to match intervention cases (n = 150) to nonintervention controls (n = 971) using a 1:5 matching ratio based on a bias-corrected nearest-neighbor algorithm.Results: Approximately 7% of NYC adults (approximately 425,000 persons) reported receiving employer-sponsored, worksite crisis interventions related to the WTCD provided by mental health professionals. In addition, analyses indicated that attending 1 to 3 brief worksite sessions was associated with positive outcomes up to 2 years after the WTCD across a spectrum of results, including reduced alcohol dependence, binge drinking, depression, PTSD severity, and reduced anxiety symptoms.Conclusions: Although our study had limitations, it is one of the few to suggest that brief postdisaster crisis interventions may be effective for employees after mass exposure to psychologically traumatic events. The reasons for the effectiveness of these interventions are unclear at this time and warrant further investigation. [ABSTRACT FROM AUTHOR]

The attack on the World Trade Center (WTC) created an acute environmental disaster of enormous magnitude. This study characterizes the environmental exposures resulting from destruction of the WTC and assesses their effects on health. Methods include ambient air sampling; analyses of outdoor and indoor settled dust; high-altitude imaging and modeling of the atmospheric plume; inhalation studies of WTC dust in mice; and clinical examinations, community surveys, and prospective epidemiologic studies of exposed populations. WTC dust was found to consist predominantly (95%) of coarse particles and contained pulverized cement, glass fibers, asbestos, lead, polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), and polychlorinated furans and dioxins. Airborne particulate levels were highest immediately after the attack and declined thereafter. Particulate levels decreased sharply with distance from the WTC. Dust pH was highly alkaline (pH 9.0-11.0). Mice exposed to WTC dust showed only moderate pulmonary inflammation but marked bronchial hyperreactivity. Evaluation of 10,116 firefighters showed exposure-related increases in cough and bronchial hyperreactivity. Evaluation of 183 cleanup workers showed new-onset cough (33%), wheeze (18%), and phlegm production (24%). Increased frequency of new-onset cough, wheeze, and shortness of breath were also observed in community residents. Follow-up of 182 pregnant women who were either inside or near the WTC on 11 September showed a 2-fold increase in small-for-gestational-age (SGA) infants. In summary, environmental exposures after the WTC disaster were associated with significant adverse effects on health. The high alkalinity of WTC dust produced bronchial hyperreactivity, persistent cough, and increased risk of asthma. Plausible causes of the observed increase in SGA infants include maternal exposures to PAH and particulates. Future risk of mesothelioma may be increased, particularly among workers and volunteers exposed occupationally to asbestos. Continuing follow-up of all exposed populations is required to document the long-term consequences of the disaster. [ABSTRACT FROM AUTHOR]

Objective: To determine the number, distribution, determinants, and health consequences of occupational injuries among working adolescents in New York State.Design: A retrospective, population-based analysis of New York State workers' compensation award data and the Annual Demographic File, a supplement to the US Bureau of the Census Current Population Survey.Participants: Adolescents, aged 14 through 17 years, who received workers' compensation awards for occupational injury from 1980 through 1987.Main Outcome Measures: (1) Numbers, types, and rates of occupational injuries in working adolescents by age, sex, industry, and occupation; (2) health consequences of injury, especially disability and death; and (3) secular trends in injury award rates.Results: A total of 9656 adolescents were compensated for occupational injuries; 4201 compensated adolescents (43.5%) suffered permanent disability; 31 working adolescents died. The annual mean rate of compensated occupational injury was 28.2 per 10,000 adolescent workers. Rates were higher in males than in females and ranged from 8.2 per 10,000 in 14-year-old male workers to 46.8 per 10,000 in 17-year-old male workers. Highest rates by industry were seen in manufacturing (49.0/10,000 adolescent workers) and agriculture (46.2/10,000). Unskilled labor was the most dangerous occupation (52.3/10,000).Conclusion: Occupational injuries are a substantial and underrecognized contributor to the continuing epidemic of injury among adolescents. [ABSTRACT FROM AUTHOR]

Background: While much attention is focused on national policies intended to protect human health from environmental hazards, states can also prevent environmentally mediated disease through legislation and regulation. However, relatively few analyses have examined the extent to which states protect children from chemical factors in the environment.Methods: Using Lexis Nexis and other secondary sources, we systematically reviewed environmental regulation and legislation in the fifty states and the District of Columbia as of July 2007 intended to protect children against neurodevelopmental disabilities and asthma.Results: States rarely address children specifically in environmental regulation and legislation, though many state regulations go far to limit children's exposures to environmental hazards. Northeast and Midwest states have implemented model regulation of mercury emissions, and regulations in five states set exposure limits to volatile organic compound emissions that are more stringent than US Environmental Protection Agency standards.Discussion: Differences in state environmental regulation and legislation are likely to lead to differences in exposure, and thus to impacts on children's health. The need for further study should not inhibit other states and the federal government from pursuing the model regulation and legislation we identified to prevent diseases of environmental origin in children. [ABSTRACT FROM AUTHOR]

Background: A growing body of epidemiologic and toxicologic literature indicates that fine airborne particulate matter (PM 2.5 ) pollution is neurotoxic and threatens children's neurobehavioral development, resulting in reduced cognitive function. Understanding the magnitude of this effect is critical for establishing public health policies that will protect children's health, preserve human capital, and support societal progress., Objective: To quantify the association between ambient PM 2.5 air pollution and loss of cognitive function in children, as measured by Intelligence Quotient (IQ) scores, through a systematic literature review and meta-analysis., Methods: Following PRISMA guidelines, we conducted a systematic literature search across seven databases: Agricultural and Environmental Science, BIOSIS Citation Index, Embase, GreenFILE, PubMed, Scopus, and Web of Science to identify original scientific studies that investigated the impact of PM 2.5 exposure during pre-and postnatal periods on IQ loss during childhood. Using data from studies included for final review, we conducted a meta-analysis, using a random effects model to compute a beta coefficient that quantifies the overall effect of PM 2.5 exposure on Full-Scale IQ (FSIQ), Performance IQ (PIQ), and Verbal IQ (VIQ)., Findings: Of the 1,107 unique publications identified, six studies met the inclusion criteria for final review, representing 4,860 children across three continents (North America, Europe, and Asia). The mean PM 2.5 concentration across all studies was 30.4 ± 24.4 µg/m 3 . Exposure timing ranged from the prenatal period to mid-childhood. Children were an average of 8.9 years old at the time of cognitive testing. We found that each 1 µg/m 3 increase in PM 2.5 concentration is associated with a -0.27 point change in FSIQ (p < 0.001), 0.39 point change in PIQ (p = 0.003), and -0.24 point change in VIQ (p = 0.021)., Conclusion: Through a systematic review and meta-analysis, we identified a statistically significant relationship between increased exposure to PM 2.5 air pollution and reduced cognitive function in children, with the most pronounced impact on PIQ. This analysis will enable estimation of the burden of adverse neurobehavioral development attributable to PM 2.5 in pediatric populations and will inform local and global strategies for exposure prevention., Competing Interests: Declarations Competing interests The authors declare no competing interests., (© 2024. The Author(s).)

Competing Interests: Competing interests: No, there are no competing interests.

Lead, an element toxic to countless biological processes, occurs naturally in the earth's lithosphere and is geologically sequestered from the biosphere at the earth's surface. When humans remove lead from the lithosphere and distribute it throughout the economy, its toxic effects impact throughout the web of life. Lead mining and manufacturing is a small industry that generates enormous harms. Lead impairs the growth, development, and reproduction of microbes, insects, plants, and animals. The annual human costs of lead exposure include 5·5 million premature adult deaths from cardiovascular disease and US$1·4 trillion in losses to the global economy from lead impairing children's cognitive development. Although the lead industry touts lead as the most recycled metal, most recycling occurs within countries that are incapable of enforcing environmental regulations. Millions of metric tonnes of lead are dispersed into the environment each year, disproportionately in low-income and middle-income countries. Substitutes for lead in the economy are available and we should act in the best interests of the planet and human health by eliminating lead from the global economy by 2035., Competing Interests: Declaration of interests SPL and JEF received funding from Stanford's King Center for International Development, the Thrasher Research Fund, and Open Philanthropy via PureEarth to support research efforts. ELP received funding from the UN Sustainable Manufacturing & Environmental Program, the International Growth Center, and Stanford's King Center for International Development and Woods Institute for the Environment in Bangladesh. HH conducted research on lead exposure and toxicity supported by the US National Institutes of Health, the US National Institute for Occupational Safety and Health, and the US Environmental Protection Agency since 1991; served as an expert witness in litigation involving lead exposure and health impacts on communities; and is a member of the Board of Directors for Pure Earth, a non-governmental organisation dedicated to the clean-up of toxic waste, including lead. All other authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Emerging evidence indicates that chemical exposures in the environment are overlooked drivers of cardiovascular diseases (CVD). Recent evidence suggests that micro- and nanoplastic (MNP) particles derived largely from the chemical or mechanical degradation of plastics might represent a novel CVD risk factor. Experimental data in preclinical models suggest that MNPs can foster oxidative stress, platelet aggregation, cell senescence, and inflammatory responses in endothelial and immune cells while promoting a range of cardiovascular and metabolic alterations that can lead to disease and premature death. In humans, MNPs derived from various plastics, including polyethylene and polyvinylchloride, have been detected in atherosclerotic plaques and other cardiovascular tissues, including pericardia, epicardial adipose tissues, pericardial adipose tissues, myocardia, and left atrial appendages. MNPs have measurable levels within thrombi and seem to accumulate preferentially within areas of vascular lesions. Their presence within carotid plaques is associated with subsequent increased incidence of cardiovascular events. To further investigate the possible causal role of MNPs in CVD, future studies should focus on large, prospective cohorts assessing the exposure of individuals to plastic-related pollution, the possible routes of absorption, the existence of a putative safety limit, the correspondence between exposure and accumulation in tissues, the timing between accumulation and CVD development, and the pathophysiological mechanisms instigated by pertinent concentrations of MNPs. Data from such studies would allow the design of preventive, or even therapeutic, strategies. Meanwhile, existing evidence suggests that reducing plastic production and use will produce benefits for the environment and for human health. This goal could be achieved through the UN Global Plastics Treaty that is currently in negotiation., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology.)

Healthy, uncontaminated soils and clean water support all life on Earth and are essential for human health. Chemical pollution of soil, water, air and food is a major environmental threat, leading to an estimated 9 million premature deaths worldwide. The Global Burden of Disease study estimated that pollution was responsible for 5.5 million deaths related to cardiovascular disease (CVD) in 2019. Robust evidence has linked multiple pollutants, including heavy metals, pesticides, dioxins and toxic synthetic chemicals, with increased risk of CVD, and some reports suggest an association between microplastic and nanoplastic particles and CVD. Pollutants in soil diminish its capacity to produce food, leading to crop impurities, malnutrition and disease, and they can seep into rivers, worsening water pollution. Deforestation, wildfires and climate change exacerbate pollution by triggering soil erosion and releasing sequestered pollutants into the air and water. Despite their varied chemical makeup, pollutants induce CVD through common pathophysiological mechanisms involving oxidative stress and inflammation. In this Review, we provide an overview of the relationship between soil and water pollution and human health and pathology, and discuss the prevalence of soil and water pollutants and how they contribute to adverse health effects, focusing on CVD., (© 2024. Springer Nature Limited.)

Planetary health is an emerging field that emphasises that humans depend on a healthy Earth for survival and, conversely, that the sustainability of Earth systems is dependent on human behaviours. In response to member demands for resources to support teaching and learning related to planetary health, the Consortium of Universities for Global Health (CUGH) convened a working group to develop a set of planetary health learning objectives (PHLOs) that would complement the existing ten CUGH global health learning objectives. The eight PHLOs feature Earth system changes, planetary boundaries, and climate change science; ecological systems and One Health; human health outcomes; risk assessment, vulnerability, and resilience; policy, governance, and laws (including the UN Framework Convention on Climate Change and the Paris Agreement); roles and responsibilities of governments, businesses, civil society organisations, other institutions, communities, and individuals for mitigation, adaptation, conservation, restoration, and sustainability; environmental ethics, human rights, and climate justice; and environmental literacy and communication. Educators who use the PHLOs as a foundation for teaching, curriculum design, and programme development related to the health-environment nexus will equip learners with a knowledge of planetary health science, interventions, and communication that is essential for future global health professionals., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

A healthy ocean is essential for human health, and yet the links between the ocean and human health are often overlooked. By providing new medicines, technologies, energy, foods, recreation, and inspiration, the ocean has the potential to enhance human health and wellbeing. However, climate change, pollution, biodiversity loss, and inequity threaten both ocean and human health. Sustainable realisation of the ocean's health benefits will require overcoming these challenges through equitable partnerships, enforcement of laws and treaties, robust monitoring, and use of metrics that assess both the ocean's natural capital and human wellbeing. Achieving this will require an explicit focus on human rights, equity, sustainability, and social justice. In addition to highlighting the potential unique role of the healthcare sector, we offer science-based recommendations to protect both ocean health and human health, and we highlight the unique potential of the healthcare sector tolead this effort., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Various forms of pollution carry a substantial burden with respect to increasing the risk of causing and exacerbating noncommunicable diseases, especially cardiovascular disease. The first part of this 2-part series on pollution and cardiovascular disease provided an overview of the impact of global warming and air pollution. This second paper provides an overview of the impact of water, soil, noise, and light pollution on the cardiovascular system. This review discusses the biological mechanisms underlying these effects and potential environmental biometrics of exposure. What is clear from both these pollution papers is that significant efforts and redoubled urgency are needed to reduce the sources of pollution in our environment, to incorporate environmental risk factors into medical education, to provide resources for research, and, ultimately, to protect those who are particularly vulnerable and susceptible., Competing Interests: Funding Support and Author Disclosures Drs Miller and Newby have received grant support from the British Heart Foundation (CH/09/002, RG/F/22/110093, RE/24/130012). Dr Arora is a founder of Linus Biotechnology Inc, a Mount Sinai start-up that develops biomarkers for precision medicine applications. Dr Münzel is the Principal Investigator for the Centre Cardiovascular Research, Partner Site Rhine-Main; and has received grant support from the Boehringer Ingelheim Foundation (“Novel and neglected cardiovascular risk factors”) and the Foundation Heart of Mainz. Dr Arora has received grant support from the National Institutes of Health (R35ES030435, P30ES023515, U2CES030859). Dr Kovacic has received research support from the National Institutes of Health (R01HL148167), New South Wales health grant (RG194194), the Bourne Foundation, Snow Medical, and Agilent. Dr Landrigan has reported that he has no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Environmental stresses are increasingly recognized as significant risk factors for adverse health outcomes. In particular, various forms of pollution and climate change are playing a growing role in promoting noncommunicable diseases, especially cardiovascular disease. Given recent trends, global warming and air pollution are now associated with substantial cardiovascular morbidity and mortality. As a vicious cycle, global warming increases the occurrence, size, and severity of wildfires, which are significant sources of airborne particulate matter. Exposure to wildfire smoke is associated with cardiovascular disease, and these effects are underpinned by mechanisms that include oxidative stress, inflammation, impaired cardiac function, and proatherosclerotic effects in the circulation. In the first part of a 2-part series on pollution and cardiovascular disease, this review provides an overview of the impact of global warming and air pollution, and because of recent events and emerging trends specific attention is paid to air pollution caused by wildfires., Competing Interests: Funding Support and Author Disclosures Dr Miller has received support from the British Heart Foundation (CH/09/002). Dr Arora is a founder of Linus Biotechnology Inc, a Mount Sinai start-up that develops biomarkers for precision medicine applications; and has received grant support from the National Institute of Health (NIH; R35ES030435, P30ES023515, and U2CES030859). Dr Newby has received support from the British Heart Foundation (CH/09/002, RG/F/22/110093, and RE/24/130012). Dr Münzel has served as a principal investigator for the Centre Cardiovascular Research, Partner Site Rhine-Main; and has received support from the Boehringer Ingelheim Foundation Novel and Neglected Cardiovascular Risk Factors grant and from the Foundation Heart of Mainz. Dr Kovacic has received research support from the NIH (grant R01HL148167), New South Wales health grant RG194194, the Bourne Foundation, Snow Medical, and Agilent. Dr Landrigan has reported that he has no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Chinese children are exposed to broad environmental risks ranging from well-known hazards, such as pesticides and heavy metals, to emerging threats including many new man-made chemicals. Although anecdotal evidence suggests that the exposure levels in Chinese children are substantially higher than those of children in developed countries, a systematic assessment is lacking. Further, while these exposures have been linked to a variety of childhood diseases, such as respiratory, endocrine, neurological, behavioral, and malignant disorders, the magnitude of the associations is often unclear. This review provides a current epidemiologic overview of commonly reported environmental contaminants and their potential impact on children's health in China. We found that despite a large volume of studies on various topics, there is a need for more high-quality research and better-coordinated regional and national data collection. Moreover, prevention of such diseases will depend not only on training of environmental health professionals and enhanced research programs, but also on public education, legislation, and networking., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Competing Interests: Disclosures None.

Competing Interests: We declare no competing interests.

Background: Rwanda, like many countries in sub-Saharan Africa, is still relatively early in development. Industrialization and urbanization are major drivers of the county's economic growth. Rwanda is also undergoing an epidemiological transition, from a pattern of morbidity and mortality dominated by infectious diseases to a pattern shaped by non-communicable diseases (NCDs). The rise in NCDs is due, in part, to increasing exposures to environmental hazards. These include emissions from the growing number of motor vehicles and toxic occupational exposures. Cardiovascular disease (CVD) is now an increasingly important cause of death in Rwanda, and ambient air pollution is a CVD risk factor of growing importance., Objectives: To quantify the burden of CVD attributable to air pollution in Rwanda and identify opportunities for prevention and control of air pollution and pollution-related disease., Methods: We relied on the 2019 Global Burden of Disease (GBD) study for information on levels, sources, and trends in household and ambient air pollution and the burden of pollution-related disease in Rwanda. Information on pollution sources was obtained from the Health Effects Institute State of Global Air 2019 report., Findings: An estimated 3,477 deaths (95% Uncertainty Interval [UI]: 2,500-4,600) in Rwanda in 2019 were attributable to air pollution-related CVD. Of these, 689 (UI: 283-1,300) deaths were from ambient air pollution-related CVD, while 2,788 (UI: 1,800-3,800) deaths were from household air pollution-related CVD., Conclusion: Rwanda is experiencing increased rates of disease and premature death from NCDs, including CVD, as the country grows economically. While household air pollution is still the top pollution-related cause of disease and premature death, rising levels of ambient air pollution are an increasingly important CVD risk factor., Recommendation: Actions taken now to curb rising levels of ambient air pollution will improve health, reduce CVD, increase longevity, and produce great economic benefit for Rwanda. The single most effective intervention against air pollution will be a rapid nationwide transition to renewable energy. We recommend additionally that Rwanda prioritize air pollution prevention and control, establish a robust, nationwide air monitoring network, support research on the health effects of air pollutants, and build national research capacity. The allocation of increased resources for rural and urban public health and health care will complement air pollution control measures and further reduce CVD. To incentivize a rapid transition to renewable energy in Rwanda and other nations, we recommend the creation of a new Global Green Development Fund., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Background: Since the Industrial Revolution, humanity has amassed great wealth and achieved unprecedented material prosperity. These advances have come, however, at great cost to the planet. They are guided by an economic model that focuses almost exclusively on short-term gain, while ignoring natural capital and human capital. They have relied on the combustion of vast quantities of fossil fuels, massive consumption of the earth's resources, and production and environmental release of enormous quantities of chemicals, pesticides, fertilizers, and plastics. They have caused climate change, pollution, and biodiversity loss, the "Triple Planetary Crisis". They are responsible for more than 9 million premature deaths per year and for widespread disease - impacts that fall disproportionately upon the poor and the vulnerable., Goals: To map the human health impacts of climate change, pollution, and biodiversity loss. To outline a framework for assessing the health benefits of interventions against these threats., Findings: Actions taken by national governments and international agencies to mitigate climate change, pollution, and biodiversity loss can improve health, prevent disease, save lives, and enhance human well-being. Yet assessment of health benefits is largely absent from evaluations of environmental remediation programs. This represents a lost opportunity to quantify the full benefits of environmental remediation and to educate policy makers and the public., Recommendations: We recommend that national governments and international agencies implementing interventions against climate change, pollution, and biodiversity loss develop metrics and strategies for quantifying the health benefits of these interventions. We recommend that they deploy these tools in parallel with assessments of ecologic and economic benefits. Health metrics developed by the Global Burden of Disease (GBD) study may provide a useful starting point.Incorporation of health metrics into assessments of environmental restoration will require building transdisciplinary collaborations. Environmental scientists and engineers will need to work with health scientists to establish evaluation systems that link environmental and economic data with health data. Such systems will assist international agencies as well as national and local governments in prioritizing environmental interventions., Competing Interests: The authors have no competing interests to declare., (Copyright: © 2024 The Author(s).)

Families increasingly raise questions about the use of genetically modified organism (GMO)-containing food products. These products are widely found in the US food supply but originate from a narrow list of crops. Although GMO technology could be used to increase the micronutrient content of foods, this does not occur in the United States; instead, GMO technology has been used to make crops resistant to chemical herbicides. As a result, herbicide use has increased exponentially. The World Health Organization's International Agency on Research for Cancer has determined that glyphosate, an herbicide widely used in producing GMO food crops, is a probable human carcinogen. Measurable quantities of glyphosate are detected in some GMO foods. Families who wish to minimize GMO food products can do so by focusing on a dietary pattern of primarily whole, plant-based foods while minimizing ultra-processed foods. Pediatricians play a vital role in their efforts to minimize fear-based messaging and support families through shared decision-making. Pediatrician awareness of GMO labeling can guide individualized conversations, particularly that non-GMO labeling does not indicate organic status and that increased cost of some non-GMO foods, especially if also organic, may limit this choice for many families., (Copyright © 2024 by the American Academy of Pediatrics.)