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The author discusses the aspects of the health of the ecosystems, which is the most significant element of the health and wellbeing of the population. It mentions that the World Health Organization (WHO) recognizes the natural ecosystems, which is the planet's life-support systems for human being and other life forms. Moreover, it notes that human activity threatens the natural functions of the world and the ability of the ecosystems to sustain future generations can no longer be ignored.

The author discusses the issues related to the health promotion program in Canada. He notes that the federal and provincial governments have generally failed to fully utilize and implement health promotion, thus realizing the health benefits that could and should have been attained by the country's citizens. He points out that the failure was caused by the political and the healthcare system leadership in the country, who failed to acknowledge the potential of health promotion.

Planetary health provides a perspective of ecological interdependence that connects the health and vitality of individuals, communities, and Earth's natural systems. It includes the social, political, and economic ecosystems that influence both individuals and whole societies. In an era of interconnected grand challenges threatening health of all systems at all scales, planetary health provides a framework for cross‐sectoral collaboration and unified systems approaches to solutions. The field of allergy is at the forefront of these efforts. Allergic conditions are a sentinel measure of environmental impact on human health in early life—illuminating how ecological changes affect immune development and predispose to a wider range of inflammatory noncommunicable diseases (NCDs). This shows how adverse macroscale ecology in the Anthropocene penetrates to the molecular level of personal and microscale ecology, including the microbial systems at the foundations of all ecosystems. It provides the basis for more integrated efforts to address widespread environmental degradation and adverse effects of maladaptive urbanization, food systems, lifestyle behaviors, and socioeconomic disadvantage. Nature‐based solutions and efforts to improve nature‐relatedness are crucial for restoring symbiosis, balance, and mutualism in every sense, recognizing that both personal lifestyle choices and collective structural actions are needed in tandem. Ultimately, meaningful ecological approaches will depend on placing greater emphasis on psychological and cultural dimensions such as mindfulness, values, and moral wisdom to ensure a sustainable and resilient future. [ABSTRACT FROM AUTHOR]

In order to successfully induce disease, the fungal pathogen Candida albicans regulates exposure of antigens like the cell wall polysaccharide ß(1,3)-glucan to the host immune system. C. albicans covers (masks) ß(1,3)-glucan with a layer of mannosylated glycoproteins, which aids in immune system evasion by acting as a barrier to recognition by host pattern recognition receptors. Consequently, enhanced ß(1,3)-glucan exposure (unmasking) makes fungal cells more visible to host immune cells and facilitates more robust fungal clearance. However, an understanding of how C. albicans regulates its exposure levels of ß(1,3)-glucan is needed to leverage this phenotype. Signal transduction pathways and their corresponding effector genes mediating these changes are only beginning to be defined. Here, we report that the phosphatase calcineurin mediates unmasking of ß(1,3)-glucan in response to inputs from the Cek1 MAPK pathway and in response to caspofungin exposure. In contrast, calcineurin reduces ß-glucan exposure in response to high levels of extracellular calcium. Thus, depending on the input, calcineurin acts as a switchboard to regulate ß(1,3)-glucan exposure levels. By leveraging these differential ß(1,3)-glucan exposure phenotypes, we identified two novel effector genes in the calcineurin regulon, FGR41 and C1_11990W_A, that encode putative cell wall proteins and mediate masking/unmasking. Loss of either effector caused unmasking and attenuated virulence during systemic infection in mice. Furthermore, immunosuppression restored the colonization decrease seen in mice infected with the fgr41Δ/Δ mutant to wild-type levels, demonstrating a reliance on the host immune system for virulence attenuation. Thus, calcineurin and its downstream regulon are general regulators of unmasking. Author summary: Candida albicans is a common cause of nosocomial systemic infections, and has an attributed mortality rate as high as ~40–60%. Thus, disease management strategies are of high medical significance. One potential immunotherapeutic approach to control disease progression is to impact the ability of C. albicans to effectively evade host immune cells. This may be achieved by increasing the exposure of the highly immunogenic cell wall epitope ß(1,3)-glucan to the host immune system. Yet, elucidation of how ß-glucan exposure is regulated is needed to leverage this approach, and signal transduction pathways and effector genes mediating this phenotype are only beginning to be defined. Here, we show that calcineurin acts as a general switchboard that can both increase and decrease ß(1,3)-glucan exposure in response to multiple stimuli. Furthermore, we identify two novel downstream effector genes within the calcineurin regulon that drive this phenotype and impact virulence during systemic infection in mice. [ABSTRACT FROM AUTHOR]

Urban living is the new reality for the majority of the world's population. Urban change is taking place in a context of other global challenges-economic globalization, climate change, financial crises, energy and food insecurity, old and emerging armed conflicts, as well as the changing patterns of communicable and noncommunicable diseases. These health and social problems, in countries with different levels of infrastructure and health system preparedness, pose significant development challenges in the 21st century. In all countries, rich and poor, the move to urban living has been both good and bad for population health, and has contributed to the unequal distribution of health both within countries (the urban-rural divide) and within cities (the rich-poor divide). In this series of papers, we demonstrate that urban planning and design and urban social conditions can be good or bad for human health and health equity depending on how they are set up. We argue that climate change mitigation and adaptation need to go hand-in-hand with efforts to achieve health equity through action in the social determinants. And we highlight how different forms of governance can shape agendas, policies, and programs in ways that are inclusive and health-promoting or perpetuate social exclusion, inequitable distribution of resources, and the inequities in health associated with that. While today we can describe many of the features of a healthy and sustainable city, and the governance and planning processes needed to achieve these ends, there is still much to learn, especially with respect to tailoring these concepts and applying them in the cities of lower- and middle-income countries. By outlining an integrated research agenda, we aim to assist researchers, policy makers, service providers, and funding bodies/donors to better support, coordinate, and undertake research that is organized around a conceptual framework that positions health, equity, and sustainability as central policy goals for urban management. [ABSTRACT FROM AUTHOR]

All three of the interacting aspects of daily urban life (physical environment, social conditions, and the added pressure of climate change) that affect health inequities are nested within the concept of urban governance, which has the task of understanding and managing the interactions among these different factors so that all three can be improved together and coherently. Governance is defined as: "the process of collective decision making and processes by which decisions are implemented or not implemented": it is concerned with the distribution, exercise, and consequences of power. Although there appears to be general agreement that the quality of governance is important for development, much less agreement appears to exist on what the concept really implies and how it should be used. Our review of the literature confirmed significant variation in meaning as well as in the practice of urban governance arrangements. The review found that the linkage between governance practices and health equity is under-researched and/or has been neglected. Reconnecting the fields of urban planning, social sciences, and public health are essential "not only for improving local governance, but also for understanding and addressing global political change" for enhanced urban health equity. Social mobilization, empowering governance, and improved knowledge for sustainable and equitable development in urban settings is urgently needed. A set of strategic research questions are suggested. [ABSTRACT FROM AUTHOR]

Climate change will likely exacerbate already existing urban social inequities and health risks, thereby exacerbating existing urban health inequities. Cities in low- and middle-income countries are particularly vulnerable. Urbanization is both a cause of and potential solution to global climate change. Most population growth in the foreseeable future will occur in urban areas primarily in developing countries. How this growth is managed has enormous implications for climate change given the increasing concentration and magnitude of economic production in urban localities, as well as the higher consumption practices of urbanites, especially the middle classes, compared to rural populations. There is still much to learn about the extent to which climate change affects urban health equity and what can be done effectively in different socio-political and socio-economic contexts to improve the health of urban dwelling humans and the environment. But it is clear that equity-oriented climate change adaptation means attention to the social conditions in which urban populations live-this is not just a climate change policy issue, it requires inter-sectoral action. Policies and programs in urban planning and design, workplace health and safety, and urban agriculture can help mitigate further climate change and adapt to existing climate change. If done well, these will also be good for urban health equity. [ABSTRACT FROM AUTHOR]

Introduction: Systemic amyloidosis is a progressive disorder characterized by the extracellular deposition of amyloid fibrils and accessory proteins in visceral organs and tissues. Amyloid accumulation causes organ dysfunction and is not generally cleared by the immune system. Current treatment focuses on reducing amyloid precursor protein synthesis and slowing amyloid deposition. However, curative interventions will likely also require removal of preexisting amyloid deposits to restore organ function. Here we describe a prototypic pan-amyloid binding peptide-antibody fusion molecule (mIgp5) that enhances macrophage uptake of amyloid., Methods: The murine IgG1-IgG2a hybrid immunoglobulin with a pan amyloid-reactive peptide, p5, fused genetically to the N-terminal of the immunoglobulin light chain was synthesized in HEK293T/17 cells. The binding of the p5 peptide moiety was assayed using synthetic amyloid-like fibrils, human amyloid extracts and amyloid-laden tissues as substrates. Binding of radioiodinated mIgp5 with amyloid deposits in vivo was evaluated in a murine model of AA amyloidosis using small animal imaging and microautoradiography. The bioactivity of mIgp5 was assessed in complement fixation and in vitro phagocytosis assays in the presence of patient-derived amyloid extracts and synthetic amyloid fibrils as substrates and in the presence or absence of human serum., Results: Murine Igp5 exhibited highly potent binding to AL and ATTR amyloid extracts and diverse types of amyloid in formalin-fixed tissue sections. In the murine model of systemic AA amyloidosis, 125 I-mIgp5 bound rapidly and specifically to amyloid deposits in all organs, including the heart, with no evidence of non-specific uptake in healthy tissues. The bioactivity of the immunoglobulin Fc domain was uncompromised in the context of mIgp5 and served as an effective opsonin. Macrophage-mediated uptake of amyloid extract and purified amyloid fibrils was enhanced by the addition of mIgp5. This effect was exaggerated in the presence of human serum coincident with deposition of complement C5b9., Conclusion: Immunostimulatory, amyloid-clearing therapeutics can be developed by incorporating pan-amyloid-reactive peptides, such as p5, as a targeting moiety. The immunologic functionality of the IgG remains intact in the context of the fusion protein. These data highlight the potential use of peptide-antibody fusions as therapeutics for all types of systemic amyloidosis., Competing Interests: EM, TR, AS, and SK are founders and shareholders, and JW is interim CSO, founder and shareholder of Attralus Inc. Attralus has licensed technology related to peptide-antibody fusion reagents that target amyloid from the University of Tennessee Research Foundation. JF and JW are inventors of intellectual property related to peptide-antibody conjugates and related molecules. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Foster, Balachandran, Hancock, Martin, Macy, Wooliver, Richey, Stuckey, Williams, Jackson, Kennel and Wall.)

Histone modifications control numerous processes in eukaryotes, including inflammation. Some bacterial pathogens alter the activity or expression of host-derived factors, including sirtuins, to modify histones and induce responses that promote infection. In this study, we identified a deacetylase encoded by Campylobacter jejuni which has sirtuin activities and contributes to activation of human neutrophils by the pathogen. This sirtuin is secreted from the bacterium into neutrophils, where it associates with and deacetylates host histones to promote neutrophil activation and extracellular trap production. Using the murine model of campylobacteriosis, we found that a mutant of this bacterial sirtuin efficiently colonized the gastrointestinal tract but was unable to induce cytokine production, gastrointestinal inflammation, and tissue pathology. In conclusion, these results suggest that secreted bacterial sirtuins represent a previously unreported class of bacterial effector and that bacterial-mediated modification of host histones is responsible for the inflammation and pathology that occurs during campylobacteriosis.

Climate change has captured much attention, but it is just one part of a much larger set of massive and rapid global ecological changes. While the United Nations has taken to referring to the "triple planetary crisis" of climate change, biodiversity loss, and pollution, even this does not capture the full extent of human impact upon the Earth-and thus upon human well-being. Canada's ecological footprint is equivalent to five planets worth of biocapacity, and healthcare's footprint is probably greater. So while health systems need to become low-carbon or net-zero, they need to go further. If healthcare is to stand by its ethical duty to do no harm, it must become a "One Planet" system. In addition to becoming a net-zero system, healthcare must reduce the consumption of material resources, the use of toxic substances, and production of all forms of waste, and protect and restore nature.

In late 2019, a novel coronavirus began circulating within humans in central China. It was designated SARS-CoV-2 because of its genetic similarities to the 2003 SARS coronavirus (SARS-CoV). Now that SARS-CoV-2 has spread worldwide, there is a risk of it establishing new animal reservoirs and recombination with native circulating coronaviruses. To screen local animal populations in the United States for exposure to SARS-like coronaviruses, we developed a serological assay using the receptor binding domain (RBD) from SARS-CoV-2. SARS-CoV-2's RBD is antigenically distinct from common human and animal coronaviruses, allowing us to identify animals previously infected with SARS-CoV or SARS-CoV-2. Using an indirect enzyme-linked immunosorbent assay (ELISA) for SARS-CoV-2's RBD, we screened serum from wild and domestic animals for the presence of antibodies against SARS-CoV-2's RBD. Surprisingly prepandemic feline serum samples submitted to the University of Tennessee Veterinary Hospital were ∼50% positive for anti-SARS RBD antibodies. Some of these samples were serologically negative for feline coronavirus (FCoV), raising the question of the etiological agent generating anti-SARS-CoV-2 RBD cross-reactivity. We also identified several white-tailed deer from South Carolina with anti-SARS-CoV-2 antibodies. These results are intriguing, as cross-reactive antibodies toward SARS-CoV-2 RBD have not been reported to date. The etiological agent responsible for seropositivity was not readily apparent, but finding seropositive cats prior to the current SARS-CoV-2 pandemic highlights our lack of information about circulating coronaviruses in other species. IMPORTANCE We report cross-reactive antibodies from prepandemic cats and postpandemic South Carolina white-tailed deer that are specific for that SARS-CoV RBD. There are several potential explanations for this cross-reactivity, each with important implications to coronavirus disease surveillance. Perhaps the most intriguing possibility is the existence and transmission of an etiological agent (such as another coronavirus) with similarity to SARS-CoV-2's RBD region. However, we lack conclusive evidence of prepandemic transmission of a SARS-like virus. Our findings provide impetus for the adoption of a One Health Initiative focusing on infectious disease surveillance of multiple animal species to predict the next zoonotic transmission to humans and future pandemics.

Background: Despite the long-standing experience of rating the evidence for clinical preventive services, the delivery of effective clinical preventive services in Canada and elsewhere is less than optimal. We outline an approach used in British Columbia to assist in determining which effective clinical preventive services are worth doing., Methods: We calculated the clinically preventable burden and cost-effectiveness for 28 clinical preventive services that received a 'strong or conditional (weak) recommendation for' by the Canadian Task Force on Preventive Health Care or an 'A' or 'B' rating by the United States Preventive Services Task Force. Clinically preventable burden is the total quality adjusted life years that could be gained if the clinical preventive services were delivered at recommended intervals to a British Columbia birth cohort of 40,000 individuals over the years of life that the service is recommended. Cost-effectiveness is the net cost per quality adjusted life year gained., Results: Clinical preventive services with the highest population impact and best value for money include services that address tobacco use in adolescents and adults, exclusive breastfeeding, and screening for hypertension and other cardiovascular disease risk factors followed by appropriate pharmaceutical treatment. In addition, alcohol misuse screening and brief counseling, one-time screening for hepatitis C virus infection in British Columbia adults born between 1945 and 1965, and screening for type 2 diabetes approach these high-value clinical preventive services., Conclusions: These results enable policy makers to say with some confidence what preventive manoeuvres are worth doing but further work is required to determine the best way to deliver these services to all those eligible and to establish what supportive services are required. After all, if a clinical preventive service is worth doing, it is worth doing well., (© 2022. The Author(s).)

Human cytomegalovirus (HCMV) is a ubiquitous pathogen infecting a majority of people worldwide, with diseases ranging from mild to life-threatening. Its clinical relevance in immunocompromised people and congenital infections have made treatment and vaccine development a top priority. Because of cytomegaloviruses' species specificity, murine cytomegalovirus (MCMV) models have historically informed and advanced translational CMV therapies. Using the phenomenon of centrifugal enhancement, we explored differences between MCMVs derived in vitro and in vivo. We found centrifugal enhancement on tissue culture-derived virus (TCV) was ~3× greater compared with salivary gland derived virus (SGV). Using novel "flow virometry", we found that TCV contained a distinct submicron particle composition compared to SGV. Using an inhibitor of exosome production, we show these submicron particles are not extracellular vesicles that contribute to centrifugal enhancement. We examined how these differences in submicron particles potentially contribute to differing centrifugal enhancement phenotypes, as well as broader in vivo vs. in vitro MCMV differences.

Campylobacter jejuni is the leading cause of bacterial-derived gastroenteritis worldwide, infecting 96 million individuals annually. During infection, inflammation and tissue pathology occur in the lower gastrointestinal tract, including the recruitment of leukocytes. Neutrophils are the most abundant leukocyte in humans, and recruitment is associated with bacterial infections and the development of various inflammatory disorders, including inflammatory bowel disease. Neutrophils possess three main antibacterial functions: phagocytosis and degradation of microbes, degranulation to release antimicrobial proteins, and extrusion of neutrophil extracellular traps (NETs). Because neutrophils are recruited to the site of C. jejuni infection and they are associated with damaging inflammation in other diseases, it is imperative to understand the immunopathology that occurs during C. jejuni infection and thoroughly study the neutrophil response to the pathogen. Detailed protocols for human and ferret neutrophil isolations, neutrophil gentamicin protection assay, neutrophil activation flow cytometry assay, NET induction and quantification, and neutrophil western blot analysis are included in this article. © 2021 Wiley Periodicals LLC. Basic Protocol 1: Isolation of human and ferret neutrophils Basic Protocol 2: Neutrophil gentamicin protection assay Basic Protocol 3: Neutrophil activation flow cytometry analyses Basic Protocol 4: Neutrophil extracellular trap induction and quantification Basic Protocol 5: Western blot detection of neutrophil-derived antimicrobial proteins., (© 2021 Wiley Periodicals LLC.)

Masking the immunogenic cell wall epitope ß(1,3)-glucan under an outer layer of mannosylated glycoproteins is an important virulence factor deployed by Candida albicans during infection. Consequently, increased ß(1,3)-glucan exposure (unmasking) reveals C. albicans to the host's immune system and attenuates its virulence. We have previously shown that activation of the Cek1 MAPK pathway via expression of a hyperactive allele of an upstream kinase (STE11ΔN467) induced unmasking. It also increased survival of mice in a murine disseminated candidiasis model and attenuated kidney fungal burden by ≥33 fold. In this communication, we utilized cyclophosphamide-induced immunosuppression to test if the clearance of the unmasked STE11ΔN467 mutant was dependent on the host immune system. Suppression of the immune response by cyclophosphamide reduced the attenuation in fungal burden caused by the STE11ΔN467 allele. Moreover, specific depletion of neutrophils via 1A8 antibody treatment also reduced STE11ΔN467-dependent fungal burden attenuation, but to a lesser extent than cyclophosphamide, demonstrating an important role for neutrophils in mediating fungal clearance of unmasked STE11ΔN467 cells. In an effort to understand the mechanism by which Ste11ΔN467 causes unmasking, transcriptomics were used to reveal that several components in the Cek1 MAPK pathway were upregulated, including the transcription factor CPH1 and the cell wall sensor DFI1. In this report we show that a cph1ΔΔ mutation restored ß(1,3)-glucan exposure to wild-type levels in the STE11ΔN467 strain, confirming that Cph1 is the transcription factor mediating Ste11ΔN467-induced unmasking. Furthermore, Cph1 is shown to induce a positive feedback loop that increases Cek1 activation. In addition, full unmasking by STE11ΔN467 is dependent on the upstream cell wall sensor DFI1. However, while deletion of DFI1 significantly reduced Ste11ΔN467-induced unmasking, it did not impact activation of the downstream kinase Cek1. Thus, it appears that once stimulated by Ste11ΔN467, Dfi1 activates a parallel signaling pathway that is involved in Ste11ΔN467-induced unmasking., Competing Interests: The authors have declared that no competing interests exist.

As a collective organized to address the education implications of calls for public health engagement on the ecological determinants of health, we, the Ecological Determinants Group on Education (cpha.ca/EDGE), urge the health community to properly understand and address the importance of the ecological determinants of the public's health, consistent with long-standing calls from many quarters-including Indigenous communities-and as part of an eco-social approach to public health education, research and practice. Educational approaches will determine how well we will be equipped to understand and respond to the rapid changes occurring for the living systems on which all life-including human life-depends. We revisit findings from the Canadian Public Health Association's discussion paper on 'Global Change and Public Health: Addressing the Ecological Determinants of Health', and argue that an intentionally eco-social approach to education is needed to better support the health sector's role in protecting and promoting health, preventing disease and injury, and reducing health inequities. We call for a proactive approach, ensuring that the ecological determinants of health become integral to public health education, practice, policy, and research, as a key part of wider societal shifts required to foster a healthy, just, and ecologically sustainable future.

Patient-oriented research (POR) aims to increase patient engagement in health research to improve health research and health services. In Canada, the Strategies for Patient-Oriented Research (SPOR) framework provides guidance for conducting POR. We critically review the SPOR framework through the lens of public health systems and services research. The SPOR framework is primarily focused on engaging individual patients in health research without attention to broader structural forces that shape health and participation in healthcare systems. Shifting from patient to public involvement and from patient to community engagement and being explicit about the range of health research that SPOR encompasses would enhance the framework and strengthen the potential of SPOR to improve health systems through health protection, promotion and prevention of disease and injury., (Copyright © 2019 Longwoods Publishing.)

The Canadian Journal of Public Health is launching a new section entitled Innovations in Policy and Practice, which will be a showcase for and reflection on innovative public health policy and practice in Canada. The section will focus on articles that describe the development and implementation of innovative policies and practices in Canada and/or that reflect on the experience of practitioners in implementation. The section is explicitly intended to attract practitioners as both readers and authors. This will involve a number of innovations for the Journal that will make the role of author easier for practitioners and result in published material that is attractive and useful, while retaining a scholarly approach. In addition, the review process for this section will be oriented to the reality of practice and undertaken by 'practitioner-scholars' in a collegial and non-anonymous manner.

Humanity is both an animal species that evolved within and is dependent upon natural ecosystems and a social animal that exists within the social systems we have created. Our health is dependent upon both these systems - natural and social - functioning well, and indeed upon their interactions. Yet our approach to improving the health of the population over the past few decades has been largely, if not exclusively, focused on the social determinants of health. A recent Canadian Public Health Association (CPHA) Discussion Document and the technical report on which it is based seek to strike a more balanced approach. First, they document the dramatic and rapid global ecological changes that humans have created and argue that they are a significant threat to the health of the population in the 21st century. Second, they identify the underlying social, cultural and economic forces that are driving these changes. Third, they argue that we need to take an eco-social approach in population health promotion, recognizing the interactions between the ecological and social determinants of health. Such an approach could be considered to be 'Population health promotion 2.0', and it has profound implications for the practice of public health.

The importance of reestablishing the link between urban planning and public health has been recognized in recent decades; this paper focuses on the relationship between urban planning/design and health equity, especially in cities in low and middle-income countries (LMICs). The physical urban environment can be shaped through various planning and design processes including urban planning, urban design, landscape architecture, infrastructure design, architecture, and transport planning. The resultant urban environment has important impacts on the health of the people who live and work there. Urban planning and design processes can also affect health equity through shaping the extent to which the physical urban environments of different parts of cities facilitate the availability of adequate housing and basic infrastructure, equitable access to the other benefits of urban life, a safe living environment, a healthy natural environment, food security and healthy nutrition, and an urban environment conducive to outdoor physical activity. A new research and action agenda for the urban environment and health equity in LMICs should consist of four main components. We need to better understand intra-urban health inequities in LMICs; we need to better understand how changes in the built environment in LMICs affect health equity; we need to explore ways of successfully planning, designing, and implementing improved health/health equity; and we need to develop evidence-based recommendations for healthy urban planning/design in LMICs.

Urban health promotion is not simply a matter of the right interventions, or even the necessary resources. Urban (and indeed global) health depends to an important extent on governance, the institutions and processes through which societies manage the course of events. This paper describes the concept of governance, distinguishing between reforms aimed at improving how government works and innovations that more fundamentally reinvent governance by developing new institutions and processes of local stakeholder control. The paper highlights strategies urban governors can use to maximize their influence on the national and international decisions that structure urban life. It concludes with some observations on the limitations of local governance strategies and the importance of establishing a "virtuous circuit" of governance through which urban dwellers play a greater role in the formation and implementation of policy at the national and global levels.

The North American population is approximately 80% urbanized and spends almost 90% of the time indoors. Accordingly, the built environment is the most important--one might almost say "natural"--human environment. Urban settlements incorporate within their boundaries natural ecosystems of plant and animal life (often highly adapted to the urban environment), and are in turn incorporated within wider bioregions and global ecosystems. But urban settlements are not just built and natural physical environments, they are social, economic, cultural and political environments; the whole constitutes an urban ecosystem. These ecosystems have profound implications for the physical, mental, social, emotional and spiritual well-being of their human inhabitants, as well as for human beings remote from these urban ecosystems. Therefore, this paper discusses urban ecosystems and human health and presents a framework for indicators of environmental health in the urban setting based on such an understanding. The concepts of environmental viability, ecological sustainability, urban livability, community conviviality, social equity, and economic adequacy are discussed in relation to human health and are used to organize proposed candidate indicators for urban ecosystems and public health.