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Copyright © eContent Management Pty Ltd. Health Sociology Review (2013) 22(1): 98–111.

Respiratory health and ecosyndemics in a time of global warming MERRILL SINGER Department of Anthropology, University of Connecticut, Mansfield, CT, USA

Abstract: Respiratory risks to human health are on the rise around the globe, at least in part, because anthropogenic environmental changes are increasing and multiplying the likelihood of respiratory disease comorbidity and disease interaction, a health consequence termed an ecosyndemic. The immediate objective of this paper is to examine the nature and growing prevalence of ecosyndemics under conditions of mounting environmental imbalance and climate change as exemplified by asthma and other increasingly frequent respiratory diseases. More broadly, the paper seeks to contribute to increased understanding of the critical role of syndemics in shaping global health and the value of a political ecology of respiratory health perspective.

Keywords: respiratory heath, ecosyndemics, asthma, health disparities, social origins of health

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he quality of the air we breathe has significantly diminished over the last several decades as a result of the interaction of global warming with other forms of anthropogenic environmental degradation, such as vehicular air pollution (Singer, 2009a). Consequently, there have been notable increases in the frequency of a range of respiratory symptoms and diseases like asthma, especially among poorer and disadvantaged populations in both developed and developing nations (World Health Organization, 2008). In coming years, respiratory health is expected to grow even worse ‘because of interaction between heavier pollen loads and increased air pollution; thunderstorms and extreme precipitation events; worsening heat-related ground-level ozone pollution; increased ambient air pollution from natural and anthropogenic sources; and air pollutionrelated to wildfires’ (Shea, Truckner, Weber, & Peden, 2008, p. 445). This conclusion, based on a review of various data sources (Beggs & Bambrick, 2005; Noyes et al., 2008; Ren, Williams, Mengersen, Morawska, & Tong, 2008), is supported by high-resolution climate/ air pollution computer modeling (Jacobson, 2008). The specific linkages between global warming, diminishing air quality, and respiratory health include: (1) the deleterious effects of air pollution produced by motor vehicles, industrial power plants, and industrial chemicals (e.g., pesticides) as a result of expanded environmental discharge and higher planetary temperatures;

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(2) forest fires that release ever greater quantities of hazardous particulate matter, carbon monoxide, and polyaromatic hydrocarbons as a result of drier environmental conditions; (3) noxious mold exposure facilitated by changes in precipitation patterns, farm land restructuring, and more frequent flooding and water intrusion in buildings; and (4) expansions in both the range and quantity of pollen from ragweed and other allergy-linked flora (Ontario Lung Association, 2008). Were this set of factors not sufficient cause for alarm, as argued in this paper, because the respiratory system is a primary body nexus for diverse environmental threats to cluster, intermingle, and multiply their adverse impacts (e.g., diesel fuel droplets and bacteria, allergens and infectious agents), there is a second set of threats to respiratory health also being ushered in by global warming. These threats – termed ecosyndemics – are defined as harmful disease interactions sparked by changing environmental conditions (Baer & Singer, 2008; Singer, 2010a; Singer, Herring, Littleton, & Rock, 2011). Respiratory risks to human health, in short, are on the rise, at least in part, because anthropogenic environmental changes are multiplying the likelihood of consequential respiratory disease comorbidity and interaction. In this light, the immediate objective of this paper is to examine the nature and growing prevalence of ecosyndemics under conditions of mounting environmental imbalance and climate change as exemplified by asthma and

Volume 22, Issue 1, March 2013

Respiratory health and ecosyndemics in a time of global warming

other increasingly frequent respiratory diseases. More broadly, the paper seeks to contribute to increased understanding of the critical role of syndemics in shaping global health and the value of a political ecology of respiratory health perspective in medical anthropology. THE

NATURE OF SYNDEMICS AND

ECOSYNDEMICS

The term syndemic, reflecting a critical biosocial understanding of disease, labels various kinds of harm-enhancing disease interactions that commonly are facilitated directly through the impact of social relations of inequality on health, or indirectly as social inequalities are mediated by environmental conditions (Singer, 2009a; Singer, 2009b; Singer & Clair, 2003; Stall, Friedman, & Catania, 2007). Unequal social relations (variously expressed as impoverishment, stigmatization, structural violence, discrimination, and marginalization) result in exposure to adverse living and working conditions in subordinate populations, which, in turn, promote the clustering of both infectious and non-infectious diseases and both organic and behavioral disorders, while weakening the body’s capacity for responding to disease challenges. An appeal of the syndemics approach within medical anthropology, as Nichter (2008, p. 159) observes, is unification of both an ‘explicit emphasis on examining connections between health and development and its attention to routes of transmission that affect clusters of interrelated health problems’. A syndemic may be unidirectional (one comorbid disease promotes or enhances the transmission, virulence or lethality of another) or bidirectional (each comorbid disease is promoted or enhanced by the co-presence of one or more other diseases), but in all cases is characterized by an increase in the burden of disease in affected populations. Additionally, and of special note with regard to respiratory health, disease interactions can be immediate or delayed. Infection caused by respiratory syncytial virus (RSV), for example, has been found to operate as a predisposing agent for bacterial infection – most commonly Streptococcus pneumoniae and Haemophilus influenzae – in the airways of children (Korppi,

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Leinonen, Koskela, Mäkelä, & Launiala, 1989). The effect of this immediate interaction has been found to be higher rates of pneumonia and acute otitis media in children with mixed RSVbacterial infections compared to children with only bacterial infections. In delayed interaction, the initial disease may predispose an individual to later, perhaps chronic disease, long after the initial disease has resolved. Notably, infection during a critical developmental life period may lead to the reallocation of energy away from the production of crucial immune and inflammatory response capacity (McDade, 2005). Thus, in utero exposure during the 1918 influenza pandemic has been found to have been associated with increased risk for an array of later in life adverse health outcomes, including cancer, hypertension, and heart disease (Almond, 2006). Similarly, early in life infection with RSV has been implicated in the later development of asthma (Openshaw, Dean, & Culley, 2003). In some cases coinfection with two or more diseases can open up multiple pathways of syndemic interaction. For example, a lethal synergism that threatens human respiratory health has been identified between influenza viruses and pneumococcus bacteria, resulting in excess mortality from secondary bacterial pneumonia during influenza epidemics. The bio-mechanisms driving this increase in disease lethality are alterations of the lungs caused by influenza viruses that increase pneumococcus adherence, invasion, and induction of disease. Other consequential changes produced by this interaction, such as an alteration of the immune response that weakens the body’s ability to eliminate pneumococcus, is also suggested by existing research (van der Sluijs et al., 2004). The importance of this syn- ED2 demic interaction is noted by McCullers (2006, p. 571): Influenza virus and Streptococcus pneumoniae rank as two of the most important pathogens affecting humans today. However, it may be their ability to work together that presents the greatest threat to world health.

On the one hand, while being highly sensitive to behavior and social patterns, some


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syndemics (e.g., HIV/TB) are less sensitive to changes in the physical environment. On the other hand, in some syndemics environmental change is critical (Bulled & Singer, 2011). Ecosyndemics – disease interactions that are the specific product of climatic and other environmental changes, commonly as a consequence of human activities – are of particular risk in the time of global warming because of the dramatic and diverse impacts of climate change on local environmental conditions (Singer, 2010a). It is likely that ecosyndemics will result in novel respiratory health profiles in diverse populations as the impacts of global warming, air pollution, and other biosphere changes progress over time. Worsening respiratory health as a consequence of ecosyndemics is likely to be most evident in the kinds of locations and populations that most commonly are studied by anthropologists traditionally, namely poor urban residents, marginalized populations, and groups subjected to environment injustices (Singer et al., 2011). ASTHMA, RHINITIS, AND RHINOSINUSITUS: A GLOBAL ALLERGY-INFECTION SYNDEMIC IN

the most common causes of hospital admission for acute conditions among children. Although more common in developed areas, increases in asthma rates are occurring worldwide, especially among the urban poor (Laurent et al., 2008). Despite the availability of treatments, ‘poorly controlled asthma continues to be reported in developed and developing countries’ alike (Hanania, 2009, p. 2). Increases in the symptom prevalence in Africa, Latin America, and sectors of Asia affirm that ‘the global burden of asthma is continuing to rise’ (Global Initiative for Asthma, 2009, p. 3). According to the United Nation’s Global Initiative for Asthma (Masoli et al., 2004, p. 1): With the projected increase in the proportion of the world’s population that is urban from 45% to 59% in 2025, there is likely to be a marked increase in the number of asthmatics worldwide over the next two decades. It is estimated that there may be an additional 100 million persons with asthma by 2025.

With reference to West Africa, for example, Gbadero, Johnson, Aderele, and Olaleye (1995, p. 739) observe that: With the inevitable atmospheric pollution from increasing urbanisation and industrialisation, paediatric asthma morbidity in the tropics may approach the current ‘epidemic’ proportions of the western world. Acute respiratory infections currently constitute a research priority area worldwide, and justifiably so in the third world where mortality related to acute respiratory infections continues to soar.

THE TIME OF CLIMATE CHANGE

Around the globe, the World Health Organization (2008) estimates that 300 million people currently suffer with asthma, and approximately a quarter of a million people, mostly in low and lower-middle income countries, die of this disease annually. This represents one of every 250 deaths in the world each year. Countries with the highest asthma mortality among 5–34 year olds are: Kazakhstan, Kyrgyzstan, Turkmenistan, South Africa, Azerbaijan, Cuba, Uzbekistan, China, Mauritius and Luxembourg. Asthma often takes a significant toll on the well-being of sufferers. In 2001, asthma was the 25th leading cause of disability-adjusted life years (DALYs) lost. Worldwide, the number of DALYs that annually are lost to asthma is estimated to be 15 million, a level that is similar to diabetes or cirrhosis (Masoli, Fabian, Holt, & Beasley, 2004). Asthma is widespread in developed countries, currently affecting about 8% of the US population (compared to 3% in 1980) and it is one of

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Similarly, in Tijuana, Mexico, along with the creation of numerous foreign-owned factories (maquiladoras) and an increase in air pollution, ‘there has been a dramatic rise in the incidence of childhood asthma’ (Schwartz, 2004, p. 215). Actual patterns of increase in asthma are seen in various local site studies. In the Republic of Malta off the coast of Sicily, for example, the International Study of Asthma and Allergies in Childhood (Montefort, Ellul, Montefort, Caruana, & Agius Muscat, 2009) collected data on asthma symptoms among school children 5–8 years of age in 1994/1995 (‘time one’) and in 2001/2002 (‘time two’). Just over 19% of children reported suffering from wheezing




at ‘time one’ compared to over 30% at ‘time two’; while 8% of the children had been diagnosed with asthma at ‘time one’, the percentage had risen to almost 15 by ‘time two’. Similarly, in Bangkok, Thailand, the ISSAC study found that rates of asthma among children increased fourfold between 1990 and 1997 (Vichyanond, Jirapongsananuruk, Visitsuntorn, & Tuchinda, 1998). Asthma has been called a strange disease because of its heterogeneous expression across patients and uncertain origin involving a mix of genetic factors and environmental exposures (Kaplan & Mascie-Taylor, 1989; Rose & Manderson, 2000). Certain processes, however, tend to central to the disease. When we breathe, air flows into the lungs and through a series of progressively smaller airways, called bronchioles into microscopic sacs (the alveoli) in which oxygen and carbon dioxide are exchanged. Asthma, which disrupts this process, is named after the ancient Greek word for panting. It is defined by the National Heart, Lung & Blood Institute (2007) of the National Institutes of Health as a chronic, noncontiguous inflammatory disorder of the air passages of the lungs characterized by wheezing, breathlessness (dyspnea), chest tightness, and coughing, especially at night and in the early morning. Inflammation is known to cause an increase in bronchial hyperresponsiveness involving exaggerated smooth muscle constriction of the airways (bronchoconstriction) that further limits the flow of air in the lungs. Additional interference with airflow may be caused by the hyper-production of mucous in the lungs caused by the arrival of white blood. The interaction of these constituents of asthma determine the specific clinical manifestations and severity of the disease. Several distinct subtypes of asthma have been described including, intermittent, persistent, exercise-associated, aspirinsensitive, and severe asthma. Over the course of time, repeated inflammatory episodes can cause permanent structural and functional changes in the air pathways, a process called remodeling that causes a persistent narrowing of the airways. A wide range of outdoor and indoor environmental factors have been shown to be triggers


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of asthmatic flare ups, including exposure to tobacco smoke, vehicular emissions, ozone, plant pollens, mold spores, skin cells and hair of common mammalian pets, waste of dust mites and cockroaches, and cold air (Adkinson et al., 2007). Notably, research with middle school children in Taiwan (Guo et al., 1999), found that traffic-related air pollutants, most notably carbon monoxide and nitrogen oxides, are positively associated with the prevalence of asthma. Additionally, there is now considerable evidence, as Murray et al. (2006, p. 376) indicate, that ‘a synergistic interaction [occurs] between allergens and viruses’ in the development of asthma attacks. To assess this syndemic interaction, over a 1 year period Murray et al. (2006) enrolled 84 children ages 3–17 admitted to South Manchester University Hospital in Manchester, UK with an acute asthma exacerbation (i.e., asthma flare up or attack). These index cases were matched for age and sex with two control groups: (1) patients with stable asthma from the outpatient department who were not admitted to the hospital and did not require oral steroids for asthma treatment within the previous 12 months (labeled ‘the stable asthma control group’); and (2) patients admitted to the hospital with non-respiratory conditions (called ‘the inpatient control group’). All control participants were enrolled within 3 weeks of their matched index case. There were no significant differences between the three groups in ethnicity. Information was collected from the parents or guardians of all study participants on the use of medications, housing conditions, deprivation (using a standard index), family health history, parental smoking, presence of pets at home, and history of hospital admissions. Study participants were tested by skin prick for allergic sensitivity to mites, cats, dogs, aspirin, and ryegrass. No significant differences between the groups were found in parental smoking, pet ownership, housing characteristics, and deprivation. Finally, participants were tested for various nasal pathogens, including rhinovirus, enterovirus, coronaviruses, RSV, influenza A and B, parainfluenza viruses 1–3, adenovirus, Chlamydophila pneumoniae and Mycoplasma pneumoniae.


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Findings showed that participants in the case group were at a significantly higher risk of having been both exposed and sensitive to allergens and of having a higher respiratory pathogen load than participants in either of the control groups. Multivariate analysis found that a combination of both risk factors (allergy and nasal pathogens) increased the risk of hospital admission by almost 20-fold. Rhinoviruses (a cause of the ‘common cold’) were the most frequently detected respiratory pathogens, accounting for 81% of viruses detected in the index group. Murray et al. (2006, pp. 381–382) conclude that their results ‘indicate that there appears to be a combined rather than an individual effect of natural virus infection and real life allergen exposure in allergic asthmatic children in inducing asthma exacerbations’. This conclusion is supported by other studies of the role of respiratory viruses in asthma attacks resulting in hospital admissions or emergency room treatment (Duff et al., 1993; Freymuth et al., 1999; Heymann et al., 2004; João Silva et al., 2007; Rakes et al., 1999; Thumerelle et al., 2003). A community study (Johnston et al., 1995) found that viral infection was a precipitating factor in 80% of asthma attacks in school children aged 9–11 years. In the study, rhinoviruses or other members of the Picornavirus family of single stranded, RNA viruses were the source of over 80% of such infections, with members of the Coronavirus family being of secondary importance. Overall, once an individual develops asthma, respiratory pathogens have been found to precipitate as much as 85% of asthma attacks in children and 44% in adults (Johnston, 1998). Consequently, respiratory infections are now seen as a primary trigger of acute asthma events across the life course. While viral respiratory infections are considered to be the most common infectious trigger of acute asthma, some studies (e.g., Brouard et al., 2002; João Silva et al., 2007; Thumerelle et al., 2003) have found other types of pathogens, such as Mycoplasma pneumoniae, a bacteria, may also contribute to asthma attacks. Bacteria (e.g., Chlamydophila pneumoniae) have also been found to be associated with adult onset asthma (Hahn, Dodge, & Golubjatnikov, 1991; Lieberman

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et al., 2003) and with both new-onset wheezing and severity of asthma (Black et al., 2000; Hahn et al., 1991; Sutherland & Martin, 2007; Wark, Johnston, Simpson, Hensley, & Gibson, 2002). In patients with asthma, antibiotic treatment for C. pneumoniae has been found to be effective in reducing asthma symptoms (Hahn, 1995; Kraft, ED3 Cassell, Pak, & Martin, 2002). Thus, Sutherland and Martin (2007, p. 1965) comment that mounting evidence from both human and animal studies ‘suggests that atypical bacterial infection is an important acquired factor in the pathogenesis and clinical expression of asthma’. Notably, because viruses and bacteria have been found to interact with adverse health consequences and are capable of exchanging genetic material (Singer, 2009b), and viruses and bacteria have been found together in nasal swab studies of asthma patients (Harju et al., 2006), biological synergy between different kinds of pathogens may also be a factor in asthma exacerbation. What are the biological pathways of syndemic interaction between allergy and infection? Several experimental studies (Calhoun, Dick, Schwartz, & Busse, 1994; Calhoun et al., 1991; Lemanske, Dick, Swenson, Vrtis, & Busse, 1989) have suggested that the key element in allergy/infection interaction is the enhancement of air pathway inflammation in sensitized individuals simultaneously exposed to allergens and infected with one or more respiratory pathogens. As Calhoun et al. (1994, p. 2207) report, their laboratory ‘observations suggest that viral infection is a critical determinant of [airway inflammation] enhancement’, although other factors, such as greater production of pro-inflammatory cytokines, a component of the immune system, may be operative. In fact, multiple pathways may promote the interaction of allergy and infection in the development and exacerbations of asthma. Note Wark and Gibson (2006, pp. 914–915):


People with asthma may frequently be exposed to more than one trigger, and these appear to interact in the development of asthma exacerbations. In experimental challenge studies, allergen responsiveness is enhanced by exposure to another trigger such as air pollution … or smoking …. A similar effect has been seen with viral infection…



In recent research, exposure to either nitrogen dioxide (NO2) (an air pollutant produced by motor vehicles among other sources), or ozone (O3) (a product of photochemical reactions between NO2 and volatile organic compounds) has been found to enhance viral- and bacterialinduced asthma flare ups (Chauhan et al., 2003; Infante Rivard, 1993). Based on animal models, this research suggests that exposure to these noxious gases plays a role in impairing immune response to respiratory pathogens by limiting the clearance of microbes from the respiratory tract and by altering the function of macrophages during infection (Frampton et al., 1989; Gilmour, Hmieleski, Stafford, & Jakab, 1991; Jakab, 1987). Jakab (1988), for example, found that: (1) the killing of Staphylococcus aureus bacteria in the lung was impaired at the exposure level of five parts per million (ppm) of NO2; and (2) this effect was found at 2.5 ppm or less when NO2 exposure occurred in lungs that were predisposed to lowered resistance by an immunosuppression drug used in the treatment of asthma (corticosteroid). Further, this research demonstrated that the macrophage phagocytic system, which includes cells in the lungs that destroy invading microbes, foreign particles, cancerous or diseased cells, and cellular debris, is the defense component of the lungs that is most susceptible to the adverse effects of air pollutants. To examine the appropriateness of extrapolating these findings to human populations, Chauhan et al. (2003) enrolled a Southampton, UK sample of 114 children (63 boys and 51 girls), 8–11 years of age, with asthma and recorded their daily upper and lower respiratory tract symptoms. Additionally, peak air flow (a standard objective gage of respiratory capacity) and NO2 exposure were measured weekly for up to 13 months. Nasal swabs were also taken during upper respiratory tract sickness events and tested for both common respiratory virus and atypical bacteria. The study found a significant association between increased exposure to NO2 and the severity of viral-induced asthma flare ups. High exposure to NO2 in the week prior to an upper respiratory infection was associated with either more intense symptoms or reductions in measured peak air flow.


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While a better understanding is needed of the precise ways and under what conditions respiratory infections of various kinds interact with allergens (and with other infections) in the development, symptoms, and impact of asthma, it is evident that syndemic interaction of this sort plays a significant role in this increasingly common respiratory syndrome. Pluralea interface between global warming and other forms of air pollution (Noyes et al., 2008; Singer, 2009a), which impacts the production of allergens, exposure to airborne toxins, and the diffusion of pathogens, may be a primary factor in the rising rates of asthma around the world. Syndemic interaction also is known to occur between asthma and other respiratory conditions, including rhinitis and rhinosinusitis. In the United States, approximately 20% of the population is afflicted with rhinitis, an irritation and inflammation of internal nose tissues (Spector, 1997). The ISAAC study found that, like asthma, there are rising rates of rhinitis in various parts of the world (Kabir, Rahman, Hassan, Ahamed, & Mridha, 2005; Montefort et al., 2009; Munivrana et al., 2005; Vichyanond et al., 1998). Rhinitis is caused by either bacterial infection or respiratory allergy, or, like asthma, interaction between pathogenic infection and allergic reaction to airborne irritants. The primary symptom of rhinitis is nasal dripping (runny nose), but the condition commonly also involves nasal congestion, and post-nasal drip. Rhinitis has also been found to adversely affect sleeping, ear health, school performance and learning, and overall quality of life (Vuurman, van Veggel, Uiterwijk, Leutner, & O’Hanlon, 1993). Summarizing the connection between rhinitis and asthma described in the literature, Leynaert, Neukirch, Demoly, and Bousquet (2000, p. S201) observe, Several studies have identified rhinitis as a risk factor for asthma, with the prevalence of allergic rhinitis in asthmatic patients being 80% to 90%. These studies and others demonstrate that the coexistence of asthma and allergic rhinitis is frequent, that allergic rhinitis usually precedes asthma, and that allergic rhinitis is a risk factor for asthma.


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Rhinosinusitus, inflammation of the sinus, also is a frequent disease, affecting over 14% of the population in the United States, where it one of the most common medically reported diseases (accounting for almost 12 million physician office visits per year), and like asthma, the frequency of this disease is increasing. Rhinosinusitus is now the fifth most frequent medical diagnosis involving the prescription of antibiotics (Smart & Slavin, 2005). Symptoms include prolonged nasal congestion and discharge, headache, facial pain or pressure, and possible reduction in olfactory capacity. Evidence for a syndemic relationship with asthma dates to the 1920s and 1930s, with studies that identified rhinosinusitis as an asthma trigger. More recent research by Bresciani et al. (2001) found that 100% of patients with severe asthma had abnormal sinus CT scans, while 88% of those with mild to moderate asthma had abnormal scans. Based on a review of the literature available at the time, Slavin (1992, p. 536) concluded that ‘sinusitis occurs not only in association with bronchial asthma but may also play a role in its pathogenesis’. More recently, the perspective has emerged that asthma, rhinitis and rhinosinusitis are all disease expressions along parallel inflammatory pathways linking the upper and lower respiratory systems and hence ‘may be progressive manifestations of a common disease process’ (Dixon, 2009, p. 23). RESPIRATORY

ECOSYNDEMICS IN

SOCIAL CONTEXT

Rising rates of respiratory disease and their adverse syndemic interactions reflect: (1) the ever expanded capacity of human societies to reshape the physical environment; (2) the nature of the social hierarchies and processes that drive these changes and facilitate resistance to the mitigate of environmental degradation; and (3) the health consequences of social disparities and environmental injustice, each of which is discussed in turn below. The growing dangers of our anthropogenic environment As Linden (2007, p. 3) observes, it is hard for some people ‘to imagine that we puny humans could affect something so all-encompassing as

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climate itself’. Indeed, global warming deniers often question the ability of our species to alter nature in a way that might diminish the stability of human life on the planet. Yet, as environmental anthropologist Moran (2006, p. 21) emphasizes, there is overwhelming scientific evidence that human activities ‘inadvertently trigger abrupt changes in the Earth system with consequences that we can only faintly imagine’. The environmental effects of human behavior are well illustrated in the Atlas of Our Changing Environment (United Nations Environment Program, 2008) which uses aerial photography and satellites images to reveal the multiple, simultaneous, and often drastic local changes that have occurred on the surface of the planet over the last 30 years. Notably, during the last quarter of the 20th century, the urban population of the planet jumped from 1.5 to 2.8 billion people (or about half of the total human population). Approximately one third of this rapidly expanding urban population (i.e., 924 million people) lives in poverty in crowded and often ecologically hazardous shantytowns with substandard housing, limited access to clean water and sanitation services, and high levels of exposure to polluted air. Driving this process, as Cohen (2004, p. 24) stresses, is ‘a new global economy that is literally changing the face of the planet’, including ‘ecological poverty’ (i.e., the loss by small farmers of entitlement to the natural resource base of traditional agriculture) (Davis, 2001), agribusiness restructuring of the land, the emergence of a global market that adversely impacts commodity pricing (e.g., for exported food produced by small farmers), and neoliberal policies that restrict access among the urban poor to government services and jobs, low-cost staple foods, and health care. The result has been the movement of large numbers of people from rural to urban areas, the emergence of a growing array of megacities (places with populations over 10 million people), and other large urban centers in which many people, like the residents of an Argentine shantytown described by Auyero and Swistun (2009), are exposed to toxins like sulfur dioxide, volatile organic compounds, particulate




matter, nitrous oxides, and carbon monoxide released into the environment by corporate manufacturers. Another of the critical environmental changes referred to by Moran is deforestation. While geological evidence suggests that 8,000 years ago forests covered about half of the plant’s land surface, this has fallen to 28% today as a result of a deforestation rate of 94,000 km2 per year (Barnéoud, 2010). According to the World Rainforest Movement (1988), ‘The most important direct causes of deforestation include logging, the conversion of forested lands for agriculture and cattle-raising, urbanization, mining and oil exploitation, acid rain and fire’. At the same time, ocean, lake, and river coastal regions – areas that both contain over 50% of the world’s human population and are critical centers of global economic activities and trade – ‘are becoming overpopulated, overexploited and their fragile balance is under threat’ (Barnéoud, 2010). Similarly, wetlands and mangroves – critical in climate stabilization, atmospheric carbon balance, flood and drought control, preservation of biodiversity, and water purification – are being destroyed by human activity (especially corporate farming) at a rapid, and in many parts of the world, intensifying, pace. It has been estimated at 50% wetlands that existed in 1,900 are already gone (Dugan, 1993). Desertification and the persistent degradation of dryland ecosystems, processes largely caused by unsustainable human land use practices and anthropogenic climate change, are additional examples of dramatic environmental changes directly or indirectly caused by human practices. Desertification, which impacts almost half of the world’s countries and threatens the livelihoods of some of the poorest populations on the planet, causes an annual loss of about 30 million acres of arable land (International Fund for Agricultural Development, 2009). Beyond surface changes, global air pollution and global warming also cause profound restructuring of the ‘natural’ environment, both on their own and through interaction with other ecocrises and, as discussed above, directly impact respiratory health. Changes in air quality and the


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release of greenhouse gases are tied to practices like ‘the existence of massive corporate support for the ongoing use of motor vehicles’ (Baer, 2009). In Hong Kong, for example, the primary source of street-level air pollution is vehicles, accounting in 1999 for 58% of particulate emissions (Stern, 2003). Ecocrises and social relationship This discussion of anthropocentric environmental changes that foster respiratory and other diseases, confirms Kirsch’s (2006, p. 129) conclusion that ‘pollution is a social relationship not simply an environmental issue’. As a result, there has emerged a need for analytic focus on what Roberts and Parks (2006, p. 118) call ‘“the polluting elites” who direct leading sectors of their economies and exercise disproportionate control over national and foreign environmental policies’ and practices. Thus, Stern argues that the exposure to and consequences of air pollution in Hong Kong reflect relations among unequal social classes: ‘everyone does not breathe the same air. Hong Kong’s poor both suffer increased exposure to air pollution and bear a heavy share of the economic costs of poor air quality’ (Stern 2003, p. 786). The same pattern obtains for blue and white collar workers in Hong Kong. The former group, including bus and taxi drivers, vendors and construction workers, is more likely to work outdoors and is significantly more likely as a result to suffer more frequently from pollution-related respiratory conditions like asthma, throat irritation, and eye/nasal allergies compared to the latter group, which is more likely to work in office buildings with filtered air. Moreover, while suffering fewer of the consequence of air pollution than poor or working people, because of their ‘ownership of cars, industry, and power plants, Hong Kong’s rich generate a significant portion of overall emissions’ (Stern, 2003, p. 791). Similarly, Namdeo and Stringer (2008), in their research on air pollution in Leeds, UK found that politically and economically disadvantaged social groups are disproportionately exposed to higher NO2 levels, while a national study in the U.K. reported that communities that have the


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lowest per capita ownership of cars suffer from the highest levels of air pollution while those with the highest rates of car ownership tend to have the cleanest air (Mitchell & Dorling, 2003). Parallel patterns have been described worldwide with a range of contaminants (Chaix et al., 2006; Perlin, Sexton, & Wong, 1999; Yamazaki, Nitta, Murakami, & Fukuhara, 2005). As has been found to be the case with greenhouse gases or other toxic waste, those who are most responsible for production are the best protected from exposure and consequent health effects, and vice versa (Baer & Singer, 2008; Checker, 2005). Environmental injustice and respiratory health Charles Dickens, one of the most popular English novelists during the Victorian era and a significant literary influence ever since, was a lifelong sufferer of asthma (Cohen, 1997). Dickens (1812–1870) grew up in London during the take-off phase of the industrial revolution when the air in the city was dank with the foul pollution of numerous unregulated smoke stacks. Reflecting the impact of living in this noxious environment, many asthmatic characters appear in Dickens’ novels, including Mr. Omer in David Copperfield and Mr. Sleary in Hard Times. Indeed, it was only the use of opium (prescribed by his physician) that allowed Dickens to sufficiently control his symptoms to remain a productive author. It is perhaps through his suffering with asthma, however, that Dickens, a noted critic of social inequality, developed some of his celebrated empathy for the poor and oppressed, social strata disproportionately afflicted with asthma and other respiratory tract diseases. As Chen et al. (2009, p. 38) indicate, Across all social factors, low socioeconomic status (SES) exhibits one of the strongest and most consistent associations with morbidity and mortality across a wide range of diseases, including childhood asthma. In particular, children with asthma from a low SES background suffer from more frequent hospitalisations, emergency department visits and more functional impairment (e.g., activity limitations, days spent in bed) compared with children from a higher SES background.

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The role of social and economic inequality in the distribution of respiratory health is reflected, in developed countries, in clear ethnic differences in rates of asthma (Canino et al., 2006). In the United States, Lara, Akinbami, Flores, and Morgenstern (2006) found that Puerto Rican children have a higher prevalence of lifetime asthma (26%) as well as recent asthma attacks (12%) than Mexican American children (10 and 4%, respectively), non-Hispanic Black children (16 and 7%, respectively), and non-Hispanic white children (13 and 6%, respectively). One consequence of this pattern is later in life health problems that contribute to the intergenerational transmission of health inequalities (Dowd, Zajacova, and Aiello, 2009). Moreover, despite the influence on the frequency of asthma diagnoses of pharmaceutical companies that manufacture asthma medications (Whitemarsh, 2008), the full extent of the asthma problem among the poor and other disadvantaged groups may be miscalculated because ‘patients’ families, and patients’ physicians frequently underestimate the severity of asthma’ (Speir, 2000, p. 8). CONCLUSION There is a widespread cultural linkage of breathing with the essence of the human soul or spirit. Thus, Genesis 2:7 of the Bible reads: ‘And the Lord God formed man [of] the dust of the ground, and breathed into his nostrils the breath of life; and man became a living soul’. The generally recognized importance of breath is reflected as well in ethnomedical healing activities, such as the practice of Qigong, therapeutic breathing, in Traditional Chinese Medicine. Through our own behaviors and our interactions with the environment, however, the ability of humans to breathe is being put at increasingly grave risk. For a growing number of people around the world, especially those from disadvantaged sectors, gasping for breath, because of asthma, chronic obstructive pulmonary disease, tuberculosis, lung cancer, or other environment-sensitive respiratory health conditions, has become a painful daily experience. The purposes of this paper have been to examine the role played by syndemic




interaction among diseases in worsening patterns of global respiratory health, to review anthropogenic causes of environmental disruption and degradation that facilitate the development of respiratory disease syndemics, and to describe the specific importance of social inequality in shaping human impacts on the environment and resulting respiratory ecosyndemics. Elsewhere (Singer, n.d.), I examine interactions between global warming and other kinds of manufactured pollution in creating an array of risks to respiratory health. The current paper adds to this line of analysis by examining the role of ecosyndemics as an additional factor in the increasing global risk to respiratory health, using asthma and related diseases to illustrate the ways in which anthropogenic environment changes in interaction with human political economies are multiplying the burden of respiratory disease within and across societies. In light of the mounting danger of environmental catastrophe, it is the premise of this paper that the tomorrow of medical anthropology will be determined by the effectiveness of our response to anthropogenic environmental threats to health and well-being. There is, as a result, an applied and theoretical need to (finally) fully heed Nader’s (1972) call ‘to study up’ by examining structural factors in the development of ecocrises. At the same time, there is a parallel need to focus both on the ways social inequalities construct environmental health injustices and on the experiences, understandings, and conceptual and behavioral responses of disadvantaged and subordinated populations to the experience of maltreatment (Brown et al., 2003; Checker, 2005). A macromicro/political ecology of health lens of this sort offers medical anthropology a strategy for impacting health in a changing environment by providing a framework for understanding ecosocial pathways to deteriorating environmental health conditions and addressing deficiencies in public health infrastructure and planning in an era of enhanced chemical, biological, and social stressors as a consequence of global warming.


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ACKNOWLEDGEMENT The author expresses his appreciation to Nicola Bulled for her comments on an earlier draft of this paper. REFERENCES Adkinson, F. N., Yunginger, J., Busse, W., Bochner, B., Simons, E., & Holgate, S. (2007). Middleton’s allergy: Principles and practice (6th ed.). St. Louis, MO: Mosby Elsevier. Almond, D. (2006). Is the 1918 influenza pandemic over? Long term effects of in utero influenza exposure in the post 1940 U.S. population. Journal of Political Economy, 114(4), 672–712. Auyero, J., & Swistun, D. (2009). Flammable: Environmental suffering in an Argentine Shantytown. Oxford, England: Oxford University Press. Baer, H. (2009). Environmental and health consequences of motor vehicles: A case study in capitalist technological hegemony and grassroots responses to it. In M. Singer & H. Baer (Eds.), Killer commodities: Public health and the corporate production of harm (pp. 95–118). Landham, MD: AltaMira. Baer, H., & Singer, M. (2008). Global warming and the political ecology of health: Emerging crises and systemic solutions. Walnut Creek, CA: Left Coast Press. Barnéoud, L. (2010). Cartography: What impact does human activity have on the planet? Science Actualités. Retrieved from http://www.cite-sciences.fr/ francais/ala_cite/science_actualites/sitesactu/question_actu.php?langue=an&id_article=4303. Beggs, P., & Bambrick, H. (2005). Is the global rise of asthma an early impact of anthropogenic climate change? Environmental Health Perspectives, 113(8), 915–919. Black, P., Scicchitano, R., Jenkins, C., Blasi, F., Allegra, L., Wlodarczyk, J., & Cooper, B. (2000). Serological evidence of infection with Chlamydia pneumoniae is related to the severity of asthma. European Respiratory Journal, 15, 254–259. Bresciani, M., Paradis, L., Des Roches, A., Vernhet, H., Vachier, I., Godard, P., … Chanez, P. (2001). Rhinosinusitis in severe asthma. Journal of Allergy and Clinical Immunology, 107, 73–80. Brouard, J., Freymuth, F., Toutain, F., Bach, N., Vabret, A., Gouarin, S., … Duhamel, J. F. (2002). Role of viral infections and Chlamydia pneumoniae and Mycoplasma pneumoniae infections in asthma in infants and young children. Epidemiologic study of 118 children. Archives de Pédiatrie, 9(Suppl. 3), 365s–371s. Brown, P., Mayer, B., Zavestoski, S., Luebke, T., Mandelbaum, J., & McCormick, S. (2003). The


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Accepted 13 August 2012

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Loss and Grief in Family Settings – Lawrie Maloney 117 pages – October 1998 http://jfs.e-contentmanagement.com/archives/vol/4/issue/2/ marketing/

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Please check the inclusion of short running title ‘Respiratory health and ecosyndemics in a time of global warming’ is fine. ‘van der Sluijs, 2006’ has been changed to ‘van der Sluijs et al., 2004’ as per reference list. ‘Hahn et al., 1995’ has been changed to ‘Hahn, 1995’ as per reference list. Please cite ‘George et al., 2006’ inside the text. Please provide Last page details for the reference ‘Jacobson, 2008’. Please cite ‘Rossi et al., 1994’ inside the text. Please cite ‘Singer, 2009c’ inside the text. Please cite ‘Singer, 2010b’ inside the text.