Open access peer-reviewed chapter - ONLINE FIRST

Malnutrition and Air Pollution in Latin America: Impact of Two Stressors on Children’s Health

Written By

Melisa Kurtz, Christian Lezon, Patricia Boyer and Deborah Tasat

Submitted: January 7th, 2022 Reviewed: March 24th, 2022 Published: May 6th, 2022

DOI: 10.5772/intechopen.104656

Malnutrition Edited by Farhan Saeed

From the Edited Volume

Malnutrition [Working Title]

Dr. Farhan Saeed, Dr. Aftab Ahmed and Mr. Muhammad Afzaal

Chapter metrics overview

4 Chapter Downloads

View Full Metrics


Nowadays, the evolution of the concept of nutrition has acquired a notion of three concurrent dimensions. Nutrition was considered an exclusively biological process while now, it comprises social and ecological aspects. Inadequate nutrition and air pollution are two major nongenetic environmental factors known to cause serious public health problems worldwide. Air pollution does not impact in the same way on the population at large, being particularly the children one of the most vulnerable subpopulations. Additionally, the nutritional status may modify the susceptibility to air pollution exposure and cause a wide range of acute and chronic cardio-respiratory diseases. Moreover, undernutrition is identified as a major health problem with devastating healthcare effects on the individual, social, and economic development. On a global scale, chronic undernourishment affects 144 million children younger than 5 years. However, the mechanism linking undernutrition and air pollution exposure still remains unclear. At present, only few epidemiological studies have been reported associating child malnutrition and air pollution. Therefore, a better understanding of the interactions between undernutrition and air pollution exposure is needed to guide action by individuals and governments.


  • malnutrition
  • air pollution
  • children
  • health

1. Introduction

From a holistic health perspective, the new concept of “nutrition” combines biological, social, and environmental dimensions as determinants of individual and collective health. The concept of “three-dimension nutrition” considers nutrition as a highly complex multidisciplinary approach to addressing health problems [1].

Thus, the concepts of nutritional adequacy and malnutrition are determined by three concurrent dimensions—(1) a biological dimension, which understands nutritional adequacy as an indispensable condition whereby the specific nutritional requirements of each stage of life are met; (2) a social dimension involving cultural factors, such as religion and education, and economic factors as determinants of eating habits; and (3) an environmental dimension, which comprises climate and geographic conditions associated with production, availability, and access to foods [1].

Inadequate nutrition and air pollution are two major nongenetic environmental factors that negatively affect body growth [2, 3]. In their 2003 report Framework for Cumulative Risk Assessment, the US Environmental Protection Agency (EPA) proposed a health risk analysis considering the combined effect of different types of stressors, including physical, chemical, biological, psychological, and social stressors, which together with the nutritional factor affect children’s respiratory system—the main target of air pollution.

There are studies reporting an association between inadequate nutrition and exposure to air pollution, suggesting that the nutritional factor can act as a stressor compromising response to pollution-related stressors [4, 5, 6, 7].

Indeed, environmental influences during prenatal and postnatal life can result in alterations in the normal patterns of epigenetic modification [2, 8]. An unbalanced diet can lead to hypomethylation, which in turn can cause genomic and chromosomal instability [2]. It is known that methyl groups are acquired through the diet and are donated to the DNA via the folate and methionine pathways. In short, qualitative-quantitative diet variations can trigger metabolic and/or neuroendocrine dysfunctions that negatively affect body growth and development, mainly during critical periods of growth, with the ensuing risk of developing diverse diseases in adulthood.

It is well documented that air pollution has devastating adverse effects on human health and is currently a significant problem that not only jeopardizes the health of thousands of millions of people [9] but also degrades the Earth’s ecosystems, undermines the economic security of nations, and is recognized as one of the main causes of disease, disability, and premature death in the world.

Lave and Seskin were among the first to demonstrate a significant association between air pollution and child death due to environment-related respiratory diseases in their study across 117 U.S. metropolitan areas [10]. Although more recent studies conducted by our research group using a model that reproduces a condition of chronic human undernutrition showed that undernourished children are potentially a high-risk group [11], there is little information on the impact of the local and systemic effect of airborne particulate matter on undernourished children (Table 1).

Pub med searchNo of publications
Infant AND [(malnutrition) OR (undernutrition)]24,710
Infant AND [(air pollution) OR (particulate matter)]6543
[(air pollution) OR (particulate matter)] AND [(malnutrition) OR (undernutrition)]252
Infant AND [(air pollution) OR (particulate matter)] AND [(malnutrition) OR (undernutrition)]71

Table 1.

Search syntax used and bibliography obtained from PubMed database.

Air pollution and undernutrition are considered a threat to world public health. Nevertheless, these risk factors can be decreased through governmental, educational, and political interventions aiming to prevent disease in the population at large, particularly in children—a vulnerable subpopulation.

The present bibliographical review study has been elaborated from a search of works published in the PubMed database. It may be accessed through several interfaces, including PubMed, Ovid Medline, and EBSCO Medline. The PubMed interface is available to anyone with an Internet connection; the Ovid and EBSCO interfaces require a subscription, either through a library or a personal account, so herein we chose to use the PubMed platform. PubMed® comprises more than 33 million citations for biomedical literature from MEDLINE, life science journals, and online books.


2. Malnutrition worldwide

2.1 Definition and classification

The World Health Organization (WHO) defines malnutrition as deficiencies, excesses, or imbalances between a person’s intake of energy and/or nutrients and his/her body requirements for proper growth, maintenance, and function.

Malnutrition comprises three physiopathological conditions—(1) (a) wasting defined as low weight for normal height for age, (b) stunting, defined as low height for age whether (normal weight for height) or not (low weight for height), and (c) underweight, defined as low weight for age; (2) micronutrient deficiencies associated with inadequate intake of vitamins and/or minerals; and (3) overweight and obesity [12, 13].

Children with wasting are dangerously thin, and their immune system is weak [14]. Delayed growth impairs both physical growth and cognitive development and increases the risk of death due to common infectious diseases [15].

Insufficient intake of vitamins A and D, iron, calcium, and zinc can severely compromise the health and development of entire populations across the globe, especially children and pregnant women in low-income countries [16, 17, 18, 19].

Worldwide, being overweight is associated with a higher intake of foods containing sugars and fats and lower physical activity levels. Its long-term consequences include cardiovascular disease, type 2 diabetes, and other metabolic diseases [20].

2.2 Nutritional insecurity

It is important to point out that the different forms of malnutrition can be aggravated by nutritional insecurity associated with poor health care, lack of safe drinking water and sanitation, poor housing conditions, and environmental crises, among other factors [21].

According to the 2021 State of Food Security and Nutrition in the World annual report prepared by the Food and Agriculture Organization of the United Nations, between 720 and 811 million people in the world faced hunger in 2020, 161 million more than in 2019 when considering the upper bound of the projected range. Of the total 768 million people facing undernutrition in the world, 282 million are in Africa and 60 million are in Latin America and the Caribbean. Thus, compared with 2019, 46 million more people in Africa, 57 million more in Asia, and almost 14 million more in Latin America and the Caribbean were affected by hunger in 2020.

Whereas the global prevalence of moderate and severe food insecurity has been increasing slowly since 2014, the estimated increase in 2020 was equal to that of the last 5 years combined. Almost one-third of the world population (2370 million people) did not have adequate access to food in 2020, nearly 320 million people more in only 1 year. The increase in food insecurity was more marked in Latin America (9%) and the Caribbean and Africa (5.4%) than in Asia (3.1%). No region in the world escaped this trend, including North America and Europe, where these figures increased for the first time since 2014. The high cost of healthy nutrition and the persistence of high poverty levels and low incomes have resulted in poor access to healthy foods for millions across the world.

The gender gap in the prevalence of moderate and severe food insecurity has increased at the global level and is 10% higher among women than men.

The COVID-19 pandemic has had a devastating impact on the global economy, triggering a recession unseen since the Second World War and affecting food security and the nutritional state of millions of people, including children. Although the impact of the COVID-19 pandemic cannot yet be determined precisely due to limitations in obtaining information, it is estimated that 22% (1492 million people) of children under the age of 5 years showed stunting, 6.7% (45.4 million) suffered wasting, and 5.7% (38.9 million) were overweight. The increase in food insecurity would seem to indicate that these figures continued to rise in 2021.

2.3 Undernutrition in Latin America

The prevalence of stunting and wasting among children under the age five years old is as follows: America: 5.6 million (2.93%), Africa: 70.2 million (36.8%), Europe: no data, Asia: 110.8 million (58%), and Australia/Oceania: 0.7 million (0.37%). Specifically, regarding the 5.6 million stunted and wasted children under 5 in America, 4.9 million (87.5%) live in Latin America and the Caribbean, and the remaining 0.7 million (12.5%) live in the US and Canada [22].

According to data on the prevalence of wasted and stunted children under the age of 5 in Latin America collected by the WHO from studies conducted in different periods, the prevalence of stunting among children under 5 was higher than 30% in Bolivia, Ecuador, Guatemala, Haiti, Honduras, and Peru, and less than 10% in Argentina, Cuba, and Costa Rica [23, 24]. The prevalence of stunting was lowest in Argentina (8.5%) and highest in Guatemala (54%). Wasting, a clear indication of severe undernutrition was highest in Haiti (20%), Honduras (13.1%), and Guatemala (18%). Prevalence was low in the remaining countries, ranging between 2.5 and 3.0% [23]. Significant surveys from 10 Latin American countries, namely Argentina, Bolivia, Brazil, Colombia, Chile, Ecuador, Guatemala, Mexico, Peru, and Uruguay conducted between 2005 and 2017 evidenced that children aged <5 years and women of reproductive age (11–49 years) were vulnerable population subgroups at high risk of all forms of malnutrition. Stunting and anemia were more prevalent among low-income and less-educated populations. Of note, Guatemala, Bolivia, and Peru had the highest stunting and anemia prevalence and the largest economic and social inequalities [24].


3. Air pollution worldwide

To a greater or lesser extent, we are all exposed to environmental pollution, and its impact on health can occur at all stages of life, from conception to old age.

Air pollution is a worldwide phenomenon and an inescapable part of modern life throughout the world. According to the World Health Organization [25], air pollution represents the largest environmental risk to global health. As shown by 2019 WHO report, 99% of the world population does not breathe clean air, and more than half the urban population is exposed to air pollution levels more than 2.5-fold higher than air quality standards. Ambient (outdoor) air pollution in both cities and rural areas was estimated to cause 4.2 million premature deaths per year. In addition to outdoor air pollution, indoor smoke is a serious health risk. In 2016, 3.8 million premature deaths were attributable to household air pollution, mainly due to the burning of biomass, kerosene fuels, and coal in inefficient stoves. Almost all of the burden was in low-middle-income countries.

Nevertheless, ambient pollution is a problem in a lot of high-income countries. Some European populations, such as those living in the United Kingdom, Germany, and France, are exposed to air pollution levels that exceed the health-based air quality guidelines set by the WHO [26]. It is estimated that even in cities where Particulate Matter (PM) concentration is within WHO air quality standards, exposure to anthropogenic PM decreases average life expectancy by 9 months [9].

At present, outdoor and indoor air pollution combined account for 7 million deaths worldwide [27].

In this context of rapid growth in population and urbanization and the challenges associated with technological and economic development and the consequent changes in land use, energy use, and transportation, careful urban planning and efficient city governance are paramount to ensure the provision of food, housing, and services while minimizing the impacts of urbanization and industry on anthropogenic and biogenic emissions that degrade air quality [28, 29, 30].

3.1 Definition and classification

Ambient air pollution is defined as the presence of substances in the atmospheric air at concentrations that can pose a risk to or damage the safety of people and the environment. Outdoor air pollution is a complex mixture of thousands of components, and from a health perspective, the important components of this mixture include airborne particulate matter (PM) and gaseous pollutants: Ozone (O3), Nitrogen Oxides (NOx), Volatile Organic Compounds (VOCs), Carbon monoxide (CO), and Sulfur Oxides (SOx). In 2006, the Environmental Protection Agency (EPA) set the National Ambient Air Quality Standards (NAAQS) for six major pollutants, including particulate matter (PM10 and PM2.5) and ozone [31]. These air pollutants can originate from natural and anthropogenic sources. The main natural sources are volcanic eruptions, forest fires, and sand and dust storms and are usually extreme and sudden events. Pollutants generated by anthropogenic activity are released continuously and persistently into the atmosphere and are mainly generated by burning petroleum and biomass fuels [32]. Particulate matter (PM) is defined as the material suspended in the air in the form of solid particles or liquid droplets. PM is generated through the burning of fossil fuels (diesel, gas, methane, and coal) in vehicles, industry, and households [33]. The adverse health effects of PM inhalation are mainly associated with the size and physical-chemical characteristics of the particles [34]. Particles can be classified into three main groups according to their aerodynamic size—coarse particles (diameter ≥2.5 and <10 μm), fine particles (diameter ≥0.1 and <2.5 μm), and ultrafine particles (<0.1 μm). Resuspension of soil and road dust by wind and moving vehicles, tire wear, construction work, and industrial emissions are the main sources of coarse particles (PM10). Fine particles (PM2.5), composed of elemental carbon, transition metals, complex organic molecules, sulfate, and nitrate, result from combustion processes. Fine particles can travel great distances (> 100 km), which can potentially lead to high concentrations over a wide area. In 2013, the International Agency for Research on Cancer (IARC) established that PM in outdoor air is carcinogenic to humans (Group 1) and causes lung cancer [35].

PM concentration is expressed as mg/m3. Different organizations have established air quality guideline values set to protect human health. Nevertheless, values differ, and WHO limits are generally stricter than the comparable politically agreed EU standards. The recently revised WHO air quality standards [36] are below those established in 2005 [37].

Even when below recommended levels, PM and O3 are linked to respiratory and cardiac morbidity and mortality, increased hospital visits, and a higher risk of adverse birth outcomes [38, 39, 40, 41, 42]. It is important to point out that the established standards cannot fully protect human health since there is no safe lower threshold of PM. Strong scientific evidence shows the negative impact of PM2.5 exposure on health [39, 43]. Particularly regarding PM2.5, long-term exposure to levels above recommended guidelines results in an increase in total, cardiopulmonary, and lung cancer mortality [44, 45, 46, 47].

3.2 Urban air pollution in Latin America

Air pollution is the largest and most persistent environmental and public health concern in Latin America and the Caribbean, where socioeconomic gradients among and inequalities within countries aggravate the impact of environmental degradation, generating different patterns of emissions and increasing exposure to pollutants and vulnerability to climate change [48, 49]. The percentage of the urban population in Latin America and the Caribbean is as high as 81%. The region is currently considered the second most urbanized region in the world, after North America [50]. These densely populated areas (medium-sized cities; 1–5 million inhabitants, large cities: 5–10 million inhabitants, and megacities: over 10 million inhabitants) are responsible for a significant amount of pollutants emitted into the atmosphere that does not necessarily remain in urban regions and can be transported over large distances, depending on the type of substance, weather conditions, topographical characteristics, etc. Cities thus contribute to background concentration in the whole hemisphere [49].

The most affected populations are located in urban areas and developing countries. The number and size of megacities in the world have increased dramatically over the last six decades—from 751 million to 4.2 billion in 2018 [49], accounting for 55% of the world population. It has been estimated that by 2050, this percentage may increase to 68% [50].

Megacities are defined as large city metropolitan areas with over 10 million inhabitants [51]. However, megacities also include high-density metropolises where more than 5 million inhabitants work, live, and commute [52]. Three of all 33 megacities, characterized as such according to the latter definition, are located in South America: Rio de Janeiro in Brazil (12.83 million people), Buenos Aires in Argentina (15.02 million), and São Paulo in Brazil (20.83 million). In 2014, megacities accounted for 12% of the world’s urban population, while large cities had 8%. In Latin America, Bogotá (Colombia) and Lima (Peru) recently reached 10 million, with 10.6 and 10.4 million inhabitants, respectively. Santiago (Chile), considered a large city, has 6.7 million inhabitants [50, 51].

Few studies have evaluated and compared regional trends of annual concentration of regulated air pollutants in South America. The main obstacles to conducting these comparative studies include the great variability in pollutant measurement techniques and protocols and the difficulty of access to information. In 2013, and for the first time since 1997, data on air pollutant concentration in 21 Latin American cities with more than one million inhabitants were gathered to establish the air quality status (baseline 2011) and trends [53].

It is important to point out that environmental pollution disproportionately affects low- and middle-income countries, with almost 90% of pollution-related deaths occurring in underdeveloped countries. In developed countries, the impact of air pollution is highest among minorities and cities with large underserved populations.

3.3 Air pollution: impact on human health

Air pollution causes a wide range of adverse health effects. As shown by toxicological and epidemiological studies across the world, it is mainly associated with an increase in cardiorespiratory metabolic diseases and cancer morbidity and mortality [54, 55, 56]. A number of variables including the use of energy, transportation, and socioeconomic factors play a major role in the generation of air pollutants. The Harvard “Six Cities” study [57] published in the 90’s was one of the first to show the lasting positive association between long-term exposure to air pollution and mortality.

Airborne PM enters the body through the skin, eyes, and respiratory mucosa. As to particle size, fine (PM2.5) and ultrafine (PM0.1) PM are considered the most deleterious to health due to their larger surface-to-volume ratio and thus greater potential to adsorb organic and inorganic compounds [58]. In addition, PM2.5 can penetrate the respiratory tract more deeply, inducing immune cell responses and morphological-functional alterations in the respiratory mucosa.

PM has adverse effects on the respiratory tract, and its main target cells are epithelial cells and lung phagocytes [59, 60]. These fine and ultrafine particles can deposit and remain in the lung alveoli over long periods of time [61]. The mucociliary clearance system is the first line of defense against exogenous agents. Mucus secretion by caliciform cells is an important factor in clearing particles from the airways but can be affected by a number of environmental factors. The latter are the main molecules that induce oxidative stress and subsequent damage to the lung [62].

Among lung phagocytes, alveolar macrophages (AM) play a key role in the biological response to air pollution.

Regarding the chemical composition of PM, metals in PM greatly contribute to the generation of reactive oxygen and nitrogen species (ROS and NOS). The latter are the main molecules that induce oxidative imbalance and subsequent damage to the lung [63, 64, 65], heart [66], and liver [67].

In addition to ROS and NOS generation, PM induces alveolar macrophage release of several mediators, including pro and anti-inflammatory interleukins (IL-1, IL-6, TNF-α e IL-10), mitogenic factors, and chemokines [68, 69, 70]. These mediators are responsible for tissue immune cell recruitment and activation [71]. This biological response involves activation of intracellular signaling pathways and transcription factors such as NFκB and Nrf2 involved in inflammatory tissue response and regulation of antioxidant genes (phase II detoxification) [72, 73]. Moreover, fine and ultrafine PM can evade this first line of defense and penetrate the alveolar-capillary barrier, thus entering the circulatory and lymphatic systems [74, 75, 76] and causing adverse effects at the systemic level and in distant organs.

It has been posited that the mechanisms through which PM exerts systemic effects include—(1) the release of pro-inflammatory and pro-oxidant mediators in the lung; (2) an imbalance in the autonomic nervous system, favoring sympathetic tone through the afferent nerves in the upper airways and/or lung; and (3) passage of ultrafine particles, or of their soluble fraction, to the bloodstream [77, 78]. Of note, one mechanism does not exclude the other, and one or more can be involved. The most relevant health effects of air pollution are induction of oxidative stress, systemic inflammation, endothelial dysfunction, atherothrombosis, and arrhythmia.

Different experimental strategies have shown the presence of soluble components of PM in the liver, kidneys, and heart [79, 80]. In their “Air Pollution and Cardiovascular Disease” report, the American Heart Association concluded that exposure to air pollution is a cardiovascular risk factor [55, 77]. Exposure to particulate matter has both short-term and long-term cardiovascular health effects [75, 81] and reduces life expectancy by months or even years [55, 82, 83].


4. Malnutrition and air pollution in children, a vulnerable population

From a nutrition perspective, the most vulnerable subpopulations are people living in poverty conditions, pregnant women, teenagers, and children in their first childhood period. Because the nutritional status during the prenatal period and childhood is the basis for healthy body growth and overall brain development and is a potential determinant of the presence of comorbidities in adulthood, attention focuses on children under the age of 5 years. In fact, inadequate nutrition is the main cause of death worldwide and accounts for half of all deaths in children under the age of five [84]. Given that nutritional status can affect a person’s susceptibility to air pollution, it follows that within the population of children less than 5 years of age, those suffering malnutrition during infancy are the most vulnerable. Forty-five percent of deaths among children aged less than five are associated with undernutrition [85]. The 2019 UNICEF reports on the global nutritional status in infancy worldwide show that at least one in three children under the age of 5 years suffers one or more of the three most visible forms of malnutrition—stunting, wasting, and overweight. Although the global prevalence of stunting among children aged less than 5 years decreased from 1995 million children in 2000 to 149.2 million in 2020, that is, 22% of infants, it is still high. A total of 6.7% of children aged less than 5 years worldwide (45.4 million) suffer from wasting and 5.7% (38.9 million) suffer from overweight.

Given that the child mortality rate is an indicator of the health of a population and that undernutrition accounted for 50% of the 5.2 million deaths among children under 5 in the world in 2019, children with inadequate nutritional status can be considered particularly vulnerable to the adverse effects of air pollution.

Although exposure to airborne pollutants is a health threat to all people across the world, whether living in urban or rural areas, certain populations are particularly vulnerable. Populations identified as being at risk include children, people over the age of 65 years, and subjects with previous cardiorespiratory diseases [86, 87, 88, 89].

There is an intuitive understanding that repeated and almost continuous exposure to air pollution in cities synergistically increases the likelihood of acute response and can even exacerbate respiratory diseases, such as asthma, chronic obstructive pulmonary disease, and lung cancer in the overall population and particularly in susceptible populations, including the elderly, subjects with the cardiorespiratory disease, pregnant women, and children under five. However, there is little awareness about the significant impact of air pollution exposure on vulnerable subpopulations, such as malnourished children.

As a result of the combination of physiological, environmental, socioeconomic, and behavioral factors, the health effects of air pollution exposure are more damaging to children than adults. Children are particularly vulnerable during prenatal development and the first years of life since their organs, especially their lungs, are still developing and their immune system is immature. In addition, children have a higher respiratory rate and therefore breathe in a larger volume of air and are exposed to a higher proportion of contaminants than adults. Furthermore, children spend more time outdoors playing or exercising in potentially contaminated environments, and they are closer to the ground where the concentration of certain pollutants can be higher [90, 91, 92, 93, 94, 95].

According to the WHO, 286000 children under the age of 5 years died due to exposure to unhealthy levels of ambient air pollution in 2016. Reported statistics show that 93% of children worldwide are exposed to particulate matter (PM2.5) levels above WHO air quality recommendations; specifically in middle- and low-income countries in Latin America, this applies to 87% of all children under five [96].

Exposure to air pollution has multiple lung and systemic effects in children. There are numerous studies showing the association between exposure during gestation and the first years of life and the development and/or exacerbation of respiratory diseases, such as asthma and allergies, as well as the incidence of pneumonia and other infectious respiratory diseases [97, 98, 99]. In addition, considering that almost 80% of alveoli develop postnatally until about the age of 6 or 7 years and that growth and maturation of the lungs and immune system continue until adolescence, the damage during the first stages of life is a determinant of lung function in later life.

As to the cardiac effects in children and adolescents, exposure to air pollution is associated with systemic inflammation, an increase in vasoconstriction molecules, an increase in arterial blood pressure, and changes in sub-clinical atherosclerosis markers, such as arterial stiffness and increase in carotid intima-media thickness, all of which can predispose to early onset of cardiovascular disease [100, 101, 102].

Worldwide, malnutrition is strongly associated with up to 19% of childhood deaths and contributes significantly to reducing life expectancy [16]. While sub-chronic nutritional deficiencies are not immediately life-threatening, these deficiencies increase susceptibility to other challenges resulting in additive and synergistic reductions in health [7]. It has been shown that exposure to ambient air pollutants is associated with concurrent poor nutritional status [103, 104]. Regarding undernutrition and air pollution, a recent study conducted by our research group using an animal model of nutritional growth retardation (NGR) showed that acute exposure to Residual Oil Fly Ash (ROFA), a substitute for ambient air pollution, causes alterations in the lung and also in distant organs, including blood vessels, heart, and liver. NGR animals showed inflammation and an ensuing decrease in alveolar space; moreover, in vitrotests showed that response to ROFA was lower in alveolar macrophages obtained from ROFA-NGR animals. As regards the heart, exposure to ROFA caused oxidative stress and alterations in blood vessel biochemical markers, which might be associated with heart contractility failure. Evaluation of ROFA effects on the liver showed an increase in the number of lymphocytes in the liver parenchyma and of binucleated hepatocytes; the latter parameter is associated with hepatic regeneration as a response to toxic tissue damage triggered by xenobiotic or dietary-induced liver damage. Our results highlight the key role of nutritional status in the ability to respond to air pollutants [11, 81, 105, 106, 107, 108].


5. Discussion

It is important to understand child malnutrition as a public health problem that threatens future generations. It is equally important to understand that the children of today are the adults of tomorrow, and ensuring nutrition safety can therefore break the vicious intergenerational cycle whereby malnutrition perpetuates poverty and poverty perpetuates malnutrition.

Environmental factors, including climate and geographical conditions, and social-economic factors are determinants of production, availability, and access to food. Because a person is a social being in constant interaction with the environment, air pollution is not merely a factor that could add to malnutrition aggravating the baseline condition but is a causal factor of malnutrition.

The United Nation’s Sustainable Development Goals (SDG) acknowledge the importance of social and environmental factors as determinants of health. All SDG are clearly linked to health-related goals and reflect an increasing awareness of the interrelation among health objectives, environmental targets, and goals to end poverty. SDG aims to guarantee a healthy life for all (Goal 3) and to make cities inclusive, safe, resilient, and sustainable (Goal 11) [109].

Despite substantial detrimental health, economic, and environmental effects, the morbidity burden associated with pollution worldwide has been underestimated and has therefore not been set as a high priority on international development agendas and in global health policies.

It is noteworthy that air pollution increases the risk of developing a number of lungs, cardiovascular, liver, and brain diseases. Other environmental factors such as temperature, noise, stress, electromagnetic fields, and built-up environments like cities also contribute to the risk of developing these diseases. Air pollution and environmental contamination—both aggravated by farming practices and other anthropogenic sources of pollution—increase global mortality and morbidity.


6. Conclusions

Among other factors, susceptibility to various diseases is influenced by the vulnerability. In this context, infants, aggravated by their nutritional status, are one of the most fragile and unprotected populations. The health effects of contamination known today may be just the tip of the iceberg. In the light of the evidence shown here, efforts to reduce exposure to air pollutants must be intensified urgently and must be endorsed by adequate and effective legislation.

Increasing the population’s awareness about the vast and terrible effects of ambient and household air pollution on the health and life expectancy of children is vitally important and must not be underestimated.



This research was funded by grants PICT 2017-1309 and PICT 2017-4549 from the National Agency for Scientific and Technological Promotion and grant number UBACyT 20020130100100BA from the University of Buenos Aires.


Conflict of interest

The authors declare no conflict of interest.


  1. 1. Macias MAI, Quintero SML, Camacho REJ, Sánchez SJM. La tridimensionalidad del concepto de nutrición: Su relación con la educación para la salud. Revista Chilena de Nutrición. 2009;36:1129-1135
  2. 2. Feil R. Environmental and nutritional effects on the epigenetic regulation of genes. Mutation Research, Fundamental and Molecular Mechanisms of Mutagenesis. 2006;600:46-57
  3. 3. Tiffon C. The impact of nutrition and environmental epigenetics on human health and disease. International Journal of Molecular Science. 2018;19:3425
  4. 4. Lewis AS, Sax SN, Wason SC, Campleman SL. Non-chemical stressors and cumulative risk assessment: An overview of current initiatives and potential air pollutant interactions. International Journal of Environmental Research and Public Health. 2011;8:2020-2073
  5. 5. Sexton K, Linder SH. Cumulative risk assessment for combined health effects from chemical and nonchemical stressors. American Journal of Public Health. 2011;101(Suppl. 1):S81-S88
  6. 6. National Research Council (US) Committee on Improving Risk Analysis Approaches Used by the U.S. EPA. Science and Decisions: Advancing Risk Assessment. National Academies Press (US); 2009
  7. 7. Miller CN, Rayalam S. The role of micronutrients in the response to ambient air pollutants: Potential mechanisms and suggestions for research design. Journal of Toxicology and Environmental Health, Part B Critical Review. 2017;20:38-53
  8. 8. Hanson MA, Gluckman PD. Early developmental conditioning of later health and disease: Physiology or pathophysiology? Physiological Review. 2014;94:1027-1076
  9. 9. World Health Organization. Air pollution [Internet]. 2018. Available from:
  10. 10. Lave LB, Seskin EP. Air Pollution and Human Health. Baltimore: Johns Hopkins University Press; 1977
  11. 11. Kurtz ML, Astort F, Lezon C, Ferraro SA, Maglione GA, Orona NS, et al. Oxidative stress response to air particle pollution in a rat nutritional growth retardation model. Journal of Toxicology and Environmental Health Part A. 2018;81:1028-1040. DOI: 10.1080/15287394.2018.1519747
  12. 12. WHO. Guideline: Assessing and managing children at primary health-care facilities to prevent overweight and obesity in the context of the double burden of malnutrition. Updates for the Integrated Management of Childhood Illness. 2017
  13. 13. WHO. Child Growth Standards Length/height-for-age, weight-for-age, weight-for-length, weight-for-height and body mass index-for-age: Methods and development. 2006
  14. 14. Caulfield LE, de Onis M, Blossner M, Black RE. Undernutrition as an underlying cause of child deaths associated with diarrhea, pneumonia, malaria, and measles. American Journal of Clinical Nutrition. 2004;80:193-198
  15. 15. Bhutta ZA, Berkley JA, Bandsma RHJ, Kerac M, Trehan I, Briend A. Severe childhood malnutrition. Nature Reviews Disease Primers. 2017;3:17067
  16. 16. Black RE, Allen LH, Bhutta ZA, Caulfield LE, de Onis M, Ezzati M, et al. Maternal and child undernutrition: Global and regional exposures and health consequences. Lancet. 2008;371:243-260
  17. 17. Black RE, Victora CG, Walker SP, Bhutta ZA, Christian P, De Onis M, et al. Maternal and child undernutrition and overweight in low-income and middle-income countries. Lancet. 2013;382:427-451
  18. 18. King JC, Brown KH, Gibson RS, Krebs NF, Lowe NM, Siekmann JH, et al. Biomarkers of nutrition for development (BOND)-Zinc Review. The Journal of Nutrition. 2015;146:858S-885S
  19. 19. López de Romaña D, Cediel G. Situation of Micronutrients in Latin America and the Caribbean: Prevalence of Defciencies and National Micronutrient Delivery Programs. Sight and Life on behalf of the World Food Programme. 2017:122-136
  20. 20. Templin T, Hashiguchi TCO, Thomson B, Dieleman J, Bendavid E. The overweight and obesity transition from the wealthy to the poor in low- and middleincome countries: A survey of household data from 103 countries. PLoS Medicine. 2019;16:e1002968
  21. 21. FAO, OPS, WFP, UNICEF. Panorama de la seguridad alimentaria y nutricional en América Latina y el Caribe 2018 [Internet]. 2019. Available from:
  22. 22. WHO, UNICEF, WBG. UNICEF/WHO/The World Bank Group joint child malnutrition estimates: Levels and trends in child malnutrition: Key findings of the 2020 edition [Internet]. 2020. Available from:
  23. 23. Kac G, Alvear JLG. Epidemiologia de la desnutricion en Latinoamerica: Situacion actual. Nutrición Hospitalaria. 2010;25(Suppl. 3):50-56
  24. 24. Batis C, Mazariegos M, Martorell R, Gil A, Rivera JA. Malnutrition in all its forms by wealth, education and ethnicity in Latin America: Who are more affected? Public Health Nutrition. 2020;23(S1):s1-s12
  25. 25. WHO. World Health Statistics 2018: Monitoring Health for the SDGs, Sustainable Development Goals. [Internet]. 2018. Available from:
  26. 26. Hannah Ritchie and Max Roser. Outdoor Air Pollution. Our World Data. 2019;6:286-304
  27. 27. WHO. Air Pollution [Internet]. 2018. Available from:
  28. 28. Gulia S, Shiva Nagendra SM, Khare M, Khanna I. Urban air quality management: A review. Atmospheric Pollution Research. 2015
  29. 29. Vilas Boas DS, Matsuda M, Toffoletto O, Garcia MLB, Saldiva PHN, Marquezini MV. Workers of São Paulo city, Brazil, exposed to air pollution: Assessment of genotoxicity. Mutatation Research: Genetic Toxicology. 2018;834:18-24
  30. 30. WMO, IGAC. Impacts of Megacities on Air Pollution and Climate [Internet]. 2021. Available from:
  31. 31. EPA. 40 CFR Part 50 National Ambient Air Quality Standards for Particulate Matter. Final Rule [Internet]. 2006. Available from:
  32. 32. EEA. Air Quality Standards [Internet]. 2021. Available from:
  33. 33. Karagulian F, Belis CA, Dora CFC, Prüss-Ustün AM, Bonjour S, Adair-Rohani H, et al. Contributions to cities’ ambient particulate matter (PM): A systematic review of local source contributions at global level. Atmospheric Environment. 2015;120:475-483
  34. 34. US-EPA USEPA. National Ambient Air Quality Standards (NAAQS) for PM. 2020
  35. 35. Loomis D, Grosse Y, Lauby-Secretan B, El Ghissassi F, Bouvard V, Benbrahim-Tallaa L, et al. The carcinogenicity of outdoor air pollution. Lancet Oncology. 2013;14:1262-1263
  36. 36. WHO. Ambient (Outdoor) Air Pollution [Internet]. 2021. Available from:
  37. 37. WHO. Air Quality Guidelines: Global Update 2005 [Internet]. 2005. Available from:
  38. 38. Brunekreef B, Holgate ST. Air pollution and health. Lancet. 2002;360:1233-1242
  39. 39. Laden F, Schwartz J, Speizer FE, Dockery DW. Reduction in fine particulate air pollution and mortality: Extended follow-up of the Harvard Six Cities Study. American Journal of Respiratory and Critical Care Medicine. 2006;173:667-672
  40. 40. Bobak M. Outdoor air pollution, low birth weight, and prematurity. Environmental Health Perspectives. 2000;108:173-176
  41. 41. Ren S, Haynes E, Hall E, Hossain M, Chen A, Muglia L, et al. Periconception exposure to air pollution and risk of congenital malformations. The Journal of Pediatrics. 2018;193:76-84.e6
  42. 42. Schwartz J, Bind MA, Koutrakis P. Estimating causal effects of local air pollution on daily deaths: Effect of low levels. Environmental Health Perspectives. 2017;125:23-29
  43. 43. Pope CA 3rd, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito K, et al. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA. 2002;287:1132-1141
  44. 44. Pope CA, Burnett RT, Thurston GD, Thun MJ, Calle EE, Krewski D, et al. Cardiovascular mortality and long-term exposure to particulate air pollution: Epidemiological evidence of general pathophysiological pathways of disease. Circulation. 2004;109:71-77
  45. 45. Krewski D, Jerrett M, Burnett RT, Ma R, Hughes E, Shi Y, et al. Extended follow-up and spatial analysis of the American Cancer Society study linking particulate air pollution and mortality. Research Report. Health Effects Institute. 2009;140:5-136
  46. 46. Apte JS, Brauer M, Cohen AJ, Ezzati M, Pope CA. Ambient PM2.5 reduces global and regional life expectancy. Environmental Science & Technology Letters. 2018;5:546−551
  47. 47. Li X, Jin L, Kan H. Air pollution: A global problem needs local fixes. Nature. 2019;570:437-439
  48. 48. WMO, IGAC. Impacts of Megacities on Air Pollution and Climate. WMO GAW report N° 205 [Internet]. 2012. Available from:
  49. 49. Baklanov A, Molina LT, Gauss M. Megacities, air quality and climate. Atmospheric Environment. 2016;126:235-249
  50. 50. UN. 2018 Revision of World Urbanization Prospects [Internet]. United Nations, Department of Economic and Social Affairs, Population Division, editor. 2018. Available from:
  51. 51. United Nations United Nations, Department of Economic and Social Affairs, Population Division. The World’s Cities in 2016 [Internet]. 2016. Available from:
  52. 52. Molina MJ, Molina LT. Megacities and atmospheric pollution. Journal of the Air & Waste Management Association. 2004;54:644-680
  53. 53. Clean Air Institute. La Calidad del Aire en América Latina: Una Visión Panorámica [Internet]. 2013. Available from:
  54. 54. Schraufnagel DE, Balmes JR, Cowl CT, De Matteis S, Jung S-H, Mortimer K, et al. Air pollution and noncommunicable diseases. Chest. 2019;155:417-426
  55. 55. Brook RD, Rajagopalan S, Pope CA 3rd, Brook JR, Bhatnagar A, Diez-Roux AV, et al. Particulate matter air pollution and cardiovascular disease: An update to the scientific statement from the American Heart Association. Circulation. 2010;121:2331-2378
  56. 56. Cohen AJ, Brauer M, Burnett R, Anderson HR, Frostad J, Estep K, et al. Estimates and 25-year trends of the global burden of disease attributable to ambient air pollution: An analysis of data from the Global Burden of Diseases Study 2015. Lancet. 2017;389:1907-1918
  57. 57. Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay ME, et al. An association between air pollution and mortality in six U.S. Cities. New England Journal of Medicine. 1993;329:1753-1759
  58. 58. Kwon HS, Ryu MH, Carlsten C. Ultrafine particles: Unique physicochemical properties relevant to health and disease. Experimental and Molecular Medicine. 2020;52:318-328
  59. 59. Zhang P, Summer WR, Bagby GJ, Nelson S. Innate immunity and pulmonary host defense. Immunology Review. 2000;173:39-51
  60. 60. Lippmann M, Yeates DB, Albert RE. Deposition, retention, and clearance of inhaled particles. British Journal of Industrial Medicine. 1980;37:337-362
  61. 61. Deng Q , Ou C, Chen J, Xiang Y. Particle deposition in tracheobronchial airways of an infant, child and adult. Science Total Environment. 2018;612:339-346
  62. 62. Riechelmann H, Kienast K, Schellenberg J, Mann WJ. An in vitro model to study effects of airborne pollutants on human ciliary activity. Rhinology. 1994;32:105-108
  63. 63. Orona NS, Ferraro SA, Astort F, Morales C, Brites F, Boero L, et al. Acute exposure to Buenos Aires air particles (UAP-BA) induces local and systemic inflammatory response in middle-aged mice: A time course study. Environmental Pollution. 2016;208(Pt A):261-270
  64. 64. Falcon-Rodriguez CI, Osornio-Vargas AR, Sada-Ovalle I, Segura-Medina P. Aeroparticles, composition, and lung diseases. Frontiers in Immunology. 2016;7:3
  65. 65. Traboulsi H, Guerrina N, Iu M, Maysinger D, Ariya P, Baglole CJ. Inhaled pollutants: The molecular scene behind respiratory and systemic diseases associated with ultrafine particulate matter. International Journal of Molecular Science. 2017;18:243
  66. 66. Marchini T, Wolf D, Michel NA, Mauler M, Dufner B, Hoppe N, et al. Acute exposure to air pollution particulate matter aggravates experimental myocardial infarction in mice by potentiating cytokine secretion from lung macrophages. Basic Research in Cardiology. 2016;111:44
  67. 67. Cano-Gutierrez G, Acevedo-Nava S, Santamaria A, Altamirano-Lozano M, Cano-Rodriguez MC, Fortoul TI. Hepatic megalocytosis due to vanadium inhalation: Participation of oxidative stress. Toxicology and Industrial Health. 2012;28:353-360
  68. 68. Hiraiwa K, van Eeden SF. Contribution of lung macrophages to the inflammatory responses induced by exposure to air pollutants. Mediators of Inflammation. 2013;2013:619523
  69. 69. González-Flecha B. Oxidant mechanisms in response to ambient air particles. Molecular Aspects of Medicine. 2004;25:169-182
  70. 70. Tao F, Gonzalez-Flecha B, Kobzik L. Reactive oxygen species in pulmonary inflammation by ambient particulates. Free Radical Biology and Medicine. 2003;35:327-340
  71. 71. Sokol CL, Luster AD. The chemokine system in innate immunity. Cold Spring Harbor Perspectives in Biology. 2015;7:a016303
  72. 72. Zhang H, Liu H, Davies KJ, Sioutas C, Finch CE, Morgan TE, et al. Nrf2-regulated phase II enzymes are induced by chronic ambient nanoparticle exposure in young mice with age-related impairments. Free Radical Biology and Medicine. 2012;52:2038-2046
  73. 73. Churg A, Xie C, Wang X, Vincent R, Wang RD. Air pollution particles activate NF-kappaB on contact with airway epithelial cell surfaces. Toxicology and Applied Pharmacology. 2005;208:37-45
  74. 74. Soukup JM, Ghio AJ, Becker S. Soluble components of Utah Valley particulate pollution alter alveolar macrophage function in vivo and in vitro. Inhalation Toxicology. 2000;12:401-414
  75. 75. Maglione GA, Kurtz ML, Orona NS, Astort F, Brites F, Morales C, et al. Changes in extrapulmonary organs and serum enzyme biomarkers after chronic exposure to Buenos Aires air pollution. Environmental Science and Pollution Research. 2020;27:14529-14542
  76. 76. Orona NS, Astort F, Maglione GA, Ferraro SA, Martin M, Morales C, et al. Hazardous effects of urban air particulate matter acute exposure on lung and extrapulmonary organs in mice. Ecotoxicology and Environmental Safety. 2020;190:110120
  77. 77. Brook RD. Cardiovascular effects of air pollution. Clinical Science. 2008;115:175-187
  78. 78. Kido T, Tamagawa E, Bai N, Suda K, Yang HH, Li Y, et al. Particulate matter induces translocation of IL-6 from the lung to the systemic circulation. American Journal of Respiratory Cell and Molecular Biology. 2011;44:197-204
  79. 79. Mani U, Prasad AK, Suresh Kumar V, Lal K, Kanojia RK, Chaudhari BP, et al. Effect of fly ash inhalation on biochemical and histomorphological changes in rat liver. Ecotoxicology and Environmental Safety. 2007;68:126-133
  80. 80. Wallenborn JG, Kovalcik KD, McGee JK, Landis MS, Kodavanti UP. Systemic translocation of (70)zinc: Kinetics following intratracheal instillation in rats. Toxicology and Applied Pharmacology. 2009;234:25-32
  81. 81. Maglione GA, Kurtz ML, Orona NS, Astort F, Busso IT, Mandalunis PM, et al. Chronic exposure to urban air pollution from Buenos Aires: The ocular mucosa as an early biomarker. Environmental Science and Pollution Research. 2019;26:27444-27456
  82. 82. Franklin BA, Brook R, Pope A, 3rd C. Air pollution and cardiovascular disease. Current Problems in Cardiology. 2015;40:207-238
  83. 83. Chen CC, Chen PS, Yang CY. Relationship between fine particulate air pollution exposure and human adult life expectancy in Taiwan. Journal of Toxicology and Environmental Health. 2019;82:826-832
  84. 84. UNICEF. Committing to Child Survival: A Promise Renewed [Internet]. 2015. Available from:
  85. 85. ANCUR. Desnutrición infantil en el mundo. 2020. Available from:
  86. 86. Saldiva PHN, Arden Pope C, Schwartz J, Dockery DW, Lichtenfels AJ, Marcos Salce J, et al. Air pollution and mortality in elderly people: Atime-series study in sao paulo, Brazil. Archives of Environmental and Health. 1995;50:159-163
  87. 87. Pope CA 3rd. Epidemiology of fine particulate air pollution and human health: Biologic mechanisms and who’s at risk? Environmental Health Perspectives. 2000;108(Suppl):713-723
  88. 88. Braga ALF, Saldiva PHN, Pereira LAA, Menezes JJC, Conceição GMS, Lin CA, et al. Health effects of air pollution exposure on children and adolescents in São Paulo, Brazil. Pediatric Pulmonology. 2001;31:106-113
  89. 89. Samet JM, Dominici F, Zeger SL, Schwartz J, Dockery DW. The National Morbidity, Mortality, and Air Pollution Study. Part I: Methods and methodologic issues. Research Reports (Health Effects Institute). 2000;94(Pt 1):5-84
  90. 90. CDC. Populations at Risk from Air Pollution—United States, 1991 [Internet]. Morb. Mortal. Wkly. Rep. 1993 [cited 2020 Apr 9]. Available from:
  91. 91. Sacks JD, Stanek LW, Luben TJ, Johns DO, Buckley BJ, Brown JS, et al. Particulate matter-induced health effects: Who is susceptible? Environmental Health Perspectives. 2011;119:446-454
  92. 92. Pinkerton KE, Joad JP. The mammalian respiratory system and critical windows of exposure for children’s health. Environmental Health Perspectives. 2000;108(Suppl. 3):457-462
  93. 93. Salvi S. Health effects of ambient air pollution in children. Paediatric Respiratory Reviews. 2007;8:275-280
  94. 94. Schwartz J. Air Pollution and Children’s Health. Pediatrics. 2004;113:1037-1043
  95. 95. UNICEF. The Climate Crisis is a Child Rights Crisis: Introducing the Children’s Climate Risk Index [Internet]. 2021. Available from:
  96. 96. WHO. Air pollution and child health: Prescribing clean air [Internet]. 2018. Available from:
  97. 97. Trasande L, Thurston GD. The role of air pollution in asthma and other pediatric morbidities. The Journal of Allergy and Clinical Immunology. 2005;115:689-699
  98. 98. Sram RJ, Binkova B, Dostal M, Merkerova-Dostalova M, Libalova H, Milcova A, et al. Health impact of air pollution to children. International Journal of Hygiene and Environmental Health. 2013;216:533-540
  99. 99. Brugha R, Grigg J. Urban air pollution and respiratory infections. Paediatric Respiratory Reviews. 2014;15:194-199
  100. 100. Lenters V, Uiterwaal CS, Beelen R, Bots ML, Fischer P, Brunekreef B, et al. Long-term exposure to air pollution and vascular damage in young adults. Epidemiology. 2010;21:512-520
  101. 101. Aragon MJ, Chrobak I, Brower J, Roldan L, Fredenburgh LE, McDonald JD, et al. Inflammatory and vasoactive effects of serum following inhalation of varied complex mixtures. Cardiovascular Toxicology. 2016;16:163-171
  102. 102. Calderón-Garcidueñas L, Villarreal-Calderon R, Valencia-Salazar G, Henríquez-Roldán C, Gutiérrez-Castrellón P, Coria-Jiménez R, et al. Systemic inflammation, endothelial dysfunction, and activation in clinically healthy children exposed to air pollutants. Inhalation Toxicology. 2008;20:499-506
  103. 103. Hennig B, Ettinger AS, Jandacek RJ, Koo S, McClain C, Seifried H, et al. Using nutrition for intervention and prevention against environmental chemical toxicity and associated diseases. Environmental Health Perspectives. 2007;115:493-495
  104. 104. Kannan S, Misra DP, Dvonch JT, Krishnakumar A. Exposures to airbone particulate matter and adverse perinatal outcomes: A biologically plausible mechanistic framework for exploring potential effect modification by nutrition. Environmental Health Perspectives. 2006;114:1636-642
  105. 105. Kurtz M, Lezón Ch, Delffose V, Viale D, Boyer, Tasat D. Cumulative Risk Factors in the Urban Environment: Interaction between Air Pollution and Malnutrition on the Immune Response of Alveolar Macrophages. Sociedad de Toxicología y Química Ambiental-Latin America (SETAC-LA) 14th Biennial Meeting. Chile; 2021
  106. 106. Kurtz M, Deza Z, Lezón Ch, Masci I, BoyerP Alvarez L and, Tasat D. Air particulate matter induces vasculature dysfunction in a nutritional growth retardation rat model. Reunión Conjunta las Sociedades Biomédicas SAIC, SAI, AAFE, Argentina 2021
  107. 107. Masci I, Lezon C, Boneto J, Boyer P, Tasat DR, Kurtz M. Impacto de la contaminación aérea en el cerebro: respuesta antioxidante en un modelo de desnutrición crónica en rata. XXIII Jornadas Anuales de la Sociedad Argentinade Biología (SAB). Argentina; 2021
  108. 108. Kurtz M, Lezón Ch, Alvarez L, Masci I, Boyer PM, Tasat DR. La contaminación aérea como factor de riesgo cardiovascular en un modelo animal de desnutrición crónica. I Congreso Virtual Iberoamericano de Salud Ambiental (SIBSA). 2021
  109. 109. United Nations. Sustainable Development Goals [Internet]. 2015 [cited 2021 Dec 28]. Available from:

Written By

Melisa Kurtz, Christian Lezon, Patricia Boyer and Deborah Tasat

Submitted: January 7th, 2022 Reviewed: March 24th, 2022 Published: May 6th, 2022