Abstract
Healthy soil is foundational to human health. Healthy soil is needed to grow crops, provides food, and sustains populations. It supports diverse ecosystems and critical ecological services such as pollination. It stores water and prevents floods. It captures carbon and slows global climate change. Soil pollution is a great and growing threat to human health. Soil may be polluted by heavy metals, organic chemicals such as pesticides, biological pathogens, and micro/nanoplastic particles. Pollution reduces soil’s ability to yield food. It results in food crop contamination and disease. Soil pollutants wash into rivers causing water pollution. Deforestation causes soil erosion, liberates sequestered pollutants, and generates airborne dust. Pollution of air, water, and soil is responsible for at least 9 million deaths each year. More than 60% of pollution-related disease and death is due to cardiovascular disease. Recognizing the importance of pollution to human health, the European Commission and the EU Action Plan for 2050: A Healthy Planet for All, have determined that air, water, and soil pollution must be reduced to levels that cause no harm to human or ecosystem health. We are thus required to create a toxic-free environment, respect the concept of a safe operating space for humanity, and sustain the health of our planet for future generations. This review article summarizes current knowledge of the links between soil health and human health and discusses the more important soil pollutants and their health effects.
Keywords: Environment, Solid pollution, Water, Pollution, Deforestation, Nanoplastic
Graphical Abstract
Graphical abstract.
Copyright information: Included images were taken from open source image databases Pixabay (https://pixabay.com/) and Unsplash (https://unsplash.com/).
1. Introduction
Healthy soil is essential for human health. While soil is not something we physicians consider very often in our daily work, soil is in fact, a key component of our planet’s infrastructure and it is foundational to human health. Healthy soil is essential for the production of safe, healthy, sufficient food. Healthy soil supports richly diverse ecosystems that provide services critical to human survival, most notably pollination. Healthy soil stores water and protects waterways, thus preventing floods and waterborne diseases. Healthy soil captures vast quantities of carbon and slows the pace of climate change.
Pollution of air, water, and soil is a great and growing threat to global health. The Lancet Commission on Pollution and Health documented that pollution is the largest environmental cause of disease and pre-mature death in the world today. Diseases caused by pollution were responsible for an estimated 9 million pre-mature deaths in 2015—16% of all deaths worldwide and three times more than from AIDS, malaria, and tuberculosis together (Figure 1A).1 Additionally, pollution was responsible in 2015 for the loss of 268 million disability-adjusted life years (DALYs)—254 million years of life lost and 14 million years lived with disability.2
Figure 1.
(A) Estimated global deaths for different pollution categories. Estimated global deaths (B) and DALYs (C) by different pollution-risk factors and age at death in 2015. Adapted from Landrigan et al.1 under the terms of the Creative Commons Attribution License (CC BY).
Despite the fact that 70% of pollution-related diseases are non-communicable diseases (NCDs) and more than 60% are cardiovascular diseases, interventions against pollution are barely mentioned in the Global Action Plan for the Prevention and Control of NCD.1 In addition to ignoring chemical pollutants, the Global NCD Action Plan also neglects the health effects of non-chemical environmental stressors such as mental stress, noise exposure, nocturnal light pollution, and climatic changes that all together may easily outcompete all genetic pre-disposition-related health-risk factors. Epidemiological data suggest that environmental-risk factors are major contributors to NCD, especially cardiovascular disease, and that they also contribute to metabolic and mental diseases including hypertension, heart failure, myocardial infarction, diabetes, arrhythmia, stroke, neurodegeneration, depression, and anxiety disorders as well as cancers.3–6
As air pollution is the leading environmental pollutant causing global pre-mature deaths in older age groups, water pollution significantly contributes to infant mortality (Figure 1B and C).1 In addition, soil and air pollution are major determinants life years lost to illness (DALYs) in infancy and childhood, whereas soil pollution is a major trigger of DALYs at higher age. The mechanisms underlying environmentally triggered NCDs are not fully understood but may comprise increased stress hormone release (cortisol, adrenaline, and noradrenaline), oxidative stress, and inflammation as well as a dysregulation of circadian rhythms leading to adverse health effects.6,7 Ambient air pollution is a major contributor to cardiovascular disease and mortality,8,9 and the incidences of stroke, arrhythmias, and acute myocardial infarction are all increased by air pollutants.10
Soil pollution is defined as contamination of soil at higher than normal concentrations by waste materials of human origin that have adverse effects on human and ecosystem health. Soil pollutants include heavy metals and toxic organic chemicals such as pesticides, biological pathogens, and plastic waste. Air pollution is the most visible and best-studied form of pollution, and images of smoke puffing out of train engines and fumes coming out of exhaust pipes are common and easily recognizable. In contrast, soil pollution is not so easily observable, and the adverse effects of soil pollution on human health are much less well characterized and are not adequately quantified.
This review article will summarize some of the more important and direct relationships between soil pollution and human health, with a particular focus on cardiovascular disease.
2. Healthy soil is essential for human health
Soil is important for human health in a number of ways. Approximately 78% of the average per capita calorie consumption worldwide comes from crops grown directly in soil, and another nearly 20% comes from terrestrial food sources that rely indirectly on soil. Soil is also a major source of nutrients, and it acts as natural filters to remove contaminants from water.
The thin crust of the Earth’s surface supports all terrestrial life and is involved in the regulation and provision of many key ecosystem services that are essential to the environment and to human health and well-being. Soil is the foundation of the agri-food system and the medium in which nearly all food-producing crops grow—about 95% of the food we eat comes from the soil. After the oceans, soil is the largest active carbon store and one cubic metre of soil can store up to 600 L of water, allowing crops to grow even during dry periods.
Biodiversity—above and below ground—is vital to ensure healthy soils and the ecosystems upon which we depend. Soil biodiversity contributes to the cycling of nutrients and carbon, regulates the emergence of pests and diseases, and serves as a source of pharmaceuticals that contribute to boost our health. Soil also provides building materials, fuel, and fibre. They are the basis for human infrastructure and preserve our cultural heritage. The main threats to healthy soil are macro- and microplastic, deforestation, pesticides, overfertilization, and heavy metals (Figure 2).
Figure 2.
Main soil pollutants and processes that contribute to poor soil quality causing important adverse health effects. Included images were taken from open source image databases Pixabay (https://pixabay.com/) and Unsplash (https://unsplash.com/).
2.1. Soil and water contamination with heavy/transition metals, pesticides, and other bioactive toxicants: mechanisms
Toxic substances such as heavy (transition) metals and metalloids or pesticides that contaminate soil frequently produce oxidative stress that is considered as a common initiating event for multiple NCDs3,6,11 (Figure 3).Epidemiological and experimental data suggest that heavy metals such as cadmium (a systematic review of 31 studies14) and lead (a systematic review of 12 studies15) as well as metalloids such as arsenic (a systematic review of 12 studies16) can trigger cardiovascular diseases. Cadmium leads to vascular damage, endothelial dysfunction, and atherosclerosis by oxidative mechanisms (e.g. by replacement of iron and copper in sulphur complexes, promoting Fenton reactions),17, 18 interference with antioxidant responses (e.g. by disruption of zinc–sulphur complexes),19 and inhibition of •NO-mediated vasodilation.20 In addition, there is also evidence for adverse effects of heavy metals and metalloids on epigenetic regulation of gene expression.3 Further reports indicate that lead contributes to oxidative stress, inflammation, endothelial dysfunction, and proliferation of vascular cells with adverse effects on heart-rate variability.15, 21 Overall, lead and cadmium have many similar biological effects.3
Figure 3.
Main effects of soil contaminants on human health, indicating the organs or systems affected and the contaminants causing them. PCBs, polychlorinated biphenyls; PBDEs, polybrominated diphenyl ethers; PFAS, per- and polyfluoroalkyl substances; POPs, persistent organic pollutants; BTEX, refers to the chemicals benzene, toluene, ethylbenzene, and xylene. Adapted from the report of the Food and Agriculture Organization of the United Nations (created from data in Agency for Toxic Substances and Disease Registry12 and Campanale et al.13), https://www.fao.org/3/cb4894en/online/src/html/chapter-04-3.html.
Chemical soil pollutants known to have adverse health effects include polychlorinated biphenyls (PCBs; e.g. dioxins), polybrominated diphenyl ethers, perfluorocarboxylic acids, perfluorooctanesulphonate, benzene, and bisphenol A (BPA). These chemicals can originate from industrial processes (e.g. material additives or combustion products) or they can be applied to soil in pesticide formulations. These compounds have proved adverse health effects that are mediated by induction of oxidative stress, inflammation, or epigenetic dysregulations (e.g. via microRNAs), all of which can increase risk for cancer, endothelial dysfunction, atherosclerosis, apoptosis, NASH, obesity, and other cardiometabolic complications22 as well as for neurodegenerative disorders.11 It is estimated that 25 million agricultural workers per year are affected by pesticide poisoning23 and that pesticides used in agricultural fields are associated with an increased risk of developing several chronic diseases such as diabetes, cancer, and asthma as well as a variety of short-term problems (e.g. dizziness, nausea, skin and eye irritation, and headaches).24 Also for ischaemic heart disease complications such as acute myocardial infarction, arrhythmia, and heart failure as well as severe arterial hypertension during pregnancy strong associations with pesticide exposure were reported, although with a large heterogeneity among the included studies.25
The mechanisms through which toxic soil pollutants induce oxidative stress are variable, but are mainly based on P450 chemistry, redox cycling, suppression of antioxidant enzymes, and uncoupling of mitochondrial respiration, all of which has been extensively reviewed.11,26,27
In addition, the impact of environmental exposures to heavy metals and their impact on circadian clock, including a detailed discussion on potential mechanisms, was previously published.28 Alterations induced by chronic lead exposure on the cells of circadian pacemaker of developing rats were reported.29 Strong evidence exists for disruption of circadian rhythm by cadmium, which is termed ‘cadmium chronotoxicity’ in the literature.6 It has been demonstrated that this effect could be partly prevented by antioxidant co-therapy (suggesting a role for oxidative stress).30 Also, elevated body burdens of copper or lead may have adverse effects on the circadian clock.31 There is also pre-clinical and clinical evidence for an impact of environmental organic chemicals on circadian pathways.6,32 According to a study in flies, different pesticides showed consistently varying LD50 values at different daytimes, which correlated well with the diurnal expression profiles of xenobiotic metabolizing genes, but also indicating that toxicity of pesticides is connected with the circadian rhythm in Drosophila flies.33,34 Vice versa, it was shown that endocrine disrupting chemicals lead to dysregulation of the endogenous circadian clock, particularly in BPA-exposed fish liver tissue, which may be explained by the presence of several xenobiotic response elements in the promoter regions of Bmal1, Cry1, Cry2, and Per2.35 The pre-clinical and clinical evidence for a crosstalk between environmental organic chemicals and circadian pathways as well as the underlying mechanisms (e.g. involvement of aryl hydrocarbon receptor-dependent detoxification36) were reviewed in detail.32,37
Disruption of circadian rhythm may promote the pathogenesis of a variety of disease including cardiovascular diseases.38,39 There is ample experimental and clinical evidence suggesting a significant link between circadian rhythms and the development or progression of cardiovascular diseases.40 Circadian misalignment is a condition highly prevalent in shift workers who have a known higher risk of cardiovascular disease.
2.2. Soil and water contamination with heavy/transition metals: clinical studies
Recent epidemiological studies have demonstrated mixed results on the effect of cadmium on cardiovascular disease outcomes. In the Korea National Health and Nutrition Examination Survey, high blood cadmium levels were associated with higher risk of prevalent stroke [odds ratio (OR) 2.39, 95% confidence interval (CI) 1.03–5.56] and hypertension (OR 1.46, 95% CI 1.20–1.76) among 10 626 participants aged 20–59 years.41 However, no association was found for ischaemic heart disease. In contrast, in the Danish Diet Cancer and Health cohort study, no substantial association between urinary cadmium per creatinine concentration and risk of stroke in never smoking men and women was found.42 Likewise, no strong evidence was found for a positive association between higher urinary cadmium and acute myocardial infarction in never smokers within the same cohort.43
In a recent cross-sectional study from China, high blood level lead was associated with higher odds of common carotid artery plaques (OR 1.53, 95% CI 1.29–1.82) and cardiovascular disease (composite measure including a previous diagnosis of coronary heart disease, myocardial infarction, or stroke; OR 1.44, 95% CI 1.17–1.76) after adjustment for potential confounders in 4234 diabetic patients.44 In good agreement, in 5348 Chinese adults blood level lead was cross-sectionally associated with cardiovascular disease (including coronary heart disease, stroke, and myocardial infarction) as well as cardiovascular-risk factors (including body mass index, fasting plasma glucose, and blood pressure) after multivariable adjustment in women, but not in men.45 Data from the National Health and Nutrition Examination Survey (NHANES) revealed that the interaction of chronic physiological stress (measured by allostatic load index) and blood lead level significantly increased the risk of cardiovascular mortality.46 The effect of low-moderate levels of arsenic exposure and metabolism on mortality was investigated in a recent US study of 3600 men and women.47 The results revealed that arsenic exposure and metabolism (defined as urine inorganic, monomethylated and demethylated arsenic compounds) were associated with all-cause [hazard ratio (HR) 1.28, 95% CI 1.16–1.41], cardiovascular (HR 1.28, 95% CI 1.08–1.52), and cancer mortality (HR 1.15, 95% CI 0.92–1.44). In 7941 Spanish mainland towns, the association between metal or metalloid levels in topsoil with all-cause and specific cardiovascular mortality endpoints was investigated through an ecological study using principal component analysis.48 For PC1, partly reflecting metals including arsenic, a strongly suggestive association with increased all-cause cardiovascular diseases mortality was observed. In a further recent ecological study, inorganic arsenic exposure from rice intake using data at local authority level across England and Wales was associated with increased risk of cardiovascular disease.49 The evidence provided here for an association between heavy metal concentrations and cardiovascular diseases, and mortality was also mirrored by the findings of a high-impact systematic review and meta-analysis (comprising 37 unique studies and 348 259 participants), indicating an association between arsenic, lead as well as cadmium exposure and increased risk of coronary heart disease and overall cardiovascular disease.50 Although soil pollution with heavy metals and its association with cardiovascular diseases is especially a problem in low- and middle-income countries since their populations are disproportionately exposed to these environmental pollutants,51 it becomes a problem for any country in the world due to the increasing globalization of food supply chains and uptake of these heavy metals with fruits, vegetables, and meat.
3. Airborne dust
In addition to the classical routes of exposure to soil pollution such as the agricultural use of pesticides and industrial or urban pollution via contaminated ground water or irrigation with polluted water, the hazards of airborne soil contamination are less acknowledged. Cultivation for agricultural production and deflation (wind erosion) from unpaved road and work sites and denuded fields can release soil into the atmosphere as dust. Airborne dust can impact human health, especially when the particles are less than 10, 2.5, or 0.1 µm in diameter.4 Airborne dust may cause irritation of the respiratory tract and increase risk for pulmonary diseases including pneumonia, chronic obstructive bronchitis, and even lung cancer. Additionally, airborne dust may carry pathogens, harmful gases, organic chemicals, nitrate and nitrite,52 heavy metals, highly reactive transition metals, aldehydes, insects, pollen, and radioactive materials, which can cause other severe health adverse effects.4,52,53
Depending on their size, airborne dust particles containing toxicants may be able to enter the pulmonary alveoli and even transmigrate the lung epithelium and enter the bloodstream, where they are taken up by the blood vessel wall and trigger inflammation and oxidative stress.4 Airborne dust from Africa represents an important contaminant in North American soil. Desert storms from the Sahara and Sahel deserts follow the trade winds across the Atlantic Ocean, and African dust has been linked to elevated levels of Hg, Se, and Pb in North American soil. Airborne dust from Africa has also been linked to increased excess air pollution deaths of cardiopulmonary origin in Europe due to the toxicity of the particles.54 Roughly 400 000–500 000 annual cardiopulmonary deaths can be attributed to natural events (e.g. desert dust, wildfires, volcanic eruptions), which makes up approximately 18% of all pre-mature deaths by air pollution.52 Since windblown sand dust can be transported over long distances, it was found that airborne dust particles originating from mineral soil in China and Mongolia increase the risk for acute myocardial infarction (OR 1.26–1.36, on Day 4 after dust exposure, depending on age and sex) in Japanese medical centres.55 The association of desert dust exposure and acute myocardial infarction remained significant even upon adjustment for other meteorologic variables such as temperature and humidity as well as other air pollutants such as photochemical oxidants, suspended particulate matter, nitrogen dioxide, and sulphur dioxide. Also the number of cardiovascular emergency department visits in Japan was increased by 20.8% (95% CI 3.5–40.9) on days with heavy Asian dust exposure.56
4. Contamination of water, air, and soil by nano- and microplastics
The production of plastics has increased exponentially, from 2.3 million tons in 1950 to 448 million tons by 2015. Production is expected to double by 2050. Every year, about 8 million tons of plastic waste escapes into the oceans from coastal nations. This is the equivalent of setting five garbage bags full of trash on every meter of coastline around the world.57
Comprehensive reviews of environmental pollution need to consider the health effects of nano- and microplastic particles,58 including particles from emerging sources that have not previously received a great deal of attention such as tyre-wear particles, and particles from synthetic carpets and clothing.57,59 Nanomaterials are already a significant component of ambient particulate matter and represent an emerging health issue.60,61 They also comprise an appreciable part of household air pollution.62,63 Nano- and microplastic particles transfer from polluted seawater and soil to the air are by-product of industrial activities, and already represent an appreciable part of household air pollution from synthetic carpets and clothing. Particles from these sources are expected to make an even greater contribution to environmental pollution in the near future due to anticipated increases in their production for research purposes and commercial use followed by their disposal, and release into the environment. More than 4000 nanomaterial-based products are today present in the market and information about them is deposited in the nanodatabase developed by the Technical University of Denmark (www.nanodb.dk).
More recently, with exponential increase in the generation of plastic waste, nano- and microplastic particles have attracted much public and scientific attention due to their great abundance and suspected adverse ecological effects in inshore waters, the sea and the soil.64 In water or soil the plastic waste is mechanically and photochemically degraded to smaller and biologically active particles. As much as 50% of the weight of manufactured plastics consists of chemical additives such as phthalates, bisphenols, flame retardants, per- and polyfluoroalkyl substances, PCBs, and heavy metals. These materials are incorporated into plastic to convey desired properties such as colour, flexibility, fire resistance, and water resistance. They include carcinogens, endocrine disruptors, and neurotoxicants. Most additives are not chemically boomed to the plastic matrix and can leach out of plastic microparticles to enter the environment or human tissues.
Although nano- and microplastics still represent an emerging research field, there have recently been a number of high quality studies on the uptake, distribution, and pathophysiological effects of nano- and microplastic particles in marine organisms such as plankton, mussels, and fish (summarized by meta-analysis65,66) as well as studies of the transfer of these particles to humans by oral uptake of these marine organisms or direct uptake of the particles by inhalation (as described above) with sustainable adverse health effects.67,68
Despite these observations and reports, the adverse health effects of nano- and microplastic particles have so far not been addressed on a mechanistic basis in mammals and humans. Mechanistic studies have been almost exclusively conducted in marine organisms and point towards oxidative stress (e.g. increased lipid peroxidation products, DNA damage, mitochondrial dysfunction) and inflammation (e.g. upregulated pro-inflammatory cytokines, infiltration of immune cells) as central pathways mediating the adverse health effects of nano- and microplastic particles that interestingly show large overlap with the toxic effects of air pollution particles.69 These outcomes have been summarized in the Adverse Outcome Pathways format based on key events, which is used by public health organizations and the OECD guidelines. This format presents a complete tabular overview of key events, adverse health outcomes and toxicological endpoints (e.g. apoptosis, impaired neuronal network function, dysregulated heart rate, fatty liver, growth inhibition, higher mortality, impaired development, and fertility). Most of these studies have been conducted in marine organisms, but some have also been undertaken in rodent models and human cell cultures. Although no controlled or population-based human studies on the association of nano- and microplastic particle exposure and cardiovascular diseases exist to date, it was recently shown that these particles can reach the blood stream and accordingly may damage any organ in the organism.70 In addition, pre-clinical studies have demonstrated that polystyrene bead ingestion promotes adiposity and cardiometabolic disease in mice,71 and induces cardiomyocyte cell death by oxidative damage and NLRP3/caspase-1-mediated pyroptosis as well as cardiac fibrosis by Wnt/β-catenin driven apoptosis in Wistar rats.72,73
Nano- and microplastic particles in polluted seawater will mostly enter the human body via consumption of contaminated seafood. However, some fraction of these particles may also transfer from polluted seawater, soil, or from household sources to the air in the form of particulates or dusts and can then be distributed over large distances and lead to inhalation exposure. Also, contamination of the drinking or irrigation water by nano- and microplastic particles as well as industrially engineered nanomaterials by wastewater is another concern and can lead to exposure via ingestion of contaminated water. The routes of uptake of nano- and microplastic particles as well as their major pathomechanisms are summarized in Figure 4, although some pathophysiological pathways are assumed from airborne particulate matter pathomechanisms.
Figure 4.
Scheme of pathomechanisms of micro- and nanoplastics (MP/NP) toxicity (combination of experimentally confirmed pathomechanisms of MP/NP as well as anticipated processes established for airborne ultrafine and fine particulate matter particles). MPs/NPs uptake is mainly based on ingestion and inhalation. MPs/NPs can on one hand increase mucosal and alveolar permeability allowing transmigration of the particles (e.g. via gut barrier breach or transcytosis). On the other hand, severe lung inflammation caused by MP/NP interaction with phagocytic cells will cause release of inflammatory cytokines such as IL-6, MCP-1, and CRP to the circulation. Once reaching the circulation and end organs, MPs/NPs can impair signalling via cell surface receptors and thereby cause changes in nuclear gene expression. Endocytosis of MPs/NPs will lead to formation of endolysosomes, release of damage-associated molecular patterns (DAMPs) and thereby activation of Toll-like receptor (TLR)-mediated inflammatory signalling and oxidative stress. NPs can also directly penetrate into mitochondria and cause multiple functional damages via swelling, cristolysis, opening of the mitochondrial permeability transition pore (mPTP), mitochondrial DNA (mtDNA) damage, and mitochondrial reactive oxygen species formation. Oxidative stress may arise from the NADPH oxidases (NOXs) and damaged mitochondria. Redrawn and modified from Yong et al.74 with permission. © 2020 by the authors (Licensee MDPI, Basel, Switzerland). This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license.
5. Deforestation
Soil under natural, tropical forests provides essential ecosystem services that have been shaped over many centuries by long-term soil–vegetation feedbacks. However, deforestation of tropical forest, with a net rate of 5.5 million hectares annually in 2010–2015, profoundly impacts soil properties and functions.75 Reforestation is also prominent in the tropics, again altering the state and functioning of the underlying soil. Changes associated with deforestation may persist for decades after forest clearing eventually extending to deep subsoil and strongly affecting soil functions, including nutrient storage and recycling, carbon storage and greenhouse gas emissions, erosion resistance and water storage, drainage and filtration.
Reforestation reverses many of the effects of deforestation, mainly in the topsoil, but such restoration can take decades and the resulting soil properties still deviate from those under natural forests. Improved management of soil organic matter in converted land uses can moderate or reduce the ecologically deleterious effects of deforestation on soil. We emphasize the importance of soil science not only in cross-disciplinary research on deforestation and reforestation but also in developing effective incentives and policies to reduce deforestation.75
6. Ecological and health consequences of overfertilization
Since the mid-1920s, humans have doubled the natural rate at which nitrogen is deposited onto land through the production and application of nitrogen fertilizers (inorganic and manure), the combustion of fossil fuels, and replacement of natural vegetation with nitrogen-fixing crops such as soya beans. The major anthropogenic source of nitrogen in the environment is nitrogen fertilizer. Most synthetic fertilizer applications to agricultural land around the world have occurred since 1980. Since approximately half of all applied nitrogen drains from agricultural fields to contaminate surface and groundwater, nitrate concentrations in our water resources have also increased.76
In terrestrial ecosystems, the addition of nitrogen to soil can lead to nutrient imbalance in trees, changes in forest health, and declines in biodiversity. With increased nitrogen availability, alteration can occur in carbon storage, thus impacting multiple ecological processes in addition to the nitrogen cycle. In agricultural systems, fertilizers are used extensively to increase plant production, but unused nitrogen, usually in the form of nitrate, can leach out of the soil, enter streams and rivers, and ultimately make its way into drinking water. The process of making synthetic fertilizers for use in agriculture by causing N2 to react with H2, known as the Haber–Bosch process, has increased significantly over the past several decades. In fact, today, nearly 80% of the nitrogen found in human tissues originated from the Haber–Bosch process.
Much of the nitrogen applied to agricultural and urban areas ultimately enters rivers and nearshore coastal systems. In nearshore marine systems, increases in nitrogen can often lead to conditions of anoxia (no dissolved oxygen in the water) or hypoxia (low oxygen), leading to reduced biodiversity. These effects can change the food-web structure and degrade the aquatic habitat. One increasingly common consequence of increased nitrogen in both fresh and salt waters is an increase in frequency of harmful algal blooms. Toxic blooms of certain types of dinoflagellates have been associated with high fish and shellfish mortality in some areas. The impacts on human health include ciguatera poisoning as well as amnesic, diarrheic, and paralytic shellfish poisoning.
Additionally, increases in nitrogen in aquatic systems can lead to increased acidification in freshwater ecosystems. Nitrogen surpluses may also have an environmental impact. Nitrogen fertilizer that is not absorbed by crops can, after being converted into nitrates, end up in neighbouring waterbodies or in the air, where it is hazardous to groundwater and drinking water and contributes to the eutrophication of surface waterbodies and terrestrial ecosystems. Nitrate air emissions provoke the eutrophication and acidification of fragile ecosystems and contribute to greenhouse gas formation. This in turn has a negative impact on landscape quality and biodiversity. The adverse health effects were colorectal cancer, bladder, and breast cancer, thyroid disease, methemoglobinaemia, and neural tube defects.76 In addition, ammonia particle emissions from agriculture to the atmosphere may be inhaled with significant health side effects of these fine and ultrafine particles.77
7. Conclusions and political implications
Soil pollution, water pollution, deforestation, excessive fertilization, and the use of pesticides and other toxic chemicals degrade the rich biodiversity of soil around the world, diminish ecosystem sustainability, reduce food crop production, and threaten human health and well-being. Soil pollution reduces the number and variety of beneficial microorganisms in the soil through chemical toxicity and chemical pollutants in soil may also become a source of pollution for groundwater through leaching of contaminants.
Along with climate change, air pollution, and species extinction, soil pollution represents an existential threat to the sustainability of human societies. All of these forms of environmental degradation are ultimately the consequence of short-term economic thinking and greed that have no respect for natural systems and no concern either for other people today or for future generations.
The many pollutants that contaminate soil increase risk of cardiovascular disease and other NCDs. While these pollutants differ in their chemical composition, they cause disease through shared pathophysiological pathways centred on oxidative stress and inflammation leading to a dysregulation of circadian rhythms.7,53 Oxidative stress and inflammation in response to contamination with plastic, heavy metals, overfertilization, pesticides, and toxic agents represent major pathophysiologic mechanisms causing cardiovascular, neurodegenerative, and metabolic diseases.
Chemical and nano/microplastic pollutants can act additively and/or synergistically with other lifestyle, metabolic and traditional health-risk factors leading to aggravated pathogenesis of NCD. The extraordinary concentration of environmental-risk factors—the exposome7 that includes light, noise, and air pollution as well as psychosocial stress—in urbanized areas has the potential to produce a disease burden associated with the sum of these environmental stressors that exceeds all previous estimations.
There is thus an urgency to act, and an opportunity for physicians and other health professionals to lead. Pollution can cause ischaemic heart disease, cancer, obstructive pulmonary disease, strokes, mental and neurological conditions, diabetes, and more.78 Despite tangible progress, in 2015 pollution still led to at least 9 million pre-mature deaths worldwide (16% of all deaths)—three times more deaths than from AIDS, tuberculosis, and malaria combined and 10 times more than from all wars and other forms of violence.1 In the EU, every year, pollution causes one in eight deaths.79 Soil pollution is definitely something that the cardiologist should worry about.
Importantly, according to the zero-pollution vision of the European Commission and the EU Action Plan for 2050 (https://ec.europa.eu/environment/strategy/zero-pollution-action-plan_de): a ‘Healthy Planet for All’, air, water, and soil pollution have to be reduced to levels no longer considered harmful to health and natural ecosystems and that respect the boundaries our planet can cope with, thus creating a non-toxic environment.
Acknowledgements
The authors thank Margot Neuser and Thilo Weckmüller for expert graphical assistance. T.M. is a PI of the DZHK Rhine-Main.
Contributor Information
Thomas Münzel, Department of Cardiology, Cardiology I, University Medical Center Mainz, Cardiology I, Geb. 605, Langenbeckstr. 1, 55131 Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Omar Hahad, Department of Cardiology, Cardiology I, University Medical Center Mainz, Cardiology I, Geb. 605, Langenbeckstr. 1, 55131 Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Leibniz Institute for Resilience Research (LIR), Mainz, Germany.
Andreas Daiber, Department of Cardiology, Cardiology I, University Medical Center Mainz, Cardiology I, Geb. 605, Langenbeckstr. 1, 55131 Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany.
Philip J Landrigan, Program for Global Public Health and the Common Good, Boston College, Chestnut Hill, MA 02467, USA; Department of Medical Biology, Centre Scientifique de Monaco, Monaco-Ville, Monaco.
Funding
The present work was supported by a vascular biology research grant from the Boehringer Ingelheim Foundation for the collaborative research group ‘Novel and neglected cardiovascular-risk factors: molecular mechanisms and therapeutic implications’ to study the effects of environmental-risk factors on vascular function and oxidative stress (A.D. and T.M.). The authors also acknowledge the continuous support by the Foundation Heart of Mainz and the DZHK (German Center for Cardiovascular Research), Partner Site Rhine-Main, Mainz, Germany.
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