Toxic Shadows And The Heart-Habitat Interface – THISDAYLIVE

By Raphael Anakwue

*Being the text of the lecture by Professor Raphael Anakwue, a Professor of Cardiology and Cardiovascular Pharmacology, at the 249th Inaugural Lecture of the University of Nigeria, Nsukka on August 20, 2026

INTRODUCTION

It is with profound gratitude, humility, and a deep sense of responsibility that I stand before you today, on this historic occasion, to deliver the 249th inaugural lecture at the University of Nigeria, Nsukka. As a Professor of Cardiology and Cardiovascular Pharmacology, I am deeply honoured to deliver this lecture, titled “Beyond Traditional Cardiovascular Risk Factors: Toxic Shadows and the Heart-Habitat Interface.”

Your presence here reflects the value you place on scholarship and the regard you hold for me. For this, I am sincerely grateful.

I wish to begin by expressing my sincere gratitude to the Vice-Chancellor, Professor Simon Uchenna Ortuanya, SJD, FCIArb, FCIA, for the privilege of delivering this inaugural lecture. Since his appointment as the 16th Vice-Chancellor of the University of Nigeria, Nsukka, he has worked tirelessly to restore and uphold the dignity of our great university, and I wish to express my appreciation for this. I also extend my appreciation to the Chairman of the Senate Ceremonials Committee, Professor Ozioma Onuzulike.

An inaugural lecture is a ceremonial academic event marking a scholar’s promotion to professorship. It celebrates achievement while offering a public window into the lecturer’s research journey. Beyond personal accomplishment, it showcases how university research challenges norms, drives societal transformation, and shapes policy and innovation. Ultimately, it aims to inspire dialogue and set the course for future inquiry.

My lecture today seeks to reshape how we assess cardiovascular disease risk. This perspective stems from a lifelong habit of questioning tradition, being broad-minded, and seeking knowledge from diverse, sometimes divergent, paths. Let me say a few words about my early life.

I was born into an ordinary family. My parents lived a simple life. My late father, Engr. Michael Anakwue, managed agricultural farm equipment on a mechanised farm in the Ministry of Agriculture and Natural Resources in Ezillo, now Ebonyi State, and my late mother taught in a primary school. The Ezillo centre, one of the legacies of the former Premier of Eastern Nigeria, Dr Michael Okpara, practised mechanised farming, including ranching. If this form of cattle rearing had been replicated across Nigeria, there would not have been any herder-farmer conflict that has killed thousands and left so many homeless.

I was a rascal as a child, and I remember that many hours after school had dismissed, I would arrive home late because of my penchant for exploring all the mango and cashew trees in the neighbourhood. This earned me some beatings at home, and I am glad my mother did not have a heart attack from my rascally behaviour.

From my earliest days in primary school, when I resolved to become a medical doctor, to my formative years at St. Patrick’s College, Asaba, I pursued science with passion while nurturing a parallel love of literature. The African Writers Series — Achebe’s Things Fall Apart and Arrow of God, Soyinka’s The Lion and the Jewel, Ekwensi’s Burning Grass, Armah’s The Beautiful Ones Are Not Yet Born, Ngũgĩ wa Thiong’o’s Weep Not Child and Petals of Blood — all left indelible marks on my imagination and worldview.

That literary grounding continues to shape me. Even today, I remain an avid reader, exploring politics, philosophy, business, spirituality, and the transcendentalist poets — Ralph Waldo Emerson, Walt Whitman, and William Wordsworth — whose voices remind us that science and art, reason and imagination, must coexist if we are to see the world as a whole.

At St. Patrick’s College, I graduated with distinction, earning prizes for best in academics, most efficient class prefect, neatest student, best-behaved student, and all-round student—though not in sports. I made efforts in sports but did not feature prominently! My secret was simple: I made friends with those who excelled in each subject, learning from them until I mastered everything myself. This is the first time I am divulging that strategy, and I suspect my schoolmates listening today will be astonished.

My focus on medicine never wavered. I entered the University of Nigeria Medical School and graduated in 1986. The valedictory lecture delivered by the late Professor Chukwuedu Nwokolo for my class became a treasured guide; I read it repeatedly throughout my early career. Determined to learn from greatness, I sought his mentorship, visiting his private clinic and later his home. As the Igbo saying goes, “nwata kwocha aka, osolu ogalanya lie ife”—a child who washes his hands may dine with elders!

Professor Nwokolo advised us then to spend a year or two in general practice before specialising, to steady our hand in managing a diverse range of cases. During that period, I began postgraduate studies in Pharmacology and Therapeutics, where I encountered another towering figure—the late Professor Gilbert Onuaguluchi, my supervisor. To be mentored by two colossi, one in Medicine and the other in Pharmacology, was a rare privilege. Professor Onuaguluchi, the first Dean of our Faculty of Medicine and the pioneer Vice-Chancellor of the University of Jos, taught pharmacology with such clarity and breadth that he transformed cardiovascular pharmacology into a lens for understanding human vulnerability and resilience. His influence remains deeply etched in my journey.

It was therefore only natural that my path led to cardiology. What began as intellectual curiosity in pharmacology matured into conviction during my early clinical experiences, when theory met the realities of human suffering. Those encounters were unsettling yet profoundly instructive, shaping the course of my career and the focus of my research. My Part 2 fellowship research focused on evaluating cardiovascular function in patients with thyrotoxicosis. I was privileged to be supervised by other high-profile mentors. Prof V. Ikeh was my main supervisor, while Prof B. Onwubere and the late Prof. B. Anisiuba were co-supervisors.

I undertook advanced training at Wockhardt Heart Hospital in India and at The Miller Family Heart, Vascular and Thoracic Institute at Cleveland Clinic in Ohio, USA. I am now a Fellow of the West African College of Physicians, the Nigerian Cardiac Society, and the American College of Cardiology, and a Member of the European Society of Cardiology, the American College of Clinical Pharmacology, the International Society of Cardio-Oncology, and the West African Society of Pharmacology, among many others.

Let me now return to today’s lecture, which focuses on the cardiovascular system. Cardiovascular diseases (CVDs) are the leading cause of mortality, accounting for about a third of all global deaths despite strides in medical advances. The estimated number of deaths due to CVDs globally increased from around 12.1 million in 1990 to 18.6 million in 2019 and 20.5 million by 2021, with an estimated death rate of 22.2 million in 2030 and 32.3 million in 2050 (World Heart Report, 2023; Lindstrom et al., 2022).

CVDs are closely linked to cardiovascular risk factors—traits, behaviours, or conditions that increase an individual’s risk of developing CVD. This relationship is causal, cumulative, and progressive. Well-established or traditional risk factors include hypertension, diabetes mellitus, dyslipidaemia, smoking, physical inactivity, unhealthy diet, and advancing age, among others.

There are millions of studies documenting traditional CVD risk factors across the globe, spanning diverse populations, ages, and genders. In line with this global effort, I have devoted much of my career to investigating these traditional risk factors within our own population.

Our research in Enugu, Southeast Nigeria, examined awareness, treatment, and control of hypertension in primary and secondary care settings. Our findings (Chijioke et al., 2016) revealed a high prevalence and poor control rates, consistent with other studies. Diabetes and hypertension frequently co-exist, compounding the cardiovascular disease (CVD) burden. Prior studies highlighted low hypertension control among diabetic patients and emphasised the importance of managing both blood glucose and blood pressure to reduce CVD risk (Anakwue et al., 2012). Additionally, poor knowledge of diabetes was associated with poorer glycaemic control, whereas greater knowledge improved outcomes (Anakwue et al., 2019).

Our research extended beyond hypertension and diabetes to explore other under-recognised contributors to cardiovascular disease. We demonstrated that thyroid hormone disorders can impair cardiac function and progress to heart failure (Anakwue et al., 2010). We also investigated the therapeutic potential of thyroid hormone replacement in patients with low hormone levels and poor systolic performance (Anakwue et al., 2017). We examined the role of coagulation factors, highlighting their impact on heart attacks, strokes, and thromboembolic events. Through studies on clinicians’ prescribing patterns and determinants of anticoagulant use (Anakwue et al., 2018), we identified determinants of anticoagulant use (Anakwue et al., 2017). By exploring anticoagulation management in critical care (Nwafor and Anakwue, 2019), we sought to develop context-appropriate anticoagulation services for Africa (Anakwue et al., 2020).

Collectively, these investigations reinforced the importance of traditional risk factors—hypertension, diabetes, obesity, dyslipidaemia, thyroid dysfunction, and coagulation abnormalities—while raising a critical question: why do some individuals develop cardiovascular disease despite not fitting the conventional risk profile? (Kumar et al.,2025) This lecture will answer the question by pointing to the environment where we live and work.

Our environment, our common home, has become a source of disease and death. The gravity of this reality moved Pope Francis to issue the encyclical Laudato Si, in which he wrote: “The post‑industrial period may well be remembered as one of the most irresponsible in history in terms of harm to our common home” (The Holy See LS, 2026).

This global concern about environmental degradation is not merely theoretical or distant; it manifests in the most personal and urgent ways within our hospitals. One particular experience remains etched in my memory. A middle-aged man was rushed into the emergency unit with hypertension, bradyarrhythmia, and altered consciousness. The diagnosis was hypertensive heart disease, based on his history of hypertension. However, there was a history of chronic exposure to agricultural chemicals on his farm, a detail that initially seemed peripheral. Further evaluation revealed features consistent with chronic toxic exposure to glyphosate herbicides, commonly called “Roundup”, with the cardiovascular system bearing the brunt of the assault. The heart was not merely failing on its own; it was responding to a toxic insult (Anakwue, 2019). That moment underscored, with striking clarity, the intimate and inseparable relationship between cardiology and toxicology.

Over time, similar cases followed—patients with unexplained arrhythmias after ingesting herbal preparations, others with cardiomyopathy linked to chronic exposure to industrial or environmental toxins, and still others who developed hypertension and heart failure months or years after exposure. Each case reinforced a simple but powerful lesson: the heart is often the final common pathway through which many toxins declare themselves. In such moments, the need for a firm grounding in both cardiovascular medicine and toxicology became unequivocally clear.

In an era saturated with countless chemicals, pollutants, medications, and synthetic substances—many beneficial, others insidiously harmful—toxicology has emerged not as a peripheral interest, but as an indispensable discipline. Understanding dose, exposure, and susceptibility often makes the difference between recovery and death.

In moments of reflection, I am often reminded of the enduring wisdom of Paracelsus (1493–1541)—physician, alchemist, astrologer, and widely regarded as the father of toxicology—who observed that “All things are poison, and nothing is without poison; the dose alone makes the poison” (dosis sola facit venenum) (Grandjean, 2016). That insight continues to resonate deeply, encapsulating both the elegance and the grave responsibility inherent in pharmacology, cardiology, and the practice of medicine.

This principle underpinned toxicology for nearly 500 years. The logic was deceptively simple: if a little does not kill you, it is probably fine. However, modern science has introduced major caveats to this linear way of thinking. While Paracelsus was not wrong, his maxim is no longer the whole truth. In the contemporary world, we confront a far more insidious reality: substances harm us not merely through high doses, but through persistent, low-level entanglement in our daily lives—silent, pervasive, and often invisible.

Today, I invite you to join me in unveiling what we now recognise as the hidden entanglement between the poisonous by-products of our civilisation and the heart and blood vessels, creating and co-creating novel cardiovascular risk factors. These toxicants, as they are now known, have emerged as a massive, population-wide, hidden driver of cardiovascular disease globally.

Indeed, these toxicants affect not only the cardiovascular system but also other organs, including the kidneys, lungs, brain, liver, skin, and reproductive organs, which have been linked to toxicant-induced disorders. One of our studies reported that chronic exposure to petroleum fuels could lead to renal echotextural changes (Anakwue et al., 2020). Our recent study on air pollution in secondary schools demonstrated a negative correlation with students’ intelligence quotient. Toxicants have also been shown to damage DNA and to initiate, promote, or accelerate the development of tumours (Pogribny and Rusyn, 2013; Newman et al., 2020).

Today, we focus on the risk posed by toxicants to the heart and blood vessels, and we will consider the relationship between these toxicants and CVD.

The Evolution of Risk: From Framingham to PREVENT

For decades, our understanding of cardiovascular disease did not include these toxicants; it centred on traditional cardiovascular risk factors—hypertension, dyslipidaemia, diabetes, smoking, physical inactivity, obesity, age and gender. These risk factors have been used as risk assessment tools to gauge future risk of cardiovascular disease (CVD) and to classify it as low, borderline, intermediate or high. A visit to the doctor is often accompanied by a litany of questions: Do you smoke? Do you have hypertension or diabetes? How often do you exercise? No doubt, the doctor means well. He wants to identify the factors that may be contributing to our medical complaints. These questions generate tools that compare one’s health information with patient data from earlier clinical studies on heart disease and are used as a lens to inform the risk of developing cardiovascular disease in 10 or more years.

The earliest risk calculator was the Framingham risk calculator (Wilson et al., 1998). It was developed in 1998 to help inform primary prevention of CVD. The calculator used data from the Framingham Heart Study, one of the first longitudinal studies of CVD.

The Predicting Risk of Cardiovascular Disease Events (PREVENT) tool is the latest, developed in 2023, based on a large observational cohort study of more than 6 million adults (Sadiya et al., 2023). The study was conducted from 1992 to 2017, making it more applicable to the current population than previous calculators, which relied on older studies.

Table 1: Comparison of the Framingham and Prevent risk calculators

Risk factor Framingham scores (1998) Prevent scores (2023)

 Age, sex Age Yes

 Blood pressure Yes Yes

 Cholesterol levels (including non-HDL cholesterol) Total cholesterol, HDL Yes

 Diabetes status / A1C Diabetes Yes

 Kidney function (eGFR and urine albumin-creatinine ratio) No Yes

 Smoking status Yes Yes

 Socioeconomic factors No Yes

 Toxicants and associated biomarkers No No

No doubt, these traditional risk factors remain foundational to cardiovascular disease prevention and treatment. However, none of these tools included toxicants or associated biomarkers as risk factors, an omission that excluded the exposome – the measure of an individual’s lifetime exposure and how these exposures relate to health. This neglect is not typically framed as intentional disregard but rather as a systemic oversight stemming from gaps in awareness, ignorance of pathophysiology, and a lack of research linking low-level exposures over time to disease. In other words, toxicants caused harm quietly over time, often through our seemingly harmless environment.

The Concept of Toxic Shadow

Firstly, toxicants often act silently, evading routine detection and awareness. Unlike traditional cardiovascular risks, they are invisible, chronic, and embedded in daily life, exerting a slow but persistent strain on the body over years or even lifetimes.

For this reason, I use the term “Toxic Shadows.” The phrase is a metaphor for the hidden yet enduring influence of environmental toxicants on cardiovascular health. Like shadows, these exposures may not always be seen, measured, or appreciated, yet their effects can be profound.

Toxicants operate silently, beyond the scope of standard clinical screening. They follow the individual day to day, sometimes throughout life, exerting a constant, invisible, and shadowy pressure. Long after exposure ends, chemicals such as pesticides can leave lasting biological imprints, subtly disrupting systems such as cardiovascular regulation. These exposures accumulate quietly in everyday environments—air, water, food, and soil—creating hidden health effects that routine clinical tests often miss.

Secondly, the toxic shadow of consumption extends across both space and time. Modern lifestyles in wealthy regions often leave hidden toxic legacies in poorer communities, such as heavy-metal exposure from informal electronic-waste recycling. While the benefits of technology are enjoyed elsewhere, the health consequences—such as cardiovascular disease—settle locally, making these shadows geographically displaced, socially invisible, yet biologically powerful.

Thirdly, toxic shadows can span generations. Environmental exposures during pregnancy may leave lasting epigenetic changes that disrupt cardiovascular and metabolic regulation in children and even grandchildren. What begins as a chemical exposure in one generation can quietly become a biological legacy for the next.

Having explored the hidden, enduring, and far-reaching nature of toxic shadows, it is important to recognise that they are not merely theoretical constructs. One of the most chilling and well-documented examples of a toxic shadow in action is air pollution—a pervasive exposure that silently undermines cardiovascular health worldwide.

The Global Toll of Air Pollution

Statistics show that air pollution, an environmental toxicant, accounts for a substantial proportion of CVD mortality globally. In 2021, according to the Global Burden of Disease Study, air pollution was the second-highest contributor to global CVD mortality. There is sufficient evidence that air pollution and other environmental factors actively create, co-create, amplify, and accelerate cardiovascular pathology, often in synergy with traditional risks (Abhishek and Singh, 2024).

WHO has provided the following chilling statistics in an effort to clear the air and address pollution’s cardiovascular health crisis, which has remained unrecognised and unattended, creating a hidden global health epidemic (WHO, 2026)

The first point is that 99% of the world’s population lives in places where air pollution exceeds WHO guideline limits (WHO, 2019; WHO, 2021).

The second point is that 8.1 million deaths in 2021 were due to air pollution, making it the second-largest risk factor for death (Global Air, 2024; Fuller et al., 2022), as shown in the figure below:

Figure 1: showing the state of Global Air/2024

Thirdly, every day almost 2,000 young children die from air pollution – more than one every minute. That makes it the second-leading cause of death among young children, after malnutrition (Global Air, 2024).

Fourthly, exposure to ambient air pollution reduces life expectancy in Nigeria and other West African countries by 3 to 4 years and globally by 1.8 years, with over 50% of those excess deaths linked to cardiovascular disease (Tunde et al.,2018)

Apart from lives lost, air pollution also causes health loss and a reduction in quality of life. The Disability-Adjusted Life Year (DALY) measures these parameters. Air pollution ranked first among 88 risk factors considered in a study of the global burden of disease across 204 countries from 1990 to 2021. Among the specific risk factors analysed in this study, particulate matter air pollution was the leading contributor to the global disease burden, accounting for 8·0% of total DALYs, followed by high systolic blood pressure (SBP; 7·8%), smoking, low birthweight and short gestation (5·6%), and high fasting plasma glucose (FPG; 5·4%). (Brauer et al., 2024)

The reality is that the high mortality figures attributable to air pollution underestimate the actual burden, as they do not fully account for other pollutants and chemicals, such as microplastic pollution, pesticides, heavy metals, and noise pollution, or for their interactions with cardiovascular risk factors such as hypertension and diabetes (Fuller et al., 2022).

The gravity of morbidity and mortality attributable to environmental toxicants has prompted four leading cardiovascular societies, the European Society of Cardiology, the American College of Cardiology, the American Heart Association and the World Heart Federation, to issue an emphatic statement in January 2026, declaring that CVD remains the leading cause of death worldwide and that environmental stressors have become its silent accelerators (Münzel et al., 2026).

Recent estimates suggest that cardiovascular risk from environmental toxicants now exceeds many conventional risk factors, contributing to ∼20 million deaths annually from ischaemic heart disease, stroke, hypertension, and type 2 diabetes (Fuller et al. 2022; GBD 2019, 2022).

The staggering global toll of air pollution underscores how environmental toxicants have become silent drivers of cardiovascular disease. Yet beyond the statistics and global statements, the reality of toxic exposures became personal for me. My journey into the world of toxicants began when I confronted the paradox of rising cardiovascular disease in low- and middle-income countries despite lower traditional risk-factor burdens.

My Journey into the Toxicant World

Let me take you back to 2008, when it was clear that a growing body of evidence showed a relentless rise in the incidence and prevalence of cardiovascular disease, particularly in low‑ and middle‑income countries. At the same time, robust epidemiological data showed that although the traditional cardiovascular risk‑factor burden—measured using tools such as the INTERHEART risk score—was lowest in low‑income countries, the rates of major cardiovascular events and cardiovascular mortality were paradoxically much higher than those observed in high‑income countries.

Indeed, contrary to several high-income countries that recorded reductions in cardiovascular deaths (Minja et al., 2022), Africa has experienced a near-50 % increase in the CVD burden over the past three decades (IHME, 2022; Gouda et al., 2019).

Figure 2 shows the rising prevalence of deaths from CVDs in Sub-Saharan African (SSA) countries from 1990 to 2019. What could be driving this increase in CVD mortality despite a documented low burden of traditional risk factors?

Figure 2: showing the absolute number of cardiovascular deaths under 70 years for four SSA regions between 1990 and 2019. The top line represents the four Sub-Saharan African regions combined (A), Western (B), Eastern (C), Central (D), and Southern (E), with numbers in 100,000s. Figures extracted from the Institute for Health Metrics and Evaluation (IHME)

This pattern could not be satisfactorily explained by the prevalence of familiar risk factors alone, such as hypertension, diabetes mellitus, or dyslipidaemia. The traditional risk factors are likely to be profoundly aggravated by environmental risk factors.

Africa is disproportionately affected by environmental toxicants, which amplify cardiovascular disease (CVD) risks. Fumes from old and poorly maintained vehicles, the widespread use of petrol/diesel generators, industries polluting the environment due to poor regulation, gas flaring exposing populations to higher levels of air pollutants, and exposure to heavy metals, coupled with rapid urbanisation and weak policies, have conspired to place Africa as the top environmental polluter.

Let me share with you some clinical cases managed under my care that provide direct evidence of the presence of environmental toxicants and their possible contribution to CVDs in Nigeria.

Case 1: Lead Poisoning and Hypertensive Heart Disease

Patient Profile: A 45-year-old male mechanic from Enugu, Nigeria, presented with chest pain, dyspnoea, and a blood pressure of 180/110 mmHg. Echocardiography revealed left ventricular hypertrophy consistent with hypertensive heart disease.

Environmental Exposure: The patient had a 20-year history of working with lead-containing batteries at an informal recycling facility. Blood lead level was 60 µg/dL (normal <10 µg/dL).

Outcome: Antihypertensive treatment improved symptoms, but the patient developed heart failure within two years. This case aligns with epidemiological data linking lead exposure to hypertension and heart failure. Chelation therapy would have improved this patient’s clinical condition.

Case 2: Household Air Pollution and Stroke

Patient Profile: A 60-year-old female presented with ischaemic stroke and a history of hypertension.

Environmental Exposure: The patient used biomass fuel for cooking in a poorly ventilated kitchen for 30 years, leading to chronic PM2.5 exposure.

Outcome: She moved to a better-ventilated kitchen and began using a gas cooker. The patient was managed appropriately and showed partial recovery of limb function.

Case 3: A 62-year-old man with ischaemic heart disease lived near a bakery in Enugu. He felt better every time he went to Lagos on holiday, but once he returned home to Achara Layout, he needed to see his doctor frequently. We saw this patient on referral, and following our advice, he relocated to another part of Enugu and has since enjoyed robust health with medication support. This is cardiotoxic fumes from the bakery in action.

It is understandable that toxicants abundant in our environment are contributing to cardiovascular morbidity and mortality. Why did we miss this epidemiological transition for so long? This question marked the beginning of my sojourn into what I now call the world of toxicants. If the visible and traditional risks did not fully account for the burden of disease, other, less obvious forces had to be at play. My attention increasingly turned to non‑traditional risk factors, particularly environmental toxicants—exposures that lie largely outside routine clinical assessment yet are deeply embedded in our everyday life.

This intellectual shift soon translated into practical action. I recall asking Professor Chioli Chijioke, then in the United Kingdom, to procure a simple carbon monoxide (CO) meter for us (Fig. 3). With that modest device, we began measuring air quality across various parts of Enugu city. Even the preliminary results were worrisome. Carbon monoxide levels were elevated in many locations.

Several years later, with access to a more sophisticated Aeroqual air‑quality monitor (fig 3), we were able to assess a wider range of air pollutants with greater accuracy. The results confirmed and extended our earlier concerns. Multiple pollutants consistently exceeded WHO permissible limits. What had initially seemed an abstract hypothesis now rested on measurable, objective evidence. The environment itself was exerting a quiet but persistent biological pressure that harmed the cardiovascular and other systems.

Figure 3: showing the Carbon monoxide meter (right) and the Aeroqual air quality monitor (left)

From Toxic Shadows to the Heart–Habitat Vision

The Heart–Habitat Project was established to translate environmental risks into measurable, controllable factors within cardiovascular care. Its vision of Green Cardiology seeks to move beyond treating disease towards preventing it at its environmental roots. Scientific evidence now shows that toxic exposures, not just cholesterol, blood pressure, and glucose, are major contributors to cardiovascular disease.

This is a call to reframe cardiology: to illuminate hidden toxic threats, apply scientific rigour to the study of environmental cardiotoxicity, and shift from a “repair shop” for broken hearts to a “shield” for populations. Achieving this requires a multi-front strategy — governments enforcing safety limits, industries innovating through green chemistry, watchdogs holding polluters to account, and individuals driving market change through healthier choices.

The remaining part of this lecture will be structured thus:

The Function of the cardiovascular system.

Toxic shadows as hidden threats to cardiovascular health

The shared pathophysiological mechanisms that position toxicants as true co-creators of cardiovascular risk

The epidemiological footprints, clinical cases and translational studies linking toxicants to cardiovascular outcome

The public health and economic cost implications of toxicant-induced cardiovascular disease

A vision for an environment supporting a healthy heart free from toxicants

THE FUNCTION OF THE CARDIOVASCULAR SYSTEM

The cardiovascular system is an intricate pump-and-plumbing system, often called the circulatory system, made up of the heart, the blood vessels, and the blood itself. It is like a vast highway network that delivers oxygen, nutrients, and other essentials to every part of our body while removing waste.

The heart is a muscular organ, about the size of a clenched fist, located in the centre of the chest and slightly tilted to the left. It’s protected by the ribcage and weighs around 250-350 grams in adults. Structurally, the heart is divided into four chambers: two upper ones called the atria and two lower ones called the ventricles. The right side (right atrium and ventricle) handles oxygen-poor blood returning from the body, while the left side (left atrium and ventricle) manages oxygen-rich blood heading to the body. This separation ensures efficient flow.

The blood vessels are made up of the arteries, veins and capillaries. The arteries are thick, muscular tubes that carry oxygen-rich blood away from the heart under high pressure. The largest is the aorta, which branches into smaller arteries and then arterioles. Their elastic walls expand and contract like rubber bands to withstand the heart’s forceful pumping.

The veins are thin-walled vessels that return oxygen-poor blood to the right side of the heart. They contain valves that prevent backflow, acting like escalators that move blood upwards. The superior and inferior vena cavae are the main veins returning blood to the right atrium.

The capillaries are tiny, web-like vessels that connect arteries and veins. They are where the real exchange occurs—oxygen and nutrients diffuse out to cells, while waste products such as carbon dioxide diffuse in.

Blood is a fluid connective tissue, about 5 litres in adults, composed of plasma (the liquid part, mostly water with proteins, hormones, and nutrients) and formed elements: red blood cells (erythrocytes, carrying oxygen via haemoglobin), white blood cells (leukocytes, fighting infections), and platelets (thrombocytes, for clotting).

The heartbeat is controlled by a network of nerve fibres that constitute the electrical system. The sinoatrial (SA) node in the right atrium initiates the signal, which spreads like a wave through the atria, then to the atrioventricular (AV) node, and down the bundle branches to the ventricles. This causes systole (contraction, when blood is ejected) and diastole (relaxation, when chambers fill). A full cycle is one heartbeat, with an average of 60-100 beats per minute at rest.

Blood flows in two circuits: pulmonary (lungs) and systemic (body).

Pulmonary Circulation: Oxygen-poor blood from the right ventricle goes to the lungs via pulmonary arteries. In the lungs’ capillaries, it picks up oxygen and dumps carbon dioxide (gas exchange). Oxygen-rich blood returns to the left atrium via pulmonary veins.

Systemic Circulation: Oxygen-rich blood from the left ventricle leaves the heart via the aorta, then travels through arteries, arterioles, and capillaries throughout the body, delivering nutrients and collecting waste. It then returns to the right atrium via the veins.

The heart functions as the central pump of the circulatory system, maintaining continuous blood flow throughout the body. At rest, it propels approximately 5 litres of blood per minute, amounting to nearly 7,200 litres per day and an estimated 200 million litres over an average lifespan of 80 years. Over that time, the heart contracts about 3 billion times, ensuring the delivery of oxygen and nutrients to every organ and tissue essential for life

Figure 4: artist impression showing the circulatory system [adapted from Chaudhry et al., 2020]

THE TOXIC SHADOWS AND HIDDEN THREAT TO CARDIOVASCULAR SYSTEM

While the cardiovascular system is remarkably efficient at sustaining life by transporting oxygen and nutrients and removing waste, it is also highly vulnerable to external influences. Among the most significant threats are toxicants—harmful substances present in our environment that can disrupt normal cardiovascular function. To understand the hidden dangers these toxicants pose, we must first explore what they are, how they are classified, and the ways they infiltrate our air, water, soil, and food. Toxins are natural toxicants—substances produced by living organisms, mainly as part of their metabolic processes. In this lecture, we will focus on toxicants that are not toxins.

Toxicants can be classified in terms of environmental media: water, soil, air, food; or in terms of their physical form: gases (e.g., carbon monoxide, ozone); vapours (e.g., Volatile organic compounds); liquids (e.g., solvents); solids/particulates (e.g., particulate matter, dusts) and aerosols/mists (Münzel et al, 2025)

Figure 5: Showing Classification of Environmental Toxicants by Media and Physical Form

Toxicants can also be classified by target organs or systems, e.g., cardiotoxicants, hepatotoxicants, neurotoxicants, and respiratory toxicants.

Cardiotoxicants are classified based on the site of activity and mechanism of activity (Lind et al., 2021)

1) impairs regulation of cardiac excitability, 2) impairs cardiac contractility and relaxation, 3) induces cardiomyocyte injury and death, 4) induces proliferation of valve stroma, 5) impacts endothelial and vascular function, 6) alters hemostasis, 7) causes dyslipidemia, 8) impairs mitochondrial function, 9) modifies autonomic nervous system activity, 10) induces oxidative stress, 11) causes inflammation, and 12) alters hormone signaling.

In this discussion, I have adopted a classification of toxicants by chemical nature/structure and functional use, as this often predicts their source, persistence, behaviour, and chemical properties (Table 2).

Table 2:   Classification of Toxicants based on their chemical nature/structure and functional use

TOXICANTS SOURCES

Particulate matter and air pollutants – PM, sulphur dioxide, ozone, nitrogen oxides, carbon monoxide Vehicle exhaust, wood, coal, natural gas burning; engines and devices that require fossil fuel combustion; tobacco smoking

Heavy metals: Lead (Pb), Mercury (Hg), Cadmium (Cd), Arsenic (As). fossil fuel combustion, urban waste disposal, mining and smelting, and the application of fertilisers and pesticides

Micro and Nanoplastics Personal care products, industrial abrasives, synthetic textiles, tyre wear, bottled water, sachet water, microwave containers, tea bags

Pesticides / Agrochemicals — e.g., Organophosphates, organochlorines, glyphosate Agricultural practices

Organic pollutants – Persistent Organic Pollutants (POPs) – Polycyclic aromatic hydrocarbons (PAHs) – Volatile organic compounds (VOCs) Vehicle emissions, industrial activity, biomass burning, tobacco smoke, forest fires, paints, personal care products, agricultural chemicals, electrical equipments

Endocrine-disrupting chemicals (EDCs) e.g., Bisphenol A (BPA), phthalates, Per- and Polyfluoroalkyl substances (forever chemicals); Food and beverage linings, water bottles, reusable food containers, thermal paper receipts, household electronics and consumer products, personal care products, home interiors

Noise/Light pollution Traffic, construction, industrial, religious worship Streetlights, building lights, advertising signs

Climate changes Extreme temperatures Wildfires, severe storms, flooding

Others Food additives and contaminants; cosmetics and personal care products

Air pollution accounts for a lion’s share of toxicant pollution globally (Global Air Report, 2024). This is because air pollution is pernicious, pervasive, persistent, and protracted, and it disperses globally, travelling across national boundaries, continents, and oceans. Particulate Matter (PM) is the most dangerous component of the air we breathe. PM is grouped by size, and the smaller fraction, PM2.5, bypasses the body’s natural filters and lodges in the lungs or even enters the bloodstream.

Figure 6: showing the size comparisons of PM

As human health patterns have evolved over time, the nature of cardiovascular risks has shifted dramatically. In earlier eras, societies grappled primarily with malnutrition and infectious diseases. However, improvements in nutrition, increased longevity, and reduced physical activity have given rise to new, less visible threats to heart health. Industrialisation and modern lifestyles have introduced a range of toxic substances into our environment, creating hidden hazards that contribute to cardiovascular disease and other degenerative conditions (McKeown, 2009).

In the 21st century, Africa’s industrial growth—led by South Africa, Egypt, Morocco, Nigeria, Algeria, and Kenya—has been driven by resource extraction, manufacturing, and urbanisation. While industries such as oil and gas, mining, textiles, chemicals, food processing, and cement have boosted economies, they also generate waste streams that release toxicants, making industrialisation both a source of prosperity and environmental risk.

NOTABLE SOURCES OF TOXICANTS IN NIGERIA

Across Nigeria, environmental pollution is reshaping the burden of heart disease. In Lagos and Onitsha, smog clouds the air; in the Niger Delta, oil spills contaminate the water; in the middle belt, pesticides saturate farmland; and in the north, slash-and-burn agriculture pollutes the air. From electronic waste recycling in Lagos to gold mining in Zamfara, toxic heavy metals such as lead and mercury enter the food chain—sometimes contaminating staples like rice and exposing consumers to cardiotoxic risks. Herbicides such as glyphosate pose further danger.

In Nigeria, toxicants pollute the air, water, land, and the food chain, with climate change further worsening cardiovascular health. A major source of air pollution is small electricity generators, widely used due to the poor public power supply. Nigeria has the world’s largest energy access deficit (IEA, IRENA, UNSD, World Bank and WHO, 2020). More than 85 million Nigerians lack access to electricity and rely on these generators, popularly called “I pass my neighbour” (IEA, IRENA, UNSD, World Bank, WHO, 2020). They are found everywhere: homes, offices, recreation centres, and religious venues. In Lagos alone, the number of generators has been reported to exceed the number of rooms, highlighting the scale of dependence and pollution.

Nigeria is home to millions of vehicles, the majority of which are old and poorly maintained, a situation that has positioned the country among those with the worst air quality globally; indeed, vehicular emissions remain one of the greatest contributors to environmental pollution in Nigeria (Ezeigwe et al., 2024).

Petroleum products are closely tied to vehicular pollution, and while petroleum has long remained the mainstay of Nigeria’s economy, the mismanagement of associated gas flaring has become a major and persistent source of air pollution. This challenge continues to pose a critical environmental and public health crisis, particularly in the Niger Delta, despite government pledges to achieve zero routine flaring by 2030.

Apart from air pollution from gas flaring, there are also multiple reports of pollution of water, food, and land, particularly from plastics, petroleum products, heavy metals, pesticides, and industrial effluents. Plastics occur as microplastics (1 µm–5 mm) and nanoplastics (smaller than 1 µm). In Nigeria, plastic pollution in water bodies stems from industrial activity, poor waste management and heavy use of single-use plastics (Cottom et al., 2024). A key source is the widespread “pure water” sachet culture—50-cl plastic sleeves of drinking water consumed in large numbers. Improper disposal creates secondary microplastics, while studies show that sachets themselves contain primary microplastic particles (Cottom et al., 2024). With over 60 million sachets consumed daily, the public health risks are significant. This industry emerged in the late 1990s and early 2000s as rapid urbanisation strained water infrastructure, offering a quick fix to the potable water crisis but leaving behind lasting environmental and health challenges (Yusuf et al., 2015).

Beyond plastic pollution from the widespread ‘pure water’ sachet culture, Nigeria also faces severe contamination from petroleum activities. An average of 240,000 barrels of crude oil are spilled annually in the Niger Delta—caused by unknown factors (31.85%), third-party activity (20.74%), and mechanical failure (17.04%). These oil spills are among the greatest pollutants of water and land in the region (Ordinioha and Brisibe, 2013).

Figure 7: Sources of air, water, land and food chain pollution in Nigeria

Other polluters of land, water and food in Nigeria include heavy metals and pesticides. The primary sources of heavy metal contamination in Nigeria are anthropogenic, stemming from dumpsites, landfill sites, mining operations, runoff and seepage from automotive repair workshops, petroleum hydrocarbon spills, and effluents from industrial plants. Elevated concentrations of heavy metals exceeding World Health Organisation/Food and Agriculture Organisation (WHO/FAO) guidelines have been documented in water, food and soil samples in Nigeria (Oloruntoba et al., 2024).

In Nigeria, the widespread use of insecticides and herbicides is a major source of pollution. Farmers often reuse empty pesticide containers for household storage, and improper disposal contaminates soil and groundwater. Some communities even apply pesticides directly to water bodies to kill fish, causing severe aquatic pollution. In urban markets, synthetic pesticides are used on stored grains to prevent spoilage, exposing consumers to harmful residues (Brantley et al., 2025). Weak regulation and poor enforcement by agencies like NAFDAC allow unregistered and hazardous agrochemicals to circulate freely, worsening environmental and public health risks (Erhunmwunse et al.,2012)

Nigeria faces serious climate-related health challenges. Rising temperatures in sub-Saharan Africa increase risks of heat stroke, heart attacks, and heart failure. Floods disrupt food and water supplies, leading to malnutrition and higher rates of cardiovascular disease. Poor nutrition contributes to hypertension, a major heart disease risk factor. Limited access to clean drinking water also spreads infections, which can indirectly worsen cardiovascular conditions (Economist Enterprise., 2026).

Exposure to toxicants is not a theory but a lived reality, amplified by ignorance, inadequate research, poor health policy and infrastructure, socioeconomic challenges, and weak regulatory frameworks. Together, these toxicants in air, water, soil, and food create a “perfect storm” for cardiovascular disease in Nigeria. This silent epidemic often goes unnoticed by clinicians and policymakers, yet it significantly increases cardiovascular risk across the population.

I hope that by unveiling the silent entanglement between the environment and the cardiovascular system, we spark renewed urgency: to integrate environmental risk assessment into routine cardiovascular care, to advocate for stronger regulatory protections, and to pursue innovative pharmacological strategies to mitigate these insidious threats.

If we are to act with conviction, we must first understand the biological pathways through which toxicants exert their influence. The silent entwinement of environment and cardiovascular health is not only a matter of policy and practice—it is rooted in shared pathophysiological mechanisms that position toxicants as true co‑creators of cardiovascular risk.

THE SHARED PATHOPHYSIOLOGICAL MECHANISMS THAT POSITION TOXICANTS AS TRUE CO-CREATORS OF CARDIOVASCULAR RISK

How do toxicants—especially at low doses sustained over long periods—undermine cardiovascular health? Modern science has uncovered three key mechanisms that Paracelsus, working with the limited tools of 1567, could never have observed:

Bioaccumulation and biomagnification. Some substances do not leave the body even when daily intake seems “safe.” Heavy metals such as lead and mercury, along with so‑called “forever chemicals,” can build up in fat or bone. Over decades, these hidden stores reach toxic levels, eventually tipping the balance toward disease.

Endocrine disruption. Certain chemicals, including BPA and phthalates, can be more dangerous at very low doses. This is because they mimic hormones, and our bodies are designed to respond to hormones at extremely low concentrations—sometimes parts per billion. Even minimal exposure can disrupt normal signalling and strain the cardiovascular system.

The Exposome. We are never exposed to one chemical in isolation. A single pesticide residue on an apple may be harmless, but combined with air pollution, microplastics, and food additives, the “cocktail effect” creates a cumulative toxic load. This combined exposure challenges the old idea that “the dose makes the poison.”

Research has demonstrated these mechanisms as central to toxicant‑induced cardiovascular disease (Aryal et al., 2021):

Oxidative Stress & ROS Generation: An imbalance where excessive Reactive Oxygen Species overwhelm the heart’s limited antioxidant capacity, causing cell damage, lipid peroxidation, and inflammation

Endothelial Dysfunction: Damage to the inner lining of blood vessels reduces nitric oxide availability, causing impaired vasodilation and increased vascular resistance.

Inflammation: Activation of immune pathways increases proinflammatory cytokines (e.g., TNF-α, IL-6), promoting atherosclerosis.

Mitochondrial Dysfunction: Impairment of cellular energy production leading to cardiac cell damage.

Autonomic Imbalance: Affects the nervous system’s control over heart rate and blood pressure.

Plaque Instability & Thrombosis: Promotes blood clot formation, leading to heart attacks and strokes.

Disruption of Ion Homeostasis: Interference with calcium handling and ion channels, causing arrhythmias and weakened cardiac contractility.

Epigenomic Effects: Alterations in DNA methylation and histone modification, influencing gene expression related to CVD.

Environmental toxicants not only cause cardiovascular disease directly through these mechanisms, but they are also co-creators of traditional CVD risk factors by worsening, mimicking, or directly triggering traditional CVD risk factors (Blaustein et al., 2024). In other words, the toxicants also accelerate the development of hypertension, diabetes, dyslipidemia and other traditional CVD risk factors.

Figure 8: How environmental toxicants cause and accelerate CVD

Understanding how toxicants act as co‑creators of cardiovascular risk factors sets the stage for examining their broader impact on populations. The biological mechanisms are compelling, but it is the epidemiological footprints—tragic episodes of pollution and their documented outcomes—that reveal how these silent exposures translate into real‑world cardiovascular harm and have shaped global health policy.

THE EPIDEMIOLOGICAL FOOTPRINTS AND TRANSLATIONAL STUDIES LINKING TOXICANTS TO CARDIOVASCULAR OUTCOMES

It took some tragedies before the world could link exposure to environmental pollutants to any form of harm. Three episodes of exposure to air pollutants, which happened between 1930 and 1952, demonstrated the vulnerability of the cardiopulmonary system to air pollutants and helped to shape environmental health policy worldwide (Anakwue and Anakwue, 2002; Peters and Pope, 2002)

The first was in Meuse, Belgium, in 1930, where exposures to pollutants from industrial steelworks, zinc smelters, glass manufacturers, and fertiliser and explosives plants caused 60 deaths. The second was in 1948 in Donora, USA, where for over 5 days, nearly half of the town’s 14,000 residents experienced severe respiratory and cardiovascular problems, and 40 deaths occurred. The third incident was in London in 1952, where a combination of citywide household coal burning and a high-pressure weather system caused a blanket of warm, moist, polluted air over London, causing more than 3000 deaths due to cardiopulmonary disease.

The environmental factor contribution to CVD in Europe is striking, with an estimated 18% of all CVD-related deaths attributed to these toxicants (European Environmental Agency, 2023; Health Effects Institute,2024). But there is likely a strong underestimate of the environmental contribution to CVD, as current calculations focus on air pollution and often omit workplace exposures, the effects of environmental noise, and other toxic chemicals, including lead (European Environmental Agency,2023; WHF, 2023)

Environmental toxicants are major but often overlooked contributors to cardiovascular disease (CVD) in Africa. Rapid urbanisation, industrial growth, gas flaring, and heavy use of biomass fuels have increased exposure risks, making pollution a key factor in heart health across the continent. Despite this growing threat, research on how environmental toxicants affect CVD in Africa remains limited (Adeoye et al.,2024)

Toxicant-induced cardiovascular disease in Nigeria

Our Heart-Habitat Project has undertaken many projects to investigate toxicant-induced cardiovascular disease in our country. We focused on specific toxicants prevalent in Nigeria, including fumes from electricity generators, heavy metal poisoning, petroleum products, pesticide poisoning and microplastics.

Let us consider how emissions from power generators contribute to the increased incidence and prevalence of cardiovascular diseases in Nigeria. Nigeria’s unreliable electricity grid has made the widespread use of diesel and petrol generators inevitable. Carbon monoxide, a deadly constituent of generator fumes, is completely odourless and colourless. Together with other toxicants, it causes cardiovascular morbidity and mortality. Tragic stories of individuals dying in their homes and offices after breathing in the poisonous fumes from the generator set continue to this day.

We studied the effects of fumes from small electric generators, more than 22 million of which are scattered across many homes, offices, relaxation centres, business and worship centres in Nigeria (IEA, IRENA, UNSD, World Bank, WHO, 2020). Three groups of dogs were exposed to petrol generator exhaust fumes for 1 hour (B), 2 hours (C), and 3 hours (D), and an unexposed group (A) served as the control. We used dogs as experimental animals because it may be unethical to expose humans to the conditions we used in this experimental model (Eze et al., 2021). Overall, dog heart models provide a high-fidelity platform for predicting human clinical responses, especially in naturally occurring diseases. For instance, canine hearts are comparable in size, weight, heart rate, oxygen consumption, and contractility to human hearts, making them suitable for studying conditions such as heart failure, arrhythmias, and ischaemic diseases (Choro et al., 2009).

The brand-new generators used in our study produced toxicants, including particulate matter, nitrogen dioxide, hydrogen peroxide, carbon dioxide, carbon monoxide, sulphur dioxide, and volatile organic compounds.

Our study evaluated serum concentrations of Troponin I (TnI) and C-reactive protein (CRP), as well as serum levels and activities of oxidative stress markers: catalase (CAT), glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO) and superoxide dismutase (SOD) in dogs experimentally exposed to graded levels of petrol generator exhaust fumes (PGEF) at 12 metres.

Our study demonstrated that dogs exposed to exhaust fumes from petrol generators are at risk of developing cellular and systemic cardiovascular injury, as evidenced by significantly increased serum levels of TnI, CRP, and oxidative stress markers, and reduced glutathione levels. This finding is relevant to what may happen to humans who keep their electric generator close to their habitat, particularly in densely populated living quarters and marketplaces in Nigeria.

Tissue sections from the heart of the four groups of dogs studied were also processed for histopathological evaluation (Eke et al., 2025). Coagulative necrosis and severe fragmentation of cardiac myofibres were seen in groups B, C and D. Moderate infiltration of mononuclear inflammatory cells was observed in the interstitium of group D, but no significant abnormalities were found in the control group. If we extrapolate the results of this study to humans, it may suggest that people exposed to generator fumes are predisposed to subclinical injuries that are usually not included in our national CVD morbidity data.

Nigeria is on the world map for heavy metal poisoning. Heavy metals are highly toxic and play a significant role both at the population and individual level in causing cardiovascular disease. In March 2010, Médecins Sans Frontières (Human Rights Watch, 2012) discovered an unprecedented epidemic of lead poisoning in Zamfara State. The processing of lead-rich ore to obtain gold resulted in the extensive dispersal of lead dust, leading to widespread ingestion and inhalation of lead particles.

A clinical report found that blood lead levels of affected children were unprecedented (mean = 119 μm/dl) normal= <10 μm/dl). It was the largest known outbreak of lead poisoning in history, leading to the death of at least 735 children, mostly aged < 5 years, and left thousands of others ill with lead poisoning. Though lead poisoning causes multi-organ toxicity, the most common way lead causes death is through chronic cardiovascular injury through hypertension, ischaemic heart disease, atherosclerosis and stroke (Dooyema et al.,2012).

Heavy metal poisoning of the population does not arise from mining sites alone. It can occur from factories, improper disposal of electronic waste, pesticides applied in agricultural settings, lead-based paints, cosmetics and traditional medicines.

We examined the heavy metal burden in a general student population (Anakwue and Nwoke, 2024). We conducted a cross-sectional study to determine the prevalence of heavy metals among apparently healthy students in a university community. Results showed elevated levels of lead, cadmium, chromium and mercury in about 33%, 73%, 95% and 25% of participants, respectively. Dyslipidaemia was found in 37% of the study participants. Logistic regression identified cadmium as a significant predictor of dyslipidaemia (OR:1.074, p<0.05). The high burden of heavy metal exposure among students warrants public health attention, particularly regarding long-term cardiovascular disease risk.

We also documented heavy metal poisoning in rice foods sold in a marketplace (Anakwue et al., 2020). Twenty-five samples were evaluated from five rice dishes. Arsenic content ranged from 503 to 550 mg/kg and was comparable across the five dishes (P = 0.148). Copper was significantly highest (16767 mg/kg) in the white rice and tomato stew dish (P < 0.001), while mercury was significantly highest (33 mg/kg) in white rice and ofeakwu (P < 0.001). Jollof rice had the highest cadmium content (23 mg/kg), a difference that was statistically significant (P = 0.021). Lead was not detected in any of the rice dishes.

These findings on heavy-metal contamination in commonly consumed rice dishes highlight how everyday foods can silently carry toxicants with serious cardiovascular implications. Yet food is only one exposure pathway; Nigeria’s dependence on petroleum products introduces another, equally devastating source of pollution.

In Nigeria, petroleum products are the lifeblood of the economy, powering everything from heavy industries and transport networks to household kitchens. Oil pollution in the Niger Delta, driven by decades of oil spills, gas flaring, and artisanal refining, is directly linked to a high prevalence of CVDs among residents, with studies reporting rates ranging from 11.2% to 51.8%. The analysis reveals that populations in highly polluted areas experience higher rates of conditions such as hypertension, diabetes, heart failure, coronary artery disease and stroke (Essiet et al., 2024; Egwurugwu et al., 2013).

An echocardiographic study of children in Niger Delta showed a prevalence of congenital heart disease (CHD) of 14.4 per 1000 children (Otaigbe and Tabansi, 2014). The prevalence of CHD in this study is the highest in the country and Africa, and may be attributable to the increased oil spillage and gas flaring from petroleum exploitation in this region. The effect on unborn children cuts across all toxicants. A pregnant woman exposed to high PM2.5 in Nigeria is more likely to deliver a baby with congenital heart defects, showing that environmental CVD doesn’t start at 40—it starts in the womb! (Gorini and Tonacci, 2025)

We studied the effect of petroleum products on the heart. We set out to determine whether exposure to petroleum products is associated with myocardial injury and histological abnormalities, using Wistar rats as experimental models (Anakwue and Otamiri, 2018).

Why use rats, you may ask? The use of rodents for research purposes has economic advantages: mice and rats are relatively small and require little space or resources to maintain, have short gestation periods but relatively large numbers of offspring, and have fairly rapid development to adulthood and relatively short lifespans (Bryda, 2013). Laboratory rats also provide ideal animal models for biomedical research and comparative medicine studies because they have many similarities to humans in terms of anatomy and physiology and genetic makeup (Gibbs et al., 2004)

The Wistar rats used in our study were divided into five groups. Group 1 was the control; groups 2 and 3 were exposed to varying durations of inhaled kerosene, and groups 4 and 5 were exposed to varying durations of petrol. Blood samples were collected by orbital puncture, and complete necropsy of the heart was performed; gross lesions were recorded in all the animals.

The results showed increased serum levels of cardiac enzymes, including Creatine Phosphokinase, CK-MB, and troponin I, in rats exposed to petroleum products. There was also histological evidence of cardiac injury on microscopy in the experimental animals. These results provide evidence of petroleum product-induced cardiotoxicity in animals exposed to kerosene and petrol for varying durations.

If the implications of these animal research findings are extrapolated to humans in Nigeria who are exposed to petroleum products continually, it may explain some of the yet unknown causes of cardiovascular diseases in Nigeria.

Apart from petroleum, agriculture is another source of revenue for our people, and there are concerns about toxicant exposure associated with agricultural practices in Nigeria. A cross-sectional study was conducted among 48 pesticide-exposed rice farmers and 39 unexposed controls (Chukwu and Anakwue, 2024). Blood pressure was measured, and blood samples were analysed for inflammatory biomarkers (C-reactive protein [CRP], interleukin-6 [IL-6], cardiac troponin I) and a lipid profile (triglycerides [TG], high-density lipoprotein [HDL], low-density lipoprotein).

Exposed participants demonstrated significantly higher levels of CRP, IL-6, and cardiac troponin I than controls (p < 0.05), indicating marked systemic inflammation and myocardial injury. Significant dyslipidemia was also observed in the exposed group, with higher triglycerides and LDL levels and lower HDL levels (p < 0.05). The rice farmers reported a significantly higher prevalence of hypertension (88%), heart disease (85%), diabetes (62%), and stroke (71%) than controls (P < 0.05). (Chukwu and Anakwue, 2026)

Microplastics (MPs) are an emerging toxicant that have not been fully studied, especially in low- and middle-income nations, where there are numerous exposures to MPs (Anakwue, 2026). We studied the effects of subacute exposure to microplastic-contaminated sachet water on the cardiovascular system of Wistar rats through physicochemical evaluation, Fourier Transform Infrared (FTIR) spectroscopy, biochemical analysis, oxidative stress analysis, and histopathology.

Four groups of male Wistar rats were designated as experimental subjects and exposed to sachet water samples over 30 days. Control rats were exposed to water from the Enugu State water reservoir, stored in a glass bottle. After 30 days, serum cardiac troponin I and cardiac oxidative stress indicators (malondialdehyde, glutathione, superoxide dismutase, catalase and glutathione peroxidase) were measured, and histological sections of the heart were assessed.

FTIR enabled the identification of microplastics in the sachet water samples. Using FTIR analysis, several polymers, such as polyethene, polyethene terephthalate, polystyrene, polyvinyl chloride and products of nylon degradation, were detected in the sachet water samples, providing evidence of microplastics. The FTIR spectrum of the control sachet water sample showed a clean profile with few minor peaks, indicating little to no microplastics.

There was inflammatory cell infiltration and a reduction in glutathione peroxidase in the cardiac tissue of rats exposed to sachet water, suggesting subclinical cardiac injury. Control rats had normal oxidative stress markers and histological findings.

These histological and biochemical alterations, which occur with even short-term consumption of sachet water, may become more severe when Wistar rats are exposed to it for longer. When extrapolated to humans, this may explain the increasing prevalence of cardiovascular disease in Nigeria. There is a need for more studies exposing the animals to longer periods.

Despite multiple layers of evidence suggesting that these toxicants may harm the cardiovascular system, there seems to be a lack of commitment to addressing the issue. The World Health Organisation has recently warned that, despite awareness of morbidity and mortality caused by air pollution, particulate matter (PM)2.5 concentrations—the key pollutant for human health—declined globally by just 1% annually between 2010 and 2019. Global levels remained alarmingly high at 31.7 µg/m3 in 2019, far above the WHO-recommended air quality guideline of 5 µg/m3 (Thundiyil and Stobach, 2012).

While meeting these recommended targets is paramount to protecting the health and well-being of their populations, few countries have met them or are even close to doing so. While 64% of countries have legislation that includes ambient air quality standards, none of these aligns with WHO air quality guidelines (Shairsingh et al., 2024).

Why has the world been so slow to respond to the harm caused by toxicants?

Global action on pollution-related cardiovascular disease (CVD) has lagged due to scientific uncertainty, economic reliance on polluting industries, and weak governance. Chronic, low-level exposures and indirect biological pathways make causation difficult to establish. It should be noted that industrial lobbying and regulatory costs slow policy change. Vulnerable populations in low- and middle-income countries face the greatest risks with limited healthcare access. Recent scientific consensus and new policy frameworks, such as WHO’s 2021 air quality guidelines, signal momentum toward integrating environmental exposure into CVD prevention strategies worldwide.

Figure 11: showing causes of Global delay in tackling cardiovascular toxicants

Peculiar problems of toxicant pollution in Africa

Africa faces unique challenges in managing toxicant pollution due to weak infrastructure, limited awareness, and regulatory gaps. In most countries, the infrastructure in air quality monitoring systems is particularly lacking, with only a handful of countries meeting WHO standards (Anakwue et al, 2024)

Apart from these structural weaknesses, clinicians and medical curricula rarely address environmental exposures. Diagnostic tools such as biomarkers are not routinely used, leading to misattribution of toxin-related cardiovascular disease. In all of these, funding is key, and policy enforcement is so poor.

Socioeconomic inequities intensify the burden, as low-income communities experience high exposure but poor healthcare access. Research gaps further compound the issue, with African-specific exposures—such as biomass fuel, generator emissions, gas flaring, and microplastics from sachet water—largely neglected in global studies.

THE PUBLIC HEALTH AND ECONOMIC COST IMPLICATIONS OF TOXICANT‑INDUCED CARDIOVASCULAR DISEASE

The failure to recognise environmental toxicants as cardiovascular risk factors has consequences that extend far beyond academic oversight. It has profound implications for diagnosis, treatment, public health planning, and economic sustainability.

At the clinical level, this omission introduces a fundamental distortion into how we assess risk. Contemporary tools such as the ASCVD Risk Estimator and the PREVENT equations do not incorporate environmental exposure variables. As a result, individuals living in high‑pollution environments or working in toxicant‑rich occupations are systematically under‑risked.

In practical terms, this means that patients with a true biological risk that is elevated may be classified as low or intermediate risk. Consequently, preventive interventions—such as statin therapy, aggressive blood pressure control, or closer monitoring—may be delayed or withheld.

From Misclassification to Missed Opportunities

This misclassification extends into broader therapeutic gaps. When toxicant exposure is not recognised as a contributing factor:

•Clinicians do not actively investigate environmental history

•Targeted interventions—such as exposure reduction—are not initiated

•Preventive counselling remains limited to lifestyle factors alone

Thus, the neglect of toxicants does not merely obscure diagnosis; it removes entire layers of prevention from clinical care.

This reality compels a fundamental shift in thinking—from a traditional lifestyle‑based model of cardiovascular disease to a more comprehensive exposome‑based model, in which the air we breathe, the water we drink, and the environments we inhabit are recognised as integral determinants of cardiovascular health.

From Clinical Oversight to Economic Consequence

The clinical implications of this oversight are mirrored—and magnified—at the economic level.

Globally, the cost of inaction on environmental toxicants is staggering. Estimates from the Health and Environment Alliance suggest that preventable environmental exposures may account for health costs exceeding 10% of global GDP. Consider the costs of air pollution. The World Bank estimated that in 2019 alone, air pollution cost the global economy approximately $8.1 trillion, representing 6.1% of global GDP (Health and Environment Alliance,2017)

Air pollution negatively impacts the U.S. economy by up to $790billion in 2014, which is roughly 5 per cent of its yearly GDP (Robinson,2019). Despite significant progress, air pollution still causes €600 billion in losses each year in the European Union – equal to 4 per cent of its annual GDP (Mejino-López and Oliu-Barton, 2024)

For Africa as a whole, as at 2013, the estimated economic cost of premature deaths from ambient particulate matter pollution was ≈ USD 215 billion (Roy, 2016). This report estimates that illness and premature deaths from ambient air pollution resulted in losses of $2.1 billion in 2018, representing 2.1% of Lagos State’s GDP (World Bank, 2023). An economic cost study using the cost-of-illness (COI) approach estimates annual economic costs of air pollution-related diseases in the Niger Delta Region at about $3.8 billion. (Udoinyang and Jumbo, 2023)

The cost of toxicant-induced CVD must be enormous given that almost 99% of the global population is exposed to inhalation of air pollutants that exceed the air quality threshold values. An estimated 7 million people die every year from air pollution, and half of that number die from heart disease and stroke (World Heart Federation, 2024)

From Burden to Opportunity: The Economics of Prevention

While the costs of inaction are enormous, the benefits of intervention are equally compelling. Investments in clean air and environmental regulation consistently demonstrate high returns. The United States Clean Air Act, for example, has yielded a benefit‑to‑cost ratio of approximately 30:1, with the vast majority of benefits arising from reduced mortality due to improved air quality (US Environmental Protection Agency, 2020)

In the UK, introducing clean air zones, such as in Bradford, has been estimated to already have led to monthly National Health Service savings exceeding £30 000 and reductions in respiratory and cardiovascular morbidity (National Institute for Health and Care Research, 2023)

Despite these straightforward returns on investment, clean air initiatives still receive only 1% of international development funding, underscoring the need to prioritise environmental health in national and global policy agendas (Clean Air Fund, 2024).

Taken together, the evidence presents a clear and compelling narrative. The failure to integrate environmental toxicants into cardiovascular care leads not only to clinical blind spots but also to substantial economic losses—at individual, national, and global levels.

Conversely, addressing these exposures offers a rare convergence of benefits:

Improved cardiovascular health

Reduced healthcare expenditure

Increased productivity

Enhanced economic growth

In this sense, environmental health is not merely a regulatory concern—it is a cardiovascular imperative and an economic emergency.

A VISION FOR AN ENVIRONMENT THAT SUSTAINS A HEALTHY HEART

The global challenge of toxicant‑induced cardiovascular disease cannot be addressed by isolated efforts. It demands a coordinated, multi‑layered response—one that bridges science, policy, a new urban management system, reimaging of health systems, medical training and clinical practice, and a shift in societal and individual behaviour.

Our vision proposes that cardiovascular care must be embedded within global frameworks such as:

•The Paris Agreement

•The Sustainable Development Goals (SDGs 3, 11, and 13)

This integration ensures that cardiovascular health is recognised not only as a medical issue, but as a planetary one.

At its core, our vision calls for changes in cardiovascular medicine: from a discipline that responds to disease to one that proactively shapes the environments that determine health.

To achieve all these, several interconnected pathways must be pursued.

From Knowledge to Action: The Central Role of Research

The journey begins with knowledge. Research provides the foundation upon which invisible risks are transformed into measurable realities and actionable policies. We must move from knowledge to action by:

Defining safe thresholds for toxicant exposure

Identifying early biomarkers of cardiovascular injury

Understanding genetic and epigenetic susceptibility

Developing context‑specific interventions

This is not merely an academic exercise—it is the key to shifting toxicants from the realm of suspicion to the domain of policy and clinical certainty.

Bridging Science and Policy: The Need for Global Regulatory Action

Clearly, knowledge alone is insufficient. Too often, scientific evidence outpaces regulatory action, leaving populations exposed, so policy changes must chase scientific discoveries. Most chemical safety frameworks, e.g., EU REACH (Registration, Evaluation, Authorisation, and Restriction of Chemicals), established in 2007, focus on carcinogenicity or reproductive toxicity, while cardiotoxicity is often neglected (European Commission, 2024). This should be corrected so that cardiovascular endpoints in toxicological testing of industrial chemicals are mandatory.

There is a need to ensure stricter global regulations on pollutants, such as updating the WHO Air Quality Guidelines (last revised in 2021) to enforce lower limits for PM₂.₅ (annual average <5 μg/m³). There should be an international legally binding instrument on chemical and plastic pollution. EU’s REACH regulation could be scaled worldwide.

Environmental policies must:

Incorporate cardiovascular outcomes into toxicological testing

Enforce stricter air quality standards globally

Advance legally binding frameworks on chemical and plastic pollution

In doing so, we move from passive observation to active protection.

Integrating Climate, Environment, and Cardiovascular Health

The relationship between climate change and toxicant exposure further reinforces the need for integrated action. Climate extremes—wildfires, heat waves, flooding—amplify the release and dispersion of toxicants, thereby intensifying cardiovascular risk.

A programme that emphasises greenery has been shown to protect against air pollution. Urban greenery tackles air pollution by absorbing carbon dioxide and harmful gaseous pollutants through microscopic pores on its leaves; by adsorbing particulate matter and by dispersing and redirecting polluted air; and by cooling the air and creating an environment that encourages better management of toxicants.

Figure 13: showing how urban greenery reduces air pollution

From Global Vision to African Strategy

While the problem is global, the response must be context‑specific.

In Africa, where exposures are high and systems are constrained, the path forward must be grounded in science, equity, and collaboration. Here are suggested strategies:

1. Prioritising Africa-Led Research

Robust, locally driven research is critical to understanding the impact of environmental factors on cardiovascular health. Universities, including ours, must lead studies on air pollution, heavy metals, pesticides, microplastics and climate change. Establishing national registries for CVDs and environmental exposures will provide much-needed data. I urge funding agencies to support African researchers in filling these knowledge gaps.

My department is the first in Africa to pioneer a postgraduate programme in Clinical Toxicology and Forensic Pharmacology, and it is seeking to establish a department of Medical Toxicology and Forensic Pharmacology to train scholars in this critical area. The College Academic Board has already approved this proposal, pending confirmation from the university. We also plan to establish an Environmental Cardiology programme as one of the options for postgraduate training in Nigeria.

2. Promoting Clean Energy and Sustainable Systems

Nigeria’s sustainable future depends on scaling up clean energy and enforcing stricter environmental standards. Solar and other renewable sources must be integrated into the national grid, with governments providing incentives to accelerate adoption. Industrial emission limits should be tightened to curb pollution. Our Heart-Habitat Project is in touch with the National Environmental Standards and Regulations Enforcement Agency (NESREA) on this matter to emphasise the heart-environmental interface of their programme.

At the household level, transitioning to clean cooking technologies—such as gas, solar, or electric stoves—will significantly reduce indoor air pollution. On the roads, electric vehicles should gradually replace petroleum-powered fleets, supported by mandatory vehicle emissions testing. Vehicle Inspection Officers (VIOs) must prioritise emissions monitoring over paperwork or non-regulatory activities.

3. From Research to Policy and Development

Research must not remain confined within academic boundaries; it must translate into practical solutions that safeguard public health. The Federal Institute of Industrial Research, Oshodi (FIIRO) provides a compelling example. In 2013, FIIRO found that locally fabricated grinding machines used to process tomatoes, peppers, and other foods in Lagos contained heavy metals linked to heart disease and organ failure. In response, the institute developed a non-corrosive, multipurpose stainless-steel grinder to reduce contamination risks. This case shows how scientific findings can be translated into safer technologies, underscoring the importance of university–industry collaboration, technology transfer, and translational innovation. We now expect NAFDAC and NESREA to extend their oversight to ensure that all grinders on the market are standardised.

Strong policies and enforcement are the backbone of environmental change. Nigeria can strengthen implementation through agencies such as NESREA and the Federal Ministry of Environment. Key priorities include:

Raising gas flaring fines beyond the current $2 per 1,000 scf to discourage flaring, while investing in gas gathering and storage infrastructure.

Enforcing safe mining practices in Zamfara to mitigate lead poisoning from artisanal gold mining.

Funding NESREA to install stationary and mobile air quality monitors for continuous 24‑hour data collection.

Phasing out polluting “I pass my neighbour” generators in favour of renewable and nuclear energy sources.

Adopting Reduce, Reuse, Recycle principles, Extended Producer Responsibility (EPR), and infrastructure upgrades to tackle plastic pollution.

Regulating noise pollution from nightclubs, religious centres, and social events.

Heart‑Healthy City Policy as a National Development Goal

Against this backdrop, the idea of a “Heart-Healthy City” emerges as both a vision and a necessity. It calls for urban environments designed to minimise toxicant exposure, strengthen public health systems, and promote lifestyles that protect cardiovascular health. By integrating cleaner energy, better waste management, greener spaces, and stronger regulation, African cities can begin to shift from toxic landscapes to heart‑friendly environments.

The Heart‑Healthy City policy is key to sustainable development and should be embedded in Nigeria’s national development agenda, in line with global best practices (Bai, Zhang, Zotova, 2022). A Heart‑Healthy City protects the environment, designs spaces for active living, ensures clean food and cooking, separates harmful industry from communities, provides equitable healthcare, and fosters safety and equity. This is in keeping with the One Health Policy, an integrated approach that recognises the interconnections among human, animal, and environmental health, aiming to optimise all three.

Core pillars include:

Environmental Quality – Clean water, sanitation, and reduced air, noise, and light pollution.

Active & Green Urban Design – Exercise‑friendly spaces and green buffers to trap dust and cool urban heat.

Healthy Food Access – Clean cooking with LPG/electric stoves, elimination of wood/charcoal fires, and affordable nutritious food.

Industrial Safety – Separation of industrial sites from homes, schools, and hospitals.

Healthcare Access & Prevention – Equitable care, education, and regular screenings.

Commitment to Safety – Peaceful neighbourhoods and strengthened social equity.

Advocacy is already underway, with efforts to introduce a private bill in Enugu State to enshrine the Heart‑Healthy City framework into law. Nigeria can lead sub‑Saharan Africa in creating urban environments that protect cardiovascular health, foster equity, and drive national development.

Figure 14: Depicting components of a Heart-Healthy City

Strengthen Health Systems

The vision of a Heart-Healthy City emphasises clean air, safe water, healthy food, and supportive urban environments that reduce toxicant exposure and promote cardiovascular well‑being. Yet, for this vision to become reality, it must be anchored in strong health systems. Strengthening health systems ensures that the prevention, diagnosis, and treatment of toxin-related cardiovascular diseases are not overlooked. By integrating environmental health into medical training, expanding diagnostic capacity, and improving access to care, cities can move beyond aspiration to implementation—transforming heart‑friendly environments into healthier populations

Strengthening Nigeria’s health systems requires integrating environmental risk assessment, preventive policies, clinical innovations, and precision medicine into cardiovascular care.

Routine screening for environmental exposures—such as air pollution, heavy metals, pesticides, and industrial chemicals—should be integrated into cardiovascular risk models. In parallel, the development of reliable biomarkers will enable early detection of toxicant-induced cardiotoxicity, strengthening preventive strategies.

Taken together, these advances highlight an urgent need for a new specialisation that bridges environmental science and cardiovascular medicine: Environmental Cardiology.

Preventive Public Health Policies: Stricter air quality regulations, occupational health reforms, and community‑level interventions—such as clean energy adoption and urban green spaces—are essential to reduce pollutant burdens.

Clinical Management Innovations: Hospitals should establish specialised cardiotoxicity units, employ advanced resuscitation techniques and develop antidotes or immunotherapies for specific toxicant classes.

Precision Medicine & Pharmacogenomics: Genetic screening can identify individuals susceptible to toxicant‑induced cardiotoxicity, while pharmacogenomics and stem‑cell models can guide tailored therapies and predict cardiotoxic responses.

Raise Public Awareness and change individual lifestyle measures.

Strengthening Nigeria’s health systems through environmental risk assessment, preventive policies, clinical innovations, and precision medicine lays the foundation for tackling toxicant‑related cardiovascular disease. Yet, even the most advanced health systems cannot succeed in isolation. Their impact depends on an informed and engaged population. This is where raising public awareness becomes essential—empowering communities to recognise toxicant pollution not just as an environmental issue, but as a direct threat to heart health, and to adopt lifestyle measures that reinforce the gains of stronger health systems. Some of the ways to achieve this aim include:

Schools & Youth Programmes: Integrating environmental health and cardiovascular science into curricula, organising interactive activities such as science fairs and debates, and establishing student‑led clubs for clean air zones, tree planting, and reduced chemical use.

Media & Communication Strategies: Launching public service campaigns through radio, TV, and social media; using storytelling to highlight families affected by toxicant‑related heart conditions; and partnering with influencers—musicians, actors, athletes, and content creators—to amplify the message.

Figure 15: illustrating individual and lifestyle measures

FINAL REFLECTION

Vice-Chancellor, Colleagues and distinguished guests, let me conclude by putting together what I have been saying for the past one hour.

Let us step away briefly from the consulting room.

Imagine a middle-aged trader living in Enugu. She has never smoked. She is not diabetic. She exercises regularly by walking to and from her shop. Her blood pressure is reasonably controlled. Yet, over time, she develops heart disease.

Every evening, when public power fails, she starts a petrol generator positioned just outside her window. She breathes its fumes for several hours daily. She cooks with firewood at home in a poorly ventilated kitchen. Her drinking water comes from plastic sachets that have spent hours exposed to sunlight. Her rice-and-beans meal comes laden with farm-field herbicide and post-harvest storage pesticide.

In traffic, she spends hours inhaling vehicle emissions. At work, she is exposed to dust and industrial pollutants. None of these exposures appears in her medical record. None are entered into cardiovascular risk calculators. Yet they accompany her every day of her life. This is just what many Nigerians and indeed Africans go through…a perfect storm for toxicant exposure.

It is clear that we are overlooking a major part of the cardiovascular disease story in our population. The hidden toxic shadows of cardiovascular disease.

While hypertension, diabetes, obesity, dyslipidaemia, physical inactivity, thyroid disorders, and coagulation abnormalities remain established and important risk factors, they may represent only part of the picture.

Ladies and gentlemen, this lecture is a call to action:

To researchers—to deepen inquiry.

To policymakers—to strengthen protection

To clinicians—to expand vision

To society—to demand personal and group action.

Together, we can ensure that every heartbeat—across Africa and beyond—thrives in an environment that supports life, not undermines it.

WE MUST RECLAIM OUR HOME, OUR PLANETARY EARTH, KNOWING THAT WE HAVE

A silent enemy on a shadowed flight,

It drifts on the wind, unseen.

The heart once steady, beating free,

Now falters beneath polluted decree.

O chemicals, O toxic streams,

You poison our pulse, disturb our rhythm.

Yet we shall rise with steadfast spirit,

To cleanse the earth, calm the waves.

With purpose firm, with voices strong,

To reclaim our Home where hearts belong.

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