Eosinophils: Diagnostic Significance and Clinical Insights

Authors: Payal Bhandari M.D., Emilia Feria, Madison Granados 

Contributors: Vivi Chador, Hailey Chin 




Eosinophils


Eosinophils fight disease, aid tissue repair, and regulate fat glucose metabolism. High counts may signal allergies, infections, or cancer, while low counts can result from alcohol, stress hormones, or medications like steroids and contraceptives.




Typical Adult Range

Ranges and thresholds can vary due to: 

(1) Lab-specific equipment, techniques, and chemicals, and 

(2) Patient demographics, including age, sex, and ethnicity.




Key Insights


Blood contains red blood cells (RBCs), white blood cells (WBCs), and platelets. RBCs transport oxygen via hemoglobin, WBCs defend against infections and maintain immune balance, and platelets prevent blood loss by forming clots and aiding tissue repair. 

Figure 1: Blood is divided into three parts: 55% is plasma, which comprises of water (93%), salts, proteins, lipids, and glucose; 45% are red blood cells; and 1% are WBCs and platelets. 



A WBC differential measures neutrophils, lymphocytes, monocytes, eosinophils, and basophils. Monocytes eliminate pathogens and provide key diagnostic insights into inflammatory conditions like infections, autoimmune disorders, and cancer. Lifestyle factors like diet, stress, and exercise influence monocyte levels and overall health.



What Are Eosinophils?


Eosinophils (Eos) make up 5–7% of circulating WBCs and 6% of bone marrow cells,  defending against pathogens, toxins, and abnormal cells. They aid WBC maturation, debris clearance, and wound repair but can harm tissues if overactive .Excess Eos activity may label healthy tissues and molecules as antigens, increasing autoimmune risks like diabetes, IBD, asthma, and allergies.



Eosinophils regulate fat metabolism, insulin release, and glucose transport. Dysregulated activity reduces energy harvesting, triggering a cascade of metabolic disruptions:


  1. Liver cells increase glucose synthesis, convert fats and proteins to fat storage, and break down muscle protein. 

  2. Fat breakdown decreases, limiting the body’s main energy source.

  3. Rising blood glucose binds hemoglobin, reducing oxygen delivery (hypoxia).

  4. Hypoxia boosts reactive oxygen species (ROS), causing oxidative stress and cell damage.

  5. Oxidative stress raises toxic byproducts, recruiting eosinophils and WBCs to clear debris and prevent bleeding.


Eosinophils help prevent insulin resistance, excess fat storage, and conditions like obesity, atherosclerosis, and gallstones. They support organ health, including gynecological and milk-producing glands, essential for pregnancy, healthy babies, and preventing congenital conditions.  


Eosinophil Formation and Regulation


Eosinophils prevent insulin resistance, obesity, atherosclerosis, and organ fat accumulation while supporting pregnancy, baby growth, and preventing congenital issues.Hematopoietic stem cells (HSCs) produce platelets, RBCs, and WBCs. CMPs form eosinophils, basophils, monocytes, and neutrophils, while CLPs produce T cells, B cells, and natural killer cells. Most WBCs develop in bone marrow, with some in the thymus, spleen, liver, and lymph nodes.

Figure 2: Hematopoietic stem cells in bone marrow, primarily in flat bones, differentiate into red blood cells, platelets, and white blood cells, including monocytes, lymphocytes, eosinophils, neutrophils, and basophils 12 . Eosinophils are granulocytes with cytoplasmic granules containing basic proteins that bind acidic dyes like eosin.


Eosinophil development in bone marrow takes about seven days,.driven by cytokines like IL-3, GM-CSF, and IL-5, with IL-5 crucial for final maturation and release4. These cytokines are produced by immune cells, including CD34+ progenitors, ILC-2, Th2 lymphocytes, natural killer cells, and mast cells. Eosinophils also produce IL-5, extending their development and lifespan.

Eosinophils circulate for 4.5–8 hours and reside in tissues for 8–12 days, concentrating in the respiratory and gastrointestinal tracts. Upon activation, they degranulate, releasing proinflammatory proteins that aid immune cell function but can also damage host tissue. 

During inflammation, Th2 cells and ILC-2 guide eosinophils to injury sites, responding to energy expenditure and circadian rhythm genes. Proinflammatory proteins and chemoattractants like C3a and C5a from lymphocytes and mast cells further direct eosinophil migration to injured tissues. 

The heart is a common target for eosinophilic inflammation, seen in up to one-third of EGPA cases, half of HES cases, and 0.5% of heart autopsies . Proinflammatory proteins, particularly from lymphocytes, drive eosinophil migration to the heart and other tissues, including skin, mucosa, nerves, and lungs. Thymic stromal lymphopoietin (TSLP) from the thymus attracts eosinophils to the respiratory tract, potentially causing united airways disease. 

Figure 3: Eosinophil differentiation. Eosinophils develop with the help of cytokines like IL-5 and are guided to injured tissues by chemokines like CCL11. They release proteins that cause tissue damage, blood clots, atherosclerosis, and organ problems.


Clinical Significance of a High Eosinophil Count (Eosinophilia)


Eosinophilia refers to a high eosinophil count (>500/μL)and is categorized as mild (500–1500/μL), moderate (1500–5000/μL), or severe (>5000/μL). It can affect all ages but is more common in men over 50. 


Eosinophilia, often caused by hypersensitivity to foods, drugs, toxins, or infections, is usually mild and symptomless, detected during routine blood tests. It is more common in overweight individuals with higher WBC counts, elevated liver enzymes, and lower lung function. Severe cases cause symptoms in affected organs:


  • skin rashes 

  • respiratory issues (congestion, wheezing, breathlessness)

  • heart problems (chest pain, palpitations, fatigue)

  • brain issues (confusion, vision/hearing trouble)

  • abdominal pain 

  • fever 

  • weight changes

          


Figure 4: Chronic eosinophilia, driven by excess proinflammatory proteins and ROS, triggers hypersensitivity responses damaging organs and microbiota. It impairs cells, mutates genes, and reduces cell function, causing cardiovascular, lung, digestive, skin, and neurological issues across all ages.



Accordingly, eosinophilic disorders are diagnosed according to the location where the eosinophil count is elevated:


  • Eosinophilic cardiomyopathy (heart; also called Löffler endocarditis) 

  • Eosinophilic colitis (large intestine)

  • Eosinophilic enteritis (small intestine)

  • Eosinophilic esophagitis (esophagus)

  • Eosinophilic gastroenteritis (stomach)

  • Eosinophilic pneumonia or reactive pulmonary eosinophilia (lungs)

  • Eosinophilic pancreatitis (pancreas)

  • Eosinophilic leukemia (bone marrow)

  • Eosinophilic myalgia (skeletal muscles and connective tissues)


When multiple organs are affected, diagnoses may include hypereosinophilic syndrome, tropical eosinophilia, hereditary eosinophilia, Stevens-Johnson syndrome, drug or food allergies, DRESS syndrome, Sezary syndrome, Churg-Strauss syndrome, or myeloid and lymphoid neoplasms. 

Misdiagnosis of eosinophilia is common, with patients often receiving unnecessary antibiotics. Diagnosis typically requires a biopsy to detect eosinophils in affected tissues. Without treatment, severe eosinophilia has an 80% two-year mortality rate, primarily due to heart damage,26 while treatment improves survival to over 80%. Drugs for cancers and autoimmune diseases can worsen eosinophilia, leading to severe complications.

Eosinophilia is linked to dehydration and atherosclerosis, which reduce blood flow (vasoconstriction) and impair digestive functions like HCl production and gut microbiota health. This leads to nutrient deficiencies, undigested food particles, inflammation, and hypoxia, which hinders cellular function and energy harvesting. Hypoxia increases reactive oxygen species (ROS), causing oxidative stress that damages cells, mutates genes, and triggers inflammatory responses.

Figure 5: Healthy gut microbiota support digestion, nutrient absorption, and waste excretion, maintaining metabolic balance. Dysbiosis disrupts this balance, impairing metabolism and increasing harmful pathogens that affect immune response



Oxidative stress oxidizes LDL cholesterol, which deposits in injured vessels to form a temporary plug. Reactive oxygen species (ROS) activate the reticuloendothelial system to release immune cells like eosinophils, clearing debris, preventing bleeding, and repairing wounds. Platelets and endothelial cells form clots, deposit plaque, and promote angiogenesis, driving oxidative stress-induced atherosclerosis.


Figure 6: Atherosclerosis thickens vessel walls, restricts blood flow, raises pressure, and causes hypoxia. This triggers eosinophil infiltration and inflammation, damaging organ structure and function .



A 2017 study published in the American Journal of Epidemiology demonstrated that a rising Eos count is associated with the progression of atherosclerosis-induced vascular diseases and shorter lifespan 31 . Culprits responsible for causing tissue injury include ROS mutating genes involved in various metabolic processes and reducing cell division and differentiation. Eos work hard to rebalance metabolism and keep ROS levels under control. 


Infections

One of the most common causes of eosinophilia is infections. Infections, especially parasitic helminths, are a common cause of eosinophilia, affecting 1.5 billion people in tropical and subtropical regions. Helminths, including roundworms and flatworms, spread through contaminated soil, food, and water. During infections, T lymphocytes recruit eosinophils to the intestines, where they release ROS and proteins to clear debris, repair tissue, and fight pathogens. However, helminths can evade these responses, surviving for years. Persistent eosinophilia causes chronic inflammation, worsens dysbiosis, and activates dormant pathogens like viruses, which hijack host cells, produce toxins, and release ROS, promoting abnormal cell growth and dysfunction.


                          

Figure 7: Viruses infect cells by binding to surface receptors and entering through injection or endocytosis. Inside, they hijack the host’s functions to replicate and produce new viruses, spreading the infection to neighboring cells. 

A 1994 study found 78% of chronic fatigue syndrome patients had markers of chronic viral infections like Epstein-Barr virus (EBV), with 50% showing elevated antibodies to HHV and HSV, often found in elderly brains. Chronic viral infections, linked to eosinophilia-induced inflammation, contribute to learning disorders, dementia, and cancer 37 . EBV, the first known cancer-causing virus, infects over 90% of people worldwide, often asymptomatically in childhood. Stress activates dormant EBV, releasing proinflammatory proteins that trigger lymphocytes and eosinophils, causing conditions like infectious mononucleosis, autoimmune disorders, and cancers such as Hodgkin’s lymphoma and gastric carcinoma49. 

Figure 8: Chronic inflammation, driven by increased ROS, proinflammatory proteins, and oxidized cholesterol, activates leukocytes and platelets, causing tissue damage, clots, plaque, restricted blood flow, and high blood pressure. Untreated stressors exacerbate inflammation, promoting infections, cancer, vascular diseases, autoimmune disorders, and organ damage.

Figure 9: Excess oxidized cholesterol, ROS, and low nitric oxide damage tissues, mutate genes, and impair cell function. Tumor cells bind to cholesterol-thickened vessels, activate platelets, evade immune cells, and release cytokines that promote cancer growth and spread.


Inflammatory Bowel Diseases

Inflammatory bowel diseases (IBD), including Crohn’s, celiac disease, and eosinophilic colitis, are autoimmune disorders causing eosinophilia and affecting the digestive tract. Triggered by dietary proteins like gluten, IBD has an incidence of 10.9 per 100,000 person-years, peaking in the third decade of life. As of 2020, 2.39 million people in the U.S. had IBD, with higher rates among Caucasians and Mexican descendants compared to Black, Asian, and Hispanic populations.


Active IBD involves excess eosinophil and lymphocyte infiltration in the small intestine, responding to substances that threaten the intestinal barrier. Undigested food, microbes, or allergens can damage the barrier, enter circulation, and harm organs and tissues. Elevated enzymes indicate increased immune and platelet activity at injury sites.


Lung Diseases

In 2021, 14.2 million U.S. adults (6.5%) had COPD, with rates stable since 2011 and higher in rural areas due to smoking, aging, and socioeconomic challenges. About 25% of COPD patients (3.8 million) never smoked. COPD involves increased CD8+ T cells and eosinophils, which release toxic compounds that impair oxygen delivery by lung capillaries31. Stress and reduced oxygen trigger megakaryocytes from bone marrow to travel to the lungs, converting to platelets and driving inflammation . This process promotes vascular diseases, immune dysregulation, and autoimmune disorders affecting the lungs, respiratory tracts, digestive tract, bone marrow, and skin.


Figure 10: Low blood oxygen triggers megakaryocytes (MKs) to leave the bone marrow and travel to the lungs, where they convert to platelets when oxygen rises 58 . Chronic inflammation accelerates platelet degradation, reducing thrombopoietin production in the liver and suppressing bone marrow platelet production.


Clinical Significance of Low Eosinophil Count (Eosinopenia)


Eosinopenia, a low eosinophil count (<30/μL, normal 30–350/μL), impairs immune defense, increasing susceptibility to infections and hypersensitivity reactions. It is a reliable marker of sepsis, associated with rapid organ failure and poor survival in intensive care patients .

Eosinopenia can result from prolonged stress hormone production (e.g., cortisol), suppressing immune function and fat metabolism. Cortisol increases glucose synthesis, fat storage, and muscle breakdown, while elevated glucose levels drive oxidative stress, damaging cells and altering metabolic pathways. Over time, oxidative stress impairs the reticuloendothelial system, reducing blood cell production and raising the risk of multi-organ failure. Absolute eosinopenia is linked to higher respiratory support needs in hospitalized patients.

Eosinopenia is linked to autoimmune diseases affecting 3–5% of the U.S. population, driven by dysbiosis, vasoconstriction, dehydration, and chronic inflammation. These factors impair digestion, nutrient absorption, protein synthesis, and waste excretion, forcing immune cells to focus on clearing debris and repairing wounds instead of combating pathogens and cancer cells . Persistent inflammation and atherosclerosis lead to immune cells attacking healthy tissue, increasing risks for autoimmune disorders like diabetes, NAFLD, CVD, and bone marrow cancers 31 . In 2015, 415 million adults had diabetes (90% T2DM),31. and in 2021, 8.4 million people globally had T1DM, with 500,000 new cases and 35,000 undiagnosed deaths. Autoimmune conditions are characterized by low-grade inflammation and eosinopenia.

Type 1 Diabetes Mellitus


In T1DM, hypoxia reduces ATP production and increases ROS, destroying pancreatic cells and reducing hormones like insulin. Insulin deficiency prevents glucose uptake, raises blood glucose and ROS levels, and shifts the liver to produce glucose, store fat, and halt fat metabolism. This leads to undigested proteins, fats, and glucose in the blood, impairing oxygen delivery and triggering inflammation . High eosinophil levels in the pancreas are a hallmark of T1DM, contributing to beta-cell destruction, oxidative stress, and vascular inflammation.


Conclusion

Eosinophil counts indicate immune health, with high levels causing inflammation and cell damage, and low levels linked to chronic diseases like diabetes and cancer. Poor nutrition, stress, and sleep issues worsen these effects by disrupting blood flow and microbiota. Lifestyle changes, diet, exercise, and hydration can help restore balance and reduce health risks.


Source References and Supplemental Research:

  1.  Young B, Lowe jo, Stevens A, Heath JW (2006). Wheater’s Functional Histology (5th ed.). Elsevier Limited. ISBN 978-0-443-06850-8.

  2. Dean L. Blood Groups and Red Cell Antigens [Internet]. Bethesda (MD): National Center for Biotechnology Information (US); 2005. Chapter 1, Blood and the cells it contains. Available from: [PubMed] 

  3.  Berek C., Eosinophils: important players in humoral immunity, Clinical & Experimental Immunology. (2016) 183, no. 1, 57–64, https://doi.org/10.1111/cei.12695, 2-s2.0-84955407770.[PubMed] [Google Scholar]

  4.  Ramirez GA, Yacoub MR, Ripa M, et al. Eosinophils from Physiology to Disease: A Comprehensive Review. Biomed Res Int. 2018;2018:9095275. Published 2018 Jan 28. doi:10.1155/2018/9095275. [PubMed]

  5.  Chu V. T., Fröhlich A., Steinhauser G., Scheel T., Roch T., Fillatreau S., Lee J. J., Löhning M., and Berek C., Eosinophils are required for the maintenance of plasma cells in the bone marrow, Nature Immunology. (2011) 12, no. 2, 151–159, 2-s2.0-78751627318, https://doi.org/10.1038/ni.1981.[PubMed]

  6.  Chu V. T., Beller A., Rausch S., Strandmark J., Zänker M., Arbach O., Kruglov A., and Berek C., Eosinophils promote generation and maintenance of immunoglobulin-a-expressing plasma cells and contribute to gut immune homeostasis, Immunity. (2014) 40, no. 4, 582–593, https://doi.org/10.1016/j.immuni.2014.02.014, 2-s2.0-84898681828. [PubMed] [Google Scholar]

  7.  Aoki A, Hirahara K, Kiuchi M, Nakayama T. Eosinophils: Cells known for over 140 years with broad and new functions. Allergology International. 2021;70(1):3-8. doi:10.1016/j.alit.2020.09.002 [Crosslink]

  8.  Diny N. L., Rose N. R., and Čiháková D., Eosinophils in autoimmune diseases, Frontiers in Immunology. (2017) 8, article no. 484, 2-s2.0-85018409319, https://doi.org/10.3389/fimmu.2017.00484. [Web of Science®] [Google Scholar]

  9.  Lee J. J., Jacobsen E. A., McGarry M. P., Schleimer R. P., and Lee N. A., Eosinophils in health and disease: the LIAR hypothesis, Clinical & Experimental Allergy. (2010) 40, no. 4, 563–575, https://doi.org/10.1111/j.1365-2222.2010.03484.x, 2-s2.0-77949349992. [PubMed] [Google Scholar]

  10.  Shi H.-Z., Humbles A., Gerard C., Jin Z., and Weller P. F., Lymph node trafficking and antigen presentation by endobronchial eosinophils, The Journal of Clinical Investigation. (2000) 105, no. 7, 945–953, 2-s2.0-0034086376, https://doi.org/10.1172/JCI8945. [CAS] [PubMed] [Google Scholar]

  11.  Marichal T., Mesnil C., and Bureau F., Homeostatic eosinophils: characteristics and functions, Frontiers in Medicine. (2017) 4, https://doi.org/10.3389/fmed.2017.00101.[Google Scholar]

  12.  Grinenko T, Eugster A, Thielecke L, et al. Hematopoietic stem cells can differentiate into restricted myeloid progenitors before cell division in mice. Nat Commun. 2018;9(1):1898. Published 2018 May 15. doi:10.1038/s41467-018-04188-7 [PMC Full Text] [PubMed] [Crosslink] 

  13.  Kovalszki A, Weller PF. Eosinophilia. Prim Care. 2016 Dec;43(4):607-617. [PMC free article] [PubMed] 

  14.  “What is an Eosinophil? | Definition & Function | CCED”. www.cincinnatichildrens.org. Retrieved 14 June 2018.

  15.  Fulkerson PC, Rothenberg ME. Eosinophil Development, Disease Involvement, and Therapeutic Suppression. Adv Immunol. 2018;138:1-34. [PubMed] 

  16.  Nussbaum J. C., van Dyken S. J., von Moltke J., Cheng L. E., Mohapatra A., Molofsky A. B., Thornton E. E., Krummel M. F., Chawla A., Liang H.-E., and Locksley R. M., Type 2 innate lymphoid cells control eosinophil homeostasis, Nature. (2013) 502, no. 7470, 245–248, https://doi.org/10.1038/nature12526, 2-s2.0-84885572626.[PubMed] [Google Scholar]

  17.  Chen R., Smith S. G., Salter B., El-Gammal A., Oliveria J. P., Obminski C., Watson R., O’Byrne P. M., Gauvreau G. M., and Sehmi R., Allergen-induced increases in sputum levels of group 2 innate lymphoid cells in subjects with asthma, American Journal of Respiratory and Critical Care Medicine. (2017) 196, no. 6, 700–712, 2-s2.0-85029587825, https://doi.org/10.1164/rccm.201612-2427OC.[PubMed]

  18.  Bass D. A., Behavior of eosinophil leukocytes in acute inflammation. II. Eosinophil dynamics during acute inflammation, The Journal of Clinical Investigation. (1975) 56, no. 4, 870–879, 2-s2.0-0016791578, https://doi.org/10.1172/JCI108166.[PubMed] [Google Scholar]

  19.  Sheikh J. and Weller P. F., Advances in diagnosis and treatment of eosinophilia, Current Opinion in Hematology. (2009) 16, no. 1, 3–8, 2-s2.0-58149127252, https://doi.org/10.1097/MOH.0b013e32831c841f. [PubMed] [Google Scholar]

  20.  Séguéla P. E., Iriart X., Acar P., Montaudon M., Roudaut R., and Thambo J. B., Eosinophilic cardiac disease: molecular, clinical and imaging aspects, Archives of Cardiovascular Diseases. (2015) 108, no. 4, 258–268, https://doi.org/10.1016/j.acvd.2015.01.006. [PubMed] [Google Scholar]

  21.  Ong S., Ligons D. L., Barin J. G., Wu L., Talor M. V., Diny N., Fontes J. A., Gebremariam E., Kass D. A., Rose N. R., and Čiháková D., Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration, The American Journal of Pathology. (2015) 185, no. 3, 847–861, 2-s2.0-84925070755, https://doi.org/10.1016/j.ajpath.2014.11.023. [PubMed]

  22.  Hui C. C. K., Yu A., Heroux D., Akhabir L., Sandford A. J., Neighbour H., and Denburg J. A., Thymic stromal lymphopoietin (TSLP) secretion from human nasal epithelium is a function of TSLP genotype, Mucosal Immunology. (2015) 8, no. 5, 993–999, 2-s2.0-84939474269, https://doi.org/10.1038/mi.2014.126. [PubMed]

  23.  Bachert C., Patou J., and Cauwenberge P. V., The role of sinus disease in asthma, Current Opinion in Allergy and Clinical Immunology. (2006) 6, no. 1, 29–36, 2-s2.0-33744494085, https://doi.org/10.1097/01.all.0000200504.54425.0e. [PubMed]

  24.  Uhm TG, Kim BS, Chung IY (March 2012). “Eosinophil development, regulation of eosinophil-specific genes, and role of eosinophils in the pathogenesis of asthma”. Allergy, Asthma & Immunology Research. 4 (2): 68–79.[PubMed] 

  25.  Kanuru S, Sapra A. Eosinophilia. [Updated 2023 Jun 21]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560929/

  26.  Park TY, Jung JW, Jang JY, et al. Peripheral Eosinophilia and Clinico-radiological Characteristics among Health Screening Program Recipients. Tuberc Respir Dis (Seoul). 2018;81(2):156-162. doi:10.4046/trd.2017.0039 [PubMed] [PMC Full Text] [Crosslink]

  27.  Dale, David. Eosinophilic Disorders. April 023. [MerckManuals]

  28.  Larsen RL, Savage NM. How I investigate Eosinophilia. Int J Lab Hematol. 2019 Apr;41(2):153-161. [PubMed]

  29.  What Is Gut Dysbiosis? Cleveland Clinic. [Cleveland Clinic] 

  30.  Hansson GK, Hermansson A. The immune system in atherosclerosis. Nat Immunol. 2011;12:204–12. [PubMed] [Crosslink]. 

  31.  Herrero-Cervera, A., Soehnlein, O. & Kenne, E. Neutrophils in chronic inflammatory diseases. Cell Mol Immunol. 2022;19(2):177-191. doi:10.1038/s41423-021-00832-3 [PubMed] [PMC Full Text] [Crosslink]  [Nature]

  32.  Nordestgaard, B. G., & Varbo, A. (2014). Triglycerides and cardiovascular disease. The Lancet, 384(9943), 626–635. https://doi.org/10.1016/s0140-6736(14)61177-6 [Science Direct] [Scopus] [Google Scholar] 

  33.  Varbo, A., Benn, M., Tybjærg-Hansen, A., & Nordestgaard, B. G. (2013). Elevated remnant cholesterol causes both Low-Grade inflammation and ischemic heart disease, whereas elevated Low-Density lipoprotein cholesterol causes ischemic heart disease without inflammation. Circulation, 128(12), 1298–1309. https://doi.org/10.1161/circulationaha.113.003008 [Scopus] [Google Scholar]

  34.  Silvestre-Roig C, Braster Q, Ortega-Gomez A, Soehnlein O. Neutrophils as regulators of cardiovascular inflammation. Nat Rev Cardiol. 2020;17:327–40. [PubMed] [Crosslink]. 

  35.  Soehnlein O, Steffens S, Hidalgo A, Weber C. Neutrophils as protagonists and targets in chronic inflammation. Nat Rev Immunol. 2017;17:248–61. [PubMed] [Crosslink]. 

  36.  Soehnlein O, Libby P. Targeting inflammation in atherosclerosis — from experimental insights to the clinic. Nat Rev Drug Discov. 2021;20:589–610. [PubMed]. 

  37.  Kabat GC, Kim MY, Manson JE, et al. White Blood Cell Count and Total and Cause-Specific Mortality in the Women’s Health Initiative. Am J Epidemiol. 2017;186(1):63-72. doi:10.1093/aje/kww226. [PubMed] 

  38.  Martviset P, Phadungsil W, Na-Bangchang K, et al. Current prevalence and geographic distribution of helminth infections in the parasitic endemic areas of rural Northeastern Thailand. BMC Public Health. 2023;23(1):448. Published 2023 Mar 8. doi:10.1186/s12889-023-15378-4 [PubMed] [PMC Full Text] [Crosslink]

  39.  Shin MH, Lee YA, Min DY. Eosinophil-mediated tissue inflammatory responses in helminth infection. Korean J Parasitol. 2009;47 Suppl(Suppl):S125-S131. doi:10.3347/kjp.2009.47.S.S125 [PubMed] [PMC Full Text] [Crosslink]

  40.  Godkin A, Smith KA. Chronic infections with viruses or parasites: breaking bad to make good. Immunology. 2017;150(4):389-396. doi:10.1111/imm.12703 [Pubmed] [Crossref]

  41.  Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Cell Biology of Infection. Available from: [PubMed] 

  42.  Hilgers A, Frank J. Chronic Fatigue Syndrome: immune dysfunction, role of pathogens and toxic agents and neurological and cardiac changes. Wien Med Wochenschr. 1994;144(16):399-406. [Pubmed]

  43.  Wang Y, Ding L, Zhu Q, Shu M, Cai Q. Common Infections May Lead to Alzheimer’s Disease. Virol Sin. 2018;33(5):456-458. doi:10.1007/s12250-018-0049-7 [Pubmed] [Springer]

  44.  Pyzik A, Grywalska E, Matyjaszek-Matuszek B, et al. Does the Epstein-Barr Virus Play a Role in the Pathogenesis of Graves’ Disease?. Int J Mol Sci. 2019;20(13):3145. Published 2019 Jun 27. doi:10.3390/ijms20133145 [Pubmed] [MDPI] [PMC]

  45.  Alizon S, Bravo IG, Farrell PJ, Roberts S. Towards a multi-level and a multi-disciplinary approach to DNA oncovirus virulence. Philos Trans R Soc Lond B Biol Sci. 2019;374(1773):20190041. doi:10.1098/rstb.2019.0041 [Pubmed] [The Royal Society] [PMC]

  46.  Yu H, Robertson ES. Epstein-Barr Virus History and Pathogenesis. Viruses. 2023;15(3):714. Published 2023 Mar 9. doi:10.3390/v15030714 [PubMed] [PMC Full Text] [Crosslink]

  47.  Smatti MK, Al-Sadeq DW, Ali NH, Pintus G, Abou-Saleh H, Nasrallah GK. Epstein-Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update. Front Oncol. 2018;8:211. Published 2018 Jun 13. doi:10.3389/fonc.2018.00211 [PubMed] [PMC Full Text] [Crosslink]

  48.  Lin J, Chen X, Wu H, Chen X, Hu X, Xu J. Peripheral blood lymphocyte counts in patients with infectious mononucleosis or chronic active Epstein-Barr virus infection and prognostic risk factors of chronic active Epstein-Barr virus infection. Am J Transl Res. 2021;13(11):12797-12806. Published 2021 Nov 15. [PubMed] [PMC Full Text]

  49.  McDowell C, Farooq U, Haseeb M. Inflammatory Bowel Disease. [Updated 2023 Aug 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470312/

  50.  Lewis JD, Parlett LE, Jonsson Funk ML, et al. Incidence, Prevalence, and Racial and Ethnic Distribution of Inflammatory Bowel Disease in the United States. Gastroenterology. 2023;165(5):1197-1205.e2. doi:10.1053/j.gastro.2023.07.003 [PubMed] [Crosslink]

  51.  Zhang YZ, Li YY. Inflammatory bowel disease: pathogenesis. World J Gastroenterol 2014;20:91–9. [PubMed] [PMC Full Text] [Crosslink]. 

  52.  Gomez-Bris R, Saez A, Herrero-Fernandez B, Rius C, Sanchez-Martinez H, Gonzalez-Granado JM. CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease. International Journal of Molecular Sciences. 2023; 24(3):2696. https://doi.org/10.3390/ijms24032696. [MDPI]

  53.  Nikolakis D, de Voogd FAE, Pruijt MJ, Grootjans J, van de Sande MG, D’Haens GR. The Role of the Lymphatic System in the Pathogenesis and Treatment of Inflammatory Bowel Disease. International Journal of Molecular Sciences. 2022; 23(3):1854. https://doi.org/10.3390/ijms23031854. [MDPI]

  54.  Liu Y, Carlson SA, Watson KB, Xu F, Greenlund KJ. Trends in the Prevalence of Chronic Obstructive Pulmonary Disease Among Adults Aged ≥18 Years — United States, 2011–2021. MMWR Morb Mortal Wkly Rep 2023;72:1250–1256. DOI: http://dx.doi.org/10.15585/mmwr.mm7246a1.

  55.  Williams, M., Todd, I. & Fairclough, L.C. The role of CD8 + T lymphocytes in chronic obstructive pulmonary disease: a systematic review. Inflamm. Res. 70, 11–18 (2021). https://doi.org/10.1007/s00011-020-01408-z. [SpringerLink]

  56.  Zhao. Platelet generation from circulating megakaryocytes is triggered in the lung vasculature. BioRXiv (2021) bioRxiv 2021.11.01.466743. doi: 10.21203/rs.3.rs-690639/v1 [BioRXiv Full Text] [Crosslink] 

  57.  Gelon L, Fromont L, Lefrançais E. Occurrence and role of lung megakaryocytes in infection and inflammation. Frontiers in Immunology. 2022;13. doi:10.3389/fimmu.2022.1029223 [PubMed] [PMC Full Text] [Crosslink]

  58.  Lefrançais, E., Ortiz-Muñoz, G., Caudrillier, A. et al. The lung is a site of platelet biogenesis and a reservoir for haematopoietic progenitors. Nature 544, 105–109 (2017). https://doi.org/10.1038/nature21706. [Nature]. [NIH].

  59. Cleveland Clinic. Eosinophil & Eosinophilic Disorders. Cleveland Clinic. Published 2022. [Cleveland Clinic] 

  60.  Abidi K, Khoudri I, Belayachi J, et al. Eosinopenia is a reliable marker of sepsis on admission to medical intensive care units. Crit Care. 2008;12(2):R59. doi:10.1186/cc6883 [PubMed] [PMC Full Text] [Crosslink]

  61.  Wang X, Dian Y, Zhou Q, Deng G, Wei R, Zeng F. Association of eosinopenia with worsening prognosis in hospitalized Azvudine-treated COVID-19 patients: a retrospective cohort study. Front Immunol. 2023;14:1320973. Published 2023 Dec 15. doi:10.3389/fimmu.2023.1320973 [PubMed] [PMC Full Text] [Crosslink]

  62.  Lambrecht BN, Hammad H. The immunology of asthma. Nat Immunol. 2015;16(1):45-56. doi:10.1038/ni.3049 [Pubmed] [Nature]

  63.  Sebastian, S., Lucey, B.C. (2008). Reticuloendothelium Malignancy: Current Role of Imaging. In: Blake, M.A., Kalra, M.K. (eds) Imaging in Oncology. Cancer Treatment and Research, vol 143. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-75587-8_17. [SpringerLink]

  64.  Shah AD, Denaxas S, Nicholas O, Hingorani AD, Hemingway H. Low eosinophil and low lymphocyte counts and the incidence of 12 cardiovascular diseases: A caliber cohort study. Open Heart. 2016;3(2). doi:10.1136/openhrt-2016-000477 [PubMed] [PMC Full Text] [Crosslink]

  65.  Cazzaniga M, Fumagalli LAM, D’angelo L, et al. Eosinopenia is a reliable marker of severe disease and unfavourable outcome in patients with COVID-19 pneumonia. Int J Clin Pract. 2021;75(7):e14047. doi:10.1111/ijcp.14047 [PubMed] [PMC Full Text] [Crosslink]

  66.  Wang L, Wang FS, Gershwin ME. Human autoimmune diseases: a comprehensive update. J Intern Med. 2015;278:369–95. [PubMed] [Crosslink]. 

  67.  Dasagrandhi, D., Muthuswamy, A. & Swaminathan, J.K. Atherosclerosis: nexus of vascular dynamics and cellular cross talks. Mol Cell Biochem 477, 571–584 (2022). https://doi.org/10.1007/s11010-021-04307-x. [SpringerLink]

  68.  Mandy O J Grootaert, Martin R Bennett, Vascular smooth muscle cells in atherosclerosis: time for a re-assessment, Cardiovascular Research, Volume 117, Issue 11, 1 October 2021, Pages 2326–2339, https://doi.org/10.1093/cvr/cvab046. [Oxford Academic]

  69.  Zidar DA, Al-Kindi SG, Liu Y, et al. Association of Lymphopenia With Risk of Mortality Among Adults in the US General Population. JAMA Netw Open. 2019;2(12):e1916526. Published 2019 Dec 2. doi:10.1001/jamanetworkopen.2019.16526 [PubMed] [PMC Full Text] [Crosslink]

  70.  Zheng Y, Ley SH, Hu FB. Global aetiology and epidemiology of type 2 diabetes mellitus and its complications. Nat Rev Endocrinol. 2018;14:88–98. [PubMed] [Crosslink].

  71.  Poznyak A, Grechko AV, Poggio P, Myasoedova VA, Alfieri V, Orekhov AN. The diabetes mellitus–atherosclerosis connection: the role of lipid and glucose metabolism and chronic inflammation. Int J Mol Sci. 2020;21:1835. [PMC Full Text] [Crosslink]. 

  72.  Mobasseri M, Shirmohammadi M, Amiri T, Vahed N, Hosseini Fard H, Ghojazadeh M. Prevalence and incidence of type 1 diabetes in the world: a systematic review and meta-analysis. Health Promot Perspect. 2020;10(2):98-115. Published 2020 Mar 30. doi:10.34172/hpp.2020.18 [PubMed] [PMC Full Text] [Crosslink]

  73.  Gregory GA, Robinson TIG, Linklater SE, et al. Global incidence, prevalence, and mortality of type 1 diabetes in 2021 with projection to 2040: a modeling study [published correction appears in Lancet Diabetes Endocrinol. 2022 Nov;10(11):e11. doi: 10.1016/S2213-8587(22)00280-7]. Lancet Diabetes Endocrinol. 2022;10(10):741-760. doi:10.1016/S2213-8587(22)00218-2 [PubMed] [Crosslink]

  74.  Valle A, Giamporcaro GM, Scavini M, Stabilini A, Grogan P, Bianconi E, et al. Reduction of circulating neutrophils precedes and accompanies type 1 diabetes. Diabetes. 2013;62:2072–7. [PubMed] [PMC Full Text] [Crosslink]. 

  75.  Vecchio F, Lo Buono N, Stabilini A, Nigi L, Dufort MJ, Geyer S, et al. Abnormal neutrophil signature in the blood and pancreas of presymptomatic and symptomatic type 1 diabetes. JCI Insight. 2018;3:e122146. [PMC Full Text]. 

  76.  Qin J, Fu S, Speake C, Greenbaum CJ, Odegard JM. NETosis-associated serum biomarkers are reduced in type 1 diabetes in association with neutrophil count. Clin Exp Immunol. 2016;184:318–22. [PubMed] [PMC Full Text] [Crosslink]. 

  77.  Dufort MJ, Greenbaum CJ, Speake C, Linsley PS. Cell type-specific immune phenotypes predict loss of insulin secretion in new-onset type 1 diabetes. JCI insight. 2019;4:e125556. [PMC Full Text] [Crosslink].

  78.  Tomita T, Apoptosis of pancreatic β-cells in type 1 diabetes: The role of Caspase-3 in β-cell apoptosis. Journal of Pediatrics and Pediatric Medicine. Jan 2018. https://doi.org/10.29245/2578-2940/2018/1.1107 [Pediatrics Research Journal]

  79.  Vallianou, N.G., Stratigou, T., Geladari, E. et al. Diabetes type 1: Can it be treated as an autoimmune disorder?. Rev Endocr Metab Disord 22, 859–876 (2021). https://doi.org/10.1007/s11154-021-09642-4. [SpringerLink]

  80.  Yen Jean MC, Hsu CC, Hung WC, et al. Association between lifestyle and hematological parameters: A study of Chinese male steelworkers. J Clin Lab Anal. 2019;33(7):e22946. doi:10.1002/jcla.22946 [PubMed] [PMC Full Text] [Crosslink]

  81.  Wirth MD, Sevoyan M, Hofseth L, Shivappa N, Hurley TG, Hébert JR. The Dietary Inflammatory Index is associated with elevated white blood cell counts in the National Health and Nutrition Examination Survey. Brain Behav Immun. 2018;69:296-303. doi:10.1016/j.bbi.2017.12.003 [PubMed] [PMC Full Text] [Crosslink]

  82.  Cedars-Sinai Staff. Are animal proteins better for you than plant proteins? Cedars Sinai. January 16, 2019. Accessed September 2, 2024. [Website] 

  83.  Koenig G, Seneff S. Gamma-glutamyltransferase: A predictive biomarker of cellular antioxidant inadequacy and disease risk. Dis Markers. 2015:2015:818570. PMID: 26543300. doi: 10.1155/2015/818570. [PubMed] [Wiley] [PubMed]

  84.  De Chiara, F., Checcllo, C. U., & Azcón, J. R. (2019). High protein diet and metabolic plasticity in Non-Alcoholic Fatty liver Disease: Myths and Truths. Nutrients, 11(12), 2985. https://doi.org/10.3390/nu11122985 [PubMed] 

  85.  Balkaransingh PD, Wheeler D, Ning Y, Helou MA, Massey G. Dietary determinants of the White Blood Cell Count. Blood. 2013;122(21):1705-1705. doi:10.1182/blood.v122.21.1705.1705 [Crosslink] [Full Text]

  86.  Guoyao Wu; Yun-Zhong Fang; Sheng Yang; Joanne R. Lupton; Nancy D. Turner (2004). “Glutathione Metabolism and its Implications for Health”. Journal of Nutrition. 134 (3): 489–492. doi:10.1093/jn/134.3.489. PMID 14988435 [PubMed] [Crosslink] 

  87.  Ho, P.I.; Ortiz, D.; Rogers, E.; Shea, T.B. Multiple aspects of homocysteine neurotoxicity: Glutamate excitotoxicity, kinase hyperactivation and DNA damage. J. Neurosci. Res. 2002, 70, 694–702. [Google Scholar] [CrossRef] [PubMed]

  88.  Menni C, Louca P, Berry SE, et al. High intake of vegetables is linked to lower white blood cell profile and the effect is mediated by the gut microbiome. BMC Med. 2021;19(1):37. Published 2021 Feb 11. doi:10.1186/s12916-021-01913-w [PubMed] [PMC Full Text] [Crosslink]

  89.  Hernáez Á, Lassale C, Castro-Barquero S, Babio N, Ros E, Castañer O, Tresserra-Rimbau A, Pintó X, Martínez-González MÁ, Corella D, et al. Mediterranean Diet and White Blood Cell Count—A Randomized Controlled Trial. Foods. 2021; 10(6):1268. https://doi.org/10.3390/foods10061268. [MDPII]

  90.  Moll S, Varga EA. Homocysteine and MTHFR Mutations. Circulation. 2015;132(1). doi:https://doi.org/10.1161/circulationaha.114.013311 [AHA Journals] [Crosslink] 

  91.  Esse, R.; Barroso, M.; Almeida, I.; Castro, R. The contribution of homocysteine metabolism disruption to endothelial dysfunction: State-of-the-art. Int. J. Mol. Sci. 2019, 20, 867. [Google Scholar] [CrossRef] [Green Version]. 

  92.  Kruman, I.I.; Culmsee, C.; Chan, S.L.; Kruman, Y.; Guo, Z.; Penix, L.; Mattson, M.P. Homocysteine elicits a DNA damage response in neurons that promotes apoptosis and hypersensitivity to excitotoxicity. J. Neurosci. 2000, 20, 6920–6926. [PubMed]

  93.  Ho, P.I.; Ashline, D.; Dhitavat, S.; Ortiz, D.; Collins, S.C.; Shea, T.B.; Rogers, E. Folate deprivation induces neurodegeneration: Roles of oxidative stress and increased homocysteine. Neurobiol. Dis. 2003, 14, 32–42. [PubMed]

  94.  Piskin E, Cianciosi D,  Gulec S, Tomas M, Capanoglu E. Iron Absorption: Factors, Limitations, and Improvement Methods. ACS Omega. 2022 Jun 21; 7(24): 20441–20456. doi: 10.1021/acsomega.2c01833 [PMC] [Crosslink] 

  95.  Boldt D. H. New Perspectives on Iron: An Introduction. Am. J. Med. Sci. 1999, 318 (4), 207. 10.1097/00000441-199910000-00001. [PubMed]

  96.  Smirnoff N. Ascorbic Acid Metabolism and Functions: A Comparison of Plants and Mammals. Free Radic. Biol. Med. 2018, 122, 116–129. 10.1016/j.freeradbiomed.2018.03.033. [PubMed]

  97.  Benkhedda K.; L’abbé M. R.; Cockell K. A. Effect of Calcium on Iron Absorption in Women with Marginal Iron Status. Br. J. Nutr. 2010, 103 (5), 742–748. 10.1017/S0007114509992418. [PubMed] [Cambridge Core]

  98.  Ziegler E.E. Consumption of cow’s milk as a cause of iron deficiency in infants and toddlers. Nutr. Rev. 2011;69:37–42. doi: 10.1111/j.1753-4887.2011.00431.x. [PubMed] [Oxford Academic]

  99.  Cory H, Passarelli S, Szeto J, Tamez M, Mattei J. The Role of Polyphenols in Human Health and Food Systems: A Mini-Review. Front Nutr. 2018;5:87. Published 2018 Sep 21. doi:10.3389/fnut.2018.00087 [PubMed]

  100. Zhang H, Tsao R. Dietary polyphenols, oxidative stress and antioxidant and anti-inflammatory effects. Curr Opin Food Sci. (2016) 8:33–42. 10.1016/j.cofs.2016.02.002 [CrossRef] [Google Scholar]

  101.  Sandberg A-S, Scheers N. Phytic Acid: Properties, Uses, and Determinations. In: ; :365-368. Accessed September 2, 2024. [ScienceDirect] 

  102.  Hart J. J.; Tako E.; Kochian L. V.; Glahn R. P. Identification of Black Bean (Phaseolus Vulgaris L.) Polyphenols That Inhibit and Promote Iron Uptake by Caco-2 Cells. J. Agric. Food Chem. 2015, 63 (25), 5950–5956. 10.1021/acs.jafc.5b00531. [PubMed]

  103.  Naghedi-Baghdar, H., Nematy, M., Kooshyar, M. M., Taghipour, A., Sajadi Tabassi, S. A., Shokri, S., Javan, R., & Nazari, S. M. (2018). Effect of a functional food (vegetable soup) on blood rheology in patients with polycythemia. Avicenna journal of phytomedicine, 8(5), 389–398. [PubMed]

  104. Watso, J. C., & Farquhar, W. B. (2019). Hydration Status and Cardiovascular Function. Nutrients, 11(8), 1866. https://doi.org/10.3390/nu11081866 [PubMed]

  105. Popkin BM, D’Anci KE, Rosenberg IH. Water, hydration, and health. Nutr Rev. 2010;68(8):439-458. doi:10.1111/j.1753-4887.2010.00304.x [PubMed]

  106. Billett HH. Hemoglobin and Hematocrit. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 151. Available from: [PubMed] 

  107. Kennedy M. How much water you’re actually supposed to drink each day – and why 8 cups isn’t right for everyone. Business Insider. December 14, 2021. [Website] 

  108.  Pałka T, Koteja PM, Tota Ł, et al. The Influence of Various Hydration Strategies (Isotonic, Water, and No Hydration) on Hematological Indices, Plasma Volume, and Lactate Concentration in Young Men during Prolonged Cycling in Elevated Ambient Temperatures. Biology (Basel). 2023;12(5):687. Published 2023 May 7. doi:10.3390/biology12050687 [PubMed] [PMC Full Text] [Crosslink]

  109.  Ballard H. S. (1997). The hematological complications of alcoholism. Alcohol health and research world, 21(1), 42–52. [PubMed]

  110.  Bradley CS, Erickson BA, Messersmith EE, et al. Evidence of the Impact of Diet, Fluid Intake, Caffeine, Alcohol and Tobacco on Lower Urinary Tract Symptoms: A Systematic Review. J Urol. 2017;198(5):1010-1020. doi:10.1016/j.juro.2017.04.097 [PubMed] [PMC Full Text] [Full Text]

  111.  Polhuis KCMM, Wijnen AHC, Sierksma A, Calame W, Tieland M. The Diuretic Action of Weak and Strong Alcoholic Beverages in Elderly Men: A Randomized Diet-Controlled Crossover Trial. Nutrients. 2017;9(7):660. Published 2017 Jun 28. doi:10.3390/nu9070660 [PubMed]

  112.  Chung PS, Tsai KZ, Lin YP, Lin YK, Lin GM. Association between Leukocyte Counts and Physical Fitness in Male Military Members: The CHIEF Study. Sci Rep. 2020;10(1):6082. Published 2020 Apr 8. doi:10.1038/s41598-020-63147-9 [PubMed] [PMC Full Text] [Crosslink]

  113.  Johannsen NM, Swift DL, Johnson WD, et al. Effect of different doses of aerobic exercise on total white blood cell (WBC) and WBC subfraction number in postmenopausal women: results from DREW. PLoS One. 2012;7(2):e31319. doi:10.1371/journal.pone.0031319 [PubMed] [PMC Full Text] [Crosslink]

  114.  El-Sayed M. S. (1998). Effects of exercise and training on blood rheology. Sports medicine (Auckland, N.Z.), 26(5), 281–292. https://doi.org/10.2165/00007256-199826050-00001 [PubMed] [Springer]

  115.  Kilic-Toprak, E., Ardic, F., Erken, G., Unver-Kocak, F., Kucukatay, V., & Bor-Kucukatay, M. (2012). Hemorheological responses to progressive resistance exercise training in healthy young males. Medical science monitor : international medical journal of experimental and clinical research, 18(6), CR351–CR360. https://doi.org/10.12659/msm.882878 [PubMed] [ISI] [PubMed]

  116.  Kamal A, Malik RN. Hematological Evidence of Occupational Exposure to Chemicals and Other Factors among Auto-Repair Workers in Rawalpindi, Pakistan. Osong Public Health Res Perspect. 2012;3(4):229-238. doi:10.1016/j.phrp.2012.10.003 [PubMed]

  117.  Premont RT, Reynolds JD, Zhang R, Stamler JS. Role of Nitric Oxide Carried by Hemoglobin in Cardiovascular Physiology: Developments on a Three-Gas Respiratory Cycle. Circ Res. 2020;126(1):129-158. doi:10.1161/CIRCRESAHA.119.315626 [PubMed] [PMC Full Text] [Circulation Research]

  118.  Pedersen KM, Çolak Y, Ellervik C, Hasselbalch HC, Bojesen SE, Nordestgaard BG. Smoking and Increased White and Red Blood Cells. Arterioscler Thromb Vasc Biol. 2019;39(5):965-977. doi:10.1161/ATVBAHA.118.312338 [PubMed] [Crosslink]

  119.  Carel RS, Eviatar J. Factors affecting leukocyte count in healthy adults. Prev Med. 1985;14(5):607-619. doi:10.1016/0091-7435(85)90081-7 [PubMed] [Crosslink] 

  120.  Pillai AA, Fazal S, Mukkamalla SKR, Babiker HM. Polycythemia. In: StatPearls. Treasure Island (FL): StatPearls Publishing; May 20, 2023. [PubMed]

  121.  Lewandowska AM, Rudzki M, Rudzki S, Lewandowski T, Laskowska B. Environmental risk factors for cancer – review paper. Ann Agric Environ Med. 2019;26(1):1-7. doi:10.26444/aaem/94299 [PubMed] [Full Text]