A current HOT-TOPIC in Sri Lanka is Aflatoxins in edible oils. Everybody from house wives to husbands to politicians and academic express their views. It’s good to know about the basic truths about Aflatoxins before we form our own opinion. In this post my objective is to give you the facts so that you could decide on what to do… 

The United States Food and Drug Administration (FDA) action levels for aflatoxin present in food or feed is 20 to 300 ppb.[14] The FDA has had occasion to declare both human and pet food recalls as a precautionary measure to prevent exposure.

Occurrence of aflatoxins in edible vegetable oils in Sri Lanka

Food Control Volume 101, July 2019, Pages 97-103


  • Nearly 38% of the coconut oil samples were contaminated with aflatoxins.
  • The total aflatoxin contamination in coconut oil ranged from 2.25 to 72.70μg/kg.
  • Aflatoxin B1 contamination in coconut oil ranged from 1.76 to 60.92 μg/kg.
  • Certain coconut oil products available in Sri Lanka may pose a health risk.
  • Aflatoxin contamination in six other vegetable oil types tested were below 0.8 μg/kg.

Aflatoxin contamination of coconut oil from small scale mills: toxin levels and their relation to free fatty acid content

Journal of National Science Foundation of Sri Lanka, 1983

Coconut oil which was mechanically extracted in small scale mills, from intermittently processed (sun-dried or smoked) Grade 111 or substandard copra kernels was assayed for free fatty acid and aflatoxin B1. Oil from these samples showed significantly high levels of aflatoxin B1 (mean value 186 ppb in 115 samples of oil) than the levels found in oil from adequately processed copra extracted in large scale industrial mills.

The attention of the coconut industry is drawn to this problem as a potential health hazard to humans and animals, from the consumption of the oil and press cake from such inadequately processed kernels.

The relationship between free fatty acid (FFA) content and aflatoxin B1 levels in 100 samples of coconut oil from the small scale mills has been investigated. No correlation was found. The conventionally used FFA content as a chemical index of the ‘quality’ of oil does not reflect the degree of aflatoxin contamination, making it necessary to apply separate assays for aflatoxin contamination in coconut oil, from commercial sources. Possible reasons for the absence of a correlation between FFA and aflatoxin levels in such oils are discussed.


Coconut fat, oil, and CVD – an update


Aflatoxins are poisonous carcinogens and mutagens that are produced by certain molds (Aspergillus flavus and Aspergillus parasiticus) which grow in soil, decaying vegetation, hay, and grains.

They are regularly found in improperly stored staple commodities such as cassava, chili peppers, cottonseed, millet, peanuts, rice, sesame seeds, sorghum, sunflower seeds, sweetcorn, tree nuts, wheat, and a variety of spices.

When contaminated food is processed, aflatoxins enter the general food supply where they have been found in both pet and human foods, as well as in feedstocks for agricultural animals. Animals fed contaminated food can pass aflatoxin transformation products into eggs, milk products, and meat.[1] 

Children are particularly affected by aflatoxin exposure, which is associated with stunted growth,[3] delayed development,[4] liver damage, and liver cancer. An association between childhood stunting and aflatoxin exposure[5] has been reported in some studies[6][7] but could not be detected in all.[8][9] Furthermore, a causal relationship between childhood stunting and aflatoxin exposure has yet to be conclusively shown by epidemiological studies, though such investigations are under way.[10][11] Adults have a higher tolerance to exposure, but are also at risk. No animal species is immune. Aflatoxins are among the most carcinogenic substances known.[12] After entering the body, aflatoxins may be metabolized by the liver to a reactive epoxide intermediate or hydroxylated to become the less harmful aflatoxin M1.

Aflatoxins are most commonly ingested. However the most toxic type of aflatoxin, B1, can permeate through the skin.[13]

The United States Food and Drug Administration (FDA) action levels for aflatoxin present in food or feed is 20 to 300 ppb.[14] The FDA has had occasion to declare both human and pet food recalls as a precautionary measure to prevent exposure.


Book Stat PEARLSContinuing Education Activity



  • Describe the epidemiology of aflatoxin toxicity.
  • Outline the typical presentation of a patient with aflatoxin toxicity.
  • Explain the treatment considerations for patients with aflatoxin toxicity.
  • Review the importance of improving care coordination among the interprofessional team to enhance care coordination for patients affected by aflatoxin toxicity

History and Physical

Whenever aflatoxin toxicity is suspected, a careful history regarding the dietary habits of the patient, similar features in family and community, patient occupation, and environmental exposure should be carefully assessed. Health implications from aflatoxin exposure depend on various factors ranging from dose and duration of exposure to a person’s age, gender, health, immunity, diet, and environmental factors. Patients with aflatoxin toxicity may have a range of non-specific signs and symptoms, but the predominant features are of hepatotoxicity. 

Acute toxicity results when someone takes in a high amount of aflatoxins in a very short time. Most common signs and symptoms are:

  • Nausea
  • Yellowing of skin and sclera (icterus)
  • Itching
  • Vomiting
  • Bleeding
  • Abdominal pain
  • Lethargy
  • Edema
  • Convulsions
  • Coma
  • Death

Adults usually have a good tolerance to aflatoxin, and, in the reported deaths due to acute poisonings, it is the children who usually die.

Chronic toxicity occurs by consuming small amounts of aflatoxins at a time but over a prolonged period. Chronic exposure to aflatoxin can cause:

  • Impaired growth and development especially in children 
  • Hepatocellular carcinoma presenting as weight loss, abdominal mass, anorexia, nausea, vomiting, bleeding, psychosis, etc.


An evaluation of a suspected case of aflatoxin toxicity can be done by measuring the aflatoxin level in food consumed by the patient, or the aflatoxin metabolites in the patient’s body.

Some popular methods to detect aflatoxin exposure in food and feed are:

  • Thin-layer chromatography (TLC)
  • High-performance liquid chromatography (HPLC)
  • Liquid chromatography-mass spectroscopy (LCMS)
  • Enzyme-linked immune-sorbent assay (ELISA)

ELISA using AfB1-lysine (metabolite of AFB1) concentration in the patient blood can help detect aflatoxin.

There are other techniques used to detect levels of aflatoxin in the human body. One method is the measurement of the AFB-guanine adduct in the urine of patients. This technique measures only recent exposure during the past 24 hours. Due to the varying half-life of this product, its level may vary from time to time based on diet. Therefore it is not ideal for assessment of long term exposure. Measurement of AFB-albumin adduct level in the blood serum is another method to detect Aflatoxin exposure over a long period.

Additionally, the assessment of liver function test to include prothrombin time (PT/INR), activated partial thromboplastin time (aPTT), albumin, bilirubin, aspartate transaminase, alanine transaminase) is done. Imaging of the liver using ultrasonography and CT-scan may help to study liver involvement further.

Other tests include the basic metabolic panel, complete blood count, and renal function depending upon the patient presentation and features.

Treatment / Management

Acute aflatoxicosis has no known antidote. The management is mainly focused on symptomatic and supportive care. Management options may include suitable intravenous fluids, vitamin B, and vitamin K administration. A high-quality protein-restricted diet with adequate carbohydrates is suggested. Also, fever, nausea, vomiting, and other patient complaints should be carefully addressed. If signs and symptoms are suggestive of acute liver failure, it must be recognized early, and subsequent care should follow in a critical care setting