Accidental poisoning is common in children. Potassium bromate is commonly used additive and raising agent in many edibles especially bread which is a staple food in Nigeria. This communication is that of an unusual case of acute renal failure following accidental ingestion of potassium bromate tablets

Adeleke, SI

Asani, MO

English

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Accidental Potassium Bromate Poisoning Causing Acute Renal Failure

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ISSN 0972-5997
Volume 8, Issue 1; Jan-Mar 2009
Accidental Potassium Bromate Poisoning Causing Acute Renal Failure
Authors
Adeleke SI, Asani MO,
Bayero Univeristy, Faculty Of Medicine, Dept Of Paediatrics, P. M. B. 3011, Kano, Nigeria
Address For Correspondence
Dr. SI Adeleke,
Aminu Kano Teaching Hospital,
P. M. B. 3452, Kano
E-mail: adelekesolo@yahoo.com
Citation
Adeleke SI, Asani MO. Accidental Potassium Bromate Poisoning Causing Acute Renal Failure 
Online J Health Allied Scs. 2009;8(1):11
URL
http://www.ojhas.org/issue29/2009-1-11.htm
http://ojhas.org 1
OJHAS Vol 8 Issue  1(11)   Adeleke SI, Asani MO. Accidental Potassium Bromate Poisoning Causing Acute Renal Failure
 Case Report 
Abstract:
Accidental poisoning is common in children. Potassium bromate is commonly used additive and raising 
agent in many edibles especially bread which is a staple food in Nigeria. This communication is that of an 
unusual case of acute renal failure following accidental ingestion of potassium bromate tablets.
Key Words: Childhood Poisoning, Bromate, Renal failure, Nigeria
Submitted: Nov 28, 2008; Accepted Apr 9, 2009 Published: May 5, 2009
Introduction:
Potassium bromate is an oxidizing agent used as 
food additives mainly in bread baking, but also 
as a neutralizer in many hair kits.1 It has been 
shown to cause severe and irreversible changes 
including carcinogenesis  in  experimental  anim-
als2,3 and  humans.4,5 Accidental  poisoning  by 
various agents is well documented in children.6.7 
This communication reports a case of potassium 
bromate ingestion by a child who subsequently 
developed acute renal failure.
Case Report: 
A two year old boy presented to the Emergency 
Paediatric Unit of Aminu Kano Teaching Hospital, 
(AKTH) Kano with vomiting, frequent and loose 
watery stools and weakness, all of a day’s dura-
tion. He had been well until the day of presenta-
tion. Past medical history was not contributory. 
He was the second child of a 26 year old mother 
who is a fulltime house wife while the father was 
a 35year old baker. On examination, he was well 
nourished, weighing 12kg with signs of some de-
hydration,  mild  pallor,  watery  rhinorrhea  and 
hepatosplenomegally.  An  initial  diagnosis  of 
acute diarrhea disease with some dehydration of 
acute  diarrhea  disease  with  some dehydration 
was  entertained.  He  received  oral  rehydration 
salts solution but the diarrhea and vomiting per-
sisted;  he  was therefore  commenced on  intra-
venous  ringer’s  lactate.  By  24hours  of  admis-
sion, the diarrhea and vomiting had subsided; he 
was well hydrated, ambulant and looked well. He 
was reverted to oral rehydration therapy (ORT). 
By  48hours  however,  it  was  observed  that  he 
had not  passed any urine despite good hydra-
tion. On further questioning mother volunteered 
the history of ingestion of at least one and half 
tablets of potassium broamate kept at home for 
baking bread about six hours  before presenta-
tion, but that his mouth was rinsed with water. 
At 72hours and despite good hydration, he was 
unable  to  pass  urine  despite  being  well  hy-
drated. A frusemide renal challenge was carried 
out, but a suprapubic needle aspiration yielded 
no urine.  An assessment of acute renal failure 
secondary to potassium bromate poisonings was 
made. By the following day, he had developed 
facial  puffiness  and  pedal  oedema,  his  weight 
was 12.8kg, blood pressure 140/90mmHg. Pulse 
rate  120beats  per  minutes  and  packed  cell 
volume 28 percent. The serum urea and electro-
lytes on days 4, 5, 7 and 18 are shown in Table 
1.
He had  peritoneal  dialysis  and his  fluid  intake 
was  restricted  to  400mls/m2/24hours.  He  was 
also commenced on intravenous calcium glucon-
ate and sodium bicarbonate. On the evening of 
the sixth day, he made urine (250ml in 24hours) 
and by the eighth day,  he was less puffy and 
weighed 12.5kg. By the 9th to the 12th days, he 
had entered  the polyuric  phase of  acute  renal 
failure making between 390 – 420ml of urine in 
24hours.  His  blood  pressure  was  now 
100/50mmHg. The mother then requested to be 
discharged on the 14th day. Due to financial con-
straints. He was seen in the Paediatric Nephro-
logy Clinic on the 24th day, he weighed 12.1kg 
and serum electrolyte and urea are normal.
Table 1: Serum Urea and Electrolyte levels in the patient.
 Day 4 Day 5 Day 7 Day 18
Creatinine (mmol/L) 690 590 340 145
Urea (mmol/L) 15.8 14.8 12.0 2.5
Sodium (mmol/L) 130 127 122 120
Potassium (mmol/L) 5.4 4.2 3.9 3.5
Bicarbonate (mmol/L) 25 15 18 15
Discussion
Accidental  poisoning  is  very  common  in  child-
hood, mostly in those aged five years and below. 
It usually involves a single substance often com-
monly used at home, with  ingestion being the 
most common used at home, with ingestion be-
ing the most common route of exposure. Most 
cases are also manageable at home.8 This case 
fits the above scenario except poisoning was by 
potassium  bromate,  few  cases  of  which  have 
been reported before. Potassium bromate is be-
ing use despite the well orchestrated media re-
port against it. 
Potassium bromate is an oxidizing agent widely 
consumed in bread in which it is used as an ad-
ditive  in  the baking process.9 It  is  also readily 
available  in  thioglycolate  containing  hair  kits.1 
However,  in  the  reported  case,  potassium 
bromate in the form of goppus tablet which the 
patient’s  father,  a  baker,  had stored at  home. 
Following  the  accidental  ingestion,  the  mother 
only rinsed the patient’s mouth and thought she 
had done the best for her child. He presented 
with  some  known  side  effects  of  potassium 
bromate  toxicity  which  include  vomiting, 
diarrhea,  renal  damage  with  oliguria.  Other 
known side effects include hypotension, pulmon-
ary oedema, hepatitis  and cardiac failure from 
toxic  myocarditis.10,11 None of these serious ef-
fects occurred in our patients. The acute renal 
failure was initially not noticed hence the initial 
omission of  urinalysis  and  monitoring of  blood 
pressure. 
Potassium bromate is particularly nephrotoxic.12 
It is known that death from renal failure may oc-
cur in one to two weeks in rats. It is also carcino-
genic in experimental animals12,13 and in human 
kidney tissue in vitro.14 It has also been shown to 
induce renal failure and irreversible sensorineur-
al  hearing  loss  in  guinea  pigs,4 testicular  and 
peritoneal mesotheliomas in rats15 and immedi-
ate and delayed signs of vestibular dysfunctions 
in dogs.4 The carcinogenic risks to humans have 
been evaluated and WHO has recommended ac-
ceptable limits of daily intake.3  
http://ojhas.org 2
OJHAS Vol 8 Issue  1(11)   Adeleke SI, Asani MO. Accidental Potassium Bromate Poisoning Causing Acute Renal Failure
Various  methods  have  been  described  for  the 
determination of bromate residues with accuracy 
in a variety of baked goods.16,17 The nephrotox-
icity is though to result from  an interplay of in-
creased formation of reactive oxygen speices,18 
lipid  peroxication,19 induced  DNA  fragmenta-
tion,20 micronuclei formation and induced cellu-
lar proliferation.21 A clear six difference has been 
reported in the susceptibility of rat kidney to the 
generation  of  the  oxidative  stress.20 Male  rats 
show a rapid and persistent response as against 
an increase that  only becomes apparent three 
weeks after exposure in the females, the signi-
ficance of this to humans is not known. The anti-
oxidants,  ascorbic  acid  (vit  C),  vitamin  E, 
cysteine and glutathione are the only substances 
documented  to  have potential  against  carcino-
genicity of potassium bromate.4 Attempts have 
been made to find an acceptable substance for 
potassium  bromate  in  the  baking  process.  A 
Venezuelan  study  demonstrated  the  technical 
feasibility  of  replacing  80ppm  of  potassium 
bromate for 20ppm of ascorbic acid in the flour 
without affecting the bread acceptability.1   
Potassium bromate has been banned in various 
countries. There is legislation against its use in 
the bread baking industry in Nigeria, while the 
National Agency for Food and Drug, Administra-
tion and Control had in the past destroyed bread 
made with potassium bromate in some cities in 
the  country.  The  legislation  has  however  not 
been widely enforced. As shown in this report, 
the average hospital in the country may be un-
able to cope with the effects of poisoning by this 
substance.  Therefore education on the preven-
tion of poisoning by the substance should be car-
ried out in place such as well  child clinics and 
over  the  electronic  media.  Parents  should  be 
counselled about potential  poisons and how to 
prevent access to them. They should also be in-
formed on what to do if poisoning occurs. This 
would  reduce  serious  morbidity  from such  ex-
posure.
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2. Chuu JJ, Hsu CJ, Lin-Shiau SY. The detri-
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17. Dennis MJ, Burrell A, Mathieson K, Wil-
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http://ojhas.org 4
OJHAS Vol 8 Issue  1(11)   Adeleke SI, Asani MO. Accidental Potassium Bromate Poisoning Causing Acute Renal Failure


A possible role for cell proliferation in potassium bromate

A possible role for oxid-ative stress in potassium bromate carci-nogenesis 1995;16:593–597.

Acci-dents and sudden infant death syn-drome In: Campbell AGM, Mcintosh Neds. Tofar and Arneils Text Book of Paediatrics.

Correlation between induction of DNA fragmenta-tion and micronuclei formation in kid-ney cells from rats, humans and tissue specific caranogenic activity. Toxicol Appl Pharmacol

Evaluation of certain food additives and contaminants.

Experimental study of oxidative DNA damange (Re-view) Free Radic Res

Generation of active oxygen species in vitro by the interac-tion of potassioum bromate with rat kid-ney cell. Carcinogenesis

In-duction of poly (ADP-ribosylaion in the kidney after in vivo application of renal caranogens.

Lack of oxidative DNA dam-age or initiation of carcinogenesis in the kidneys of F 344 rats given subchronic exposure to P-dichbro benze (p DCB) at a carcinogenic dise.

Measurement of bromate in bread by li-quid chromatography with post column flow reactor detection.

Organotropic formation and disap-pearance of 8 hydrooxygnosine in the kidney of spraque dawley rats esposed to adriamycin and 1 & Bro3. Cancer lett 1993;74:141–145.

Origin and distribu-tion of potassium bromate induced testicular and peritoneal mesotheho-mas in rats. Toxicol Pathol

Oxidative DNA damage induced by potassium bromate in isolated rat renal proximal tubules and renal nuclei. Cancer Lett

Oxidative DNA damage induced by potassium bromate under cell free conditions and in mam-malian cells.

Poisoning in childhood In: Hendriske RG,

Potassium bromate IARC monographs on the evaluation of carci-nogenic risks to humans. WHO Mono-graph.

Requirement of ghitathione and cysteine in guinea specific oxidation of DNA by carcinogenic potassium bromate Chem Res Toxicol

Severe acute renal failure due to bromate intoxication. Report of a case and discussion of management guidelines based on a review of literat-ure.

Substitution of ascorbic acid for potassi-um bromate in making French bread. Archivos Latinoamericanos de Nutrition

The determination of the flour improver potassium bromate in bread by gas chromatographic and ICP-MS methods. Food Addit and Contam

The detri-mental effects of potassium bromate and thioglycate on audiotory branstem response in guinea pigs.

Accidental Potassium Bromate Poisoning Causing Acute Renal Failure

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