REVIEW

CURRENT
OPINION Zinc deficiency and toxicity in pediatric practice
Jennifer L. Willoughby and Christine N. Bowen

Purpose of review
Zinc is a commonly overlooked deficiency in developed countries, occurring in infants, children, and
adolescents during critical growth periods. The purpose of this review is to present the evidence of zinc
deficiencies and toxicities as well as treatment in pediatrics.
Recent findings
During the last decade, the significance of zinc deficiency in childhood growth, morbidity, and mortality
has been recognized by a number of large-scale supplementation trials in underdeveloped countries.
Recognition of the recent nationwide shortage of injectable zinc available for total parenteral nutrition
supplementation over the last 2 years focused attention on the possibility of zinc deficiency in the United
States.
Summary
Although primarily thought of as a problem reserved for underdeveloped countries, zinc deficiency has
increasing pediatric prevalence in the USA. Zinc is an essential trace element in the body that is
responsible for numerous structural, catalytic, and biochemical functions. Deficiencies can occur because of
poor dietary intake, long-term parenteral nutrition without supplementation, and enteral causes such as
malabsorption. Zinc deficiency is closely associated with stunting, respiratory infections, diarrhea, and
dermatitis. Deficiency is hard to define solely by the serum levels. Clinicians should utilize a combination of
serum zinc levels, presenting signs and symptoms, and nutritional intake via oral, enteral, and parenteral
routes to accurately assess the deficiency risk and diagnosis.
Keywords
deficiency, dermatitis, diarrhea, nutrition, pediatrics, toxicity, vegetarian, zinc

INTRODUCTION form of phytic acid, which inhibits the absorption of

Zinc is an essential trace element that the body
utilizes in many ways. Zinc functions as a com-
ponent of 200–300 enzymes to assist in the most
major metabolic pathways in the body responsible
for structural, catalytic, and biochemical functions
&
[1,2,3 ] as well as the formation and maintenance of
proteins and the regulation of gene expression [4].
Zinc also plays a role in glucose metabolism and
insulin secretion, wound healing, and immune
function. Zinc is primarily absorbed in the small
intestine, facilitated by the zinc transporters, and
stored intracellularly in the liver and kidney as zinc
&&
metalloproteins [5,6 ]. Zinc is excreted in the urine
at 0.5–0.8 mg per day or recycled back into the
intestine [5].
Zinc intake is closely related to dietary protein
&&
intake [6 ]. Natural food sources of zinc include
lean meats, shellfish, nuts, milk, and beans. Break-
fast cereals are commonly fortified with zinc.
Animal protein sources of zinc have higher bioavail-
ability than plant-based foods such as grains and
beans. These plant sources contain phytate, the salt
zinc [4].
Approximately 50% of the world’s population is
at risk of inadequate zinc intake. Epidemiological
studies have shown that adolescents usually have
dietary zinc intakes that fail to meet the require-
ments [2] and that globally, 60–80% of adolescents
suffer from micronutrient deficiencies, with zinc in
the forefront because of the nature of zinc-depend-
ent enzymes in the metabolic process and zinc’s
vital role in several body functions during this
pubertal growth spurt period [7]. It is estimated
that more than 20% of individuals worldwide are
actually zinc deficient, especially in underdeveloped
Department of Pediatric Nutrition Support, Cleveland Clinic Children’s,
Cleveland, OH, USA
Correspondence to Jennifer L. Willoughby, RD, LD, Department of
Pediatric Nutrition Support, Cleveland Clinic Children’s, 9500 Euclid
Avenue, Cleveland, OH 44195, USA. Tel: +1 216 445 1614; e-mail:
willouj3@ccf.org
Curr Opin Pediatr 2014, 26:579–584
DOI:10.1097/MOP.0000000000000132

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 Gastroenterology and nutrition

Table 1. Dietary reference intakes updated in 2001

KEY POINTS
(commonly referred to as Recommended Dietary
 Zinc deficiency is challenging to diagnose as serum Allowances or RDAs)
zinc levels do not always accurately affect the total
body stores of zinc, and therefore it is important to RDA/DRI ULb
(mg/day) 2001 (mg/day)
recognize the signs and symptoms in infants, children,
and adolescents. 0–6 Months 2a 4
 Physicians ordering TPN for pediatric patients should 7–12 Months 3 5
be able to recognize the potential signs and symptoms 1–3 Years 3 7
of micronutrient deficiencies, including zinc deficiency, 4–8 Years 5 12
as these patients can be at higher risk.
Male
 Oral zinc supplementation reverses most of the signs 9–13 Years 8 23
and symptoms of zinc deficiency, regardless of the 14–18 Years 11 24
underlying cause of deficiency.
Female
 Supplementation has proven beneficial for preterm 9–13 Years 8 23
infants and for those on long-term TPN. 14–18 Years 9 24
 Supplementation has been associated with significantly Pregnancy 18 years 12 34
increased length or height, particularly in those with Lactation 18 years 13 34
previously stunted growth.
Data from the National Research Council [4]. DRI, dietary reference intakes;
RDA, recommended dietary allowances; UL, upper intake level.
a
Adequate intakes (AIs) – the mean intake for healthy breastfed infants [4].
Established when evidence is insufficient to develop an RDA and is set at a
&&
countries [8 ]. In contrast, the estimated prevalence level assumed to ensure nutritional adequacy.
b
&& Tolerable Upper intake Level – the highest (average) level of daily intake that
in the United States is 1–3% [8 ], with identified is likely to pose no risk of adverse health effects to almost all persons in the
groups from neonatal through adolescence. The true general population.
prevalence of mild zinc deficiency is unknown
because of the nonspecific nature of symptoms
and the imprecise diagnostic methods [9] (Table 1). a partial defect in the gene responsible for intes-
&&
tinal zinc absorption [6 ]. A study of exclusively
breastfed infants published by the American Acad-
DEFICIENCY emy of Pediatrics (AAP) found mild persistent diar-
A review of the presentation, diagnosis, causes, and rhea and perioral, facial, scalp, and perineal skin
treatment of zinc deficiency to help practitioners lesions beginning around the corner of the mouth
execute intervention for high-risk patients. and back of the head. Dermatitis symptoms were not
resolved with topical antibiotics, antifungal agents,
or systemic antibiotics, causing attention to turn to
Presentation (clinical manifestations) zinc deficiency [5].
As a result of the nature of zinc-dependent enzymes
in the metabolic process and zinc’s vital role in several
body functions [7], deficiency affects immune com-
petence, reproductive function, neurobehavioral
&&
development, and physical growth [1,8 ,10,11].
Linear growth is most affected during infancy, child-
hood, and adolescence. Deficiency may present
in the form of skin disorders, diarrhea, short stature
with impaired development, hypogonadism, cogni-
tive dysfunction, anorexia, impaired taste and smell,
altered wound healing, and bacterial infections
&&
[6 ,12].
The most common presenting symptom of zinc
deficiency is dermatitis located around the limbs
and body orifices (Fig. 1). This can occur with either
acquired zinc deficiency or acrodermatitis entero- FIGURE 1. Erythematous, scaly dermatitis plaques on the
pathica. Acrodermatitis enteropathica is an auto- facial cheeks, perioral region, and occiput in an exclusively
somal recessive form of zinc deficiency caused by breastfed infant. Data from Leonard et al. [5].

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Upon physical examination by the clinician, all
vital signs and standard laboratory readings will be
within the normal limits, as well as normal urinal-
ysis, stool examination, serum immunoglobulins,
chest radiographs, and abdominal ultrasonography
[5]. Aside from dermatitis and short stature, other
physical findings may be normal.
Diagnosis
Dietary assessment of pediatric patients can be use-
ful in determining those at risk for zinc deficiency;
however, food recall should not be used as a sole
determinant to define zinc status or make a diag-
nosis. When dietary assessment is combined with
the signs and symptoms as well, as the biochemical
indicators such as serum zinc, conclusions regarding
the level of deficiency can be reached. Serum zinc
level has historically been regarded as the most
practical and widely used indicator for determining
zinc deficiency [13]. The diagnosis of zinc deficiency
using laboratory levels can be difficult as serum zinc
level does not always accurately reflect the total
body zinc, and circulating zinc is rapidly turned
& &
over to meet tissue requirements [14 ,15 ]. Values
can also be altered by infection, stress, and growth
rate [12]. Some investigators argue that it is possible
to be zinc deficient with a normal serum zinc level
&&
[6 ]. Normal serum zinc concentration for pediatric
populations is 70–150 mg/dl (10.7–22.9 mmol/l)
&&
[5,16 ]. For premature infants, withdrawing the
amount of blood required to measure the serum
zinc level might compromise the health of the
infant; therefore, routine testing is not performed,
&&
leading to underdiagnoses [16 ].
Alkaline phosphatase, a zinc-dependent enzyme,
has been used as an additional biological marker of
zinc status. In patients with zinc deficiency, serum
alkaline phosphatase levels for age would presumably
&& & &&
be lower [6 ,15 ,16 ].
As a final component in diagnosis, the rapid
clinical response to zinc supplementation seen in
the meta-analysis studies strongly supports the pre-
sumed diagnosis of zinc deficiency. If serum zinc
and serum alkaline phosphatase levels are normal,
but clinical suspicion from the signs and symptoms
remains high, a trial of zinc supplementation can be
conducted to assess response and aid in diagnosing a
&&
zinc deficiency [8 ].
Causes of zinc deficiency
Zinc deficiency is common in underdeveloped
countries and accompanied by a high mortality rate
in children younger than 5 years of age because
of diarrheal disease, pneumonia, and occasionally
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Zinc deficiency and toxicity Willoughby and Bowen
&
malaria [5,17 ]. Although acquired zinc deficiency is
uncommon in developed countries, it can occur as a
result of poor dietary intake, long-term parenteral
nutrition without supplementation, and enteral
causes such as malabsorption or excessive loss,
brought about by the conditions including gastro-
intestinal disorders, chronic diarrhea, intestinal fis-
&
tulae, and high ostomy outputs [5,13,18 ].
The most common cause of pediatric zinc
deficiency is transient neonatal deficiency attribu-
table to a physiological decline in the zinc content
&&
of maternal breast milk [4,19 ]. Breast milk provides
sufficient zinc in the amount of 2 mg per day for the
first 4–6 months of life. However, zinc concen-
tration in breast milk decreases over time regardless
of the maternal zinc intake, in both term and pre-
& &&
term pregnancies [17 ,20 ]. Human milk alone pro-
vides an inadequate source of zinc after the first
6 months of life, in conjunction with the increased
zinc requirements for infants 7–12 [12,21]. When
introducing baby foods, the traditional starter foods,
rice and wheat based cereals, are inadequate in zinc.
Emerging evidence supports the introduction of
meat as a first complementary food, especially for
exclusively breastfed infants, because of the benefits
&
from increased bioavailable zinc content [17 ,22].
Another cause of zinc deficiency is the inhibi-
tory effect of dietary phytate. Phytate is an abundant
food component in diets that include legumes
and unrefined cereals and whole grains, primarily
vegetarian and vegan diets. Phytate reduces zinc
absorption by forming insoluble complexes with
&&
zinc in the gastrointestinal tract [4,23,24 ].
Recent attention to zinc deficiency was created
by a national shortage of trace elements for total
&
parenteral nutrition (TPN) [3 ]. It is a recommended
additive in TPN for premature or medically com-
promised infants. Though trace elements were avail-
able during shortage, high doses of parenteral trace
elements to meet the zinc requirements could
potentially cause other trace element toxicities
& &&
[3 ,16 ]. Research shows that the time from
initiation of TPN to diagnosis of zinc deficiency
disorder ranged from 4 to 34 weeks in infants and
&&
children on exclusive TPN [16 ]. There is currently
no zinc shortage in the USA. According to the Food
and Drug Administration, only two domestic man-
ufacturers prepare injectable zinc compounds used
in TPN, posing a risk of a shortage occurring again,
leading to zinc deficiency in infants and children on
& &&
long-term TPN [3 ,16 ].
Groups at high risk for deficiency
Preterm infants(defined as birth at <37 weeks gesta-
tional age) are at increased risk because of poor
www.co-pediatrics.com 581
 Gastroenterology and nutrition
absorption, increased zinc loss in stool, increased
requirements from rapid growth and metabolism,
and inadequate zinc stores, as zinc accumulation is
&&
greatest in the third trimester [5,8 ].
Infants and children with gastrointestinal
surgery and digestive disorders, including ulcerative
colitis, Crohn’s disease, and short bowel syndrome,
may experience decreased zinc absorption and
increased endogenous zinc losses from the gastro-
intestinal tract. Other diseases at risk include
chronic liver disease (cirrhosis), chronic kidney dis-
ease, sickle cell disease, diabetes, chronic diuretic
&&
use, and chronic diarrhea [6 ,21].
Vegetarians are at risk secondary to lack of meat
sources and higher consumption of phytate-rich
legumes and whole grains. Studies recommend that
this population may require up to 50% greater
dietary zinc because of the limited absorption and
&&
bioavailability of foods consumed [4,24 ]. The ado-
lescent athletes (i.e. gymnasts, dancers, wrestlers,
etc.) and those with eating disorders such as ano-
rexia nervosa and bulimia nervosa are an additional
group at risk, secondary to the inadequate intake
associated with overall dietary restrictions caused by
a desire to maintain or lose weight and the concur-
rent potential losses in sweat from hyperactivity
&&
[6 ].
Children at risk for generalized malnutrition are
also at risk for zinc deficiency, such as those expe-
riencing food insecurity and poor access to zinc-rich
foods [25]. Many of these specific at-risk populations
are in underdeveloped countries, which is con-
sequently where the majority of the research on
zinc deficiency and supplementation has been
done, including India, China, Guatemala, Vietnam,
Mongolia, and Pakistan.
Treatment
Zinc supplementation remains the only proven,
effective intervention strategy in treating zinc
deficiency when compared with alternatives such
as fortified, processed, complementary foods and
dietary modification. The two latter mentioned
treatments have yet to demonstrate a significant
impact on the biochemical or functional indicators
& &
of zinc status [17 ]. The most widely available
supplementation products include zinc oxide, zinc
acetate, zinc sulfate, and zinc gluconate which con-
tain elemental zinc in percentages of 80, 30, 23, and
&&
14.3% respectively [8 ]. Approximately 70% of
patients with zinc deficiency respond positively to
zinc supplementation if initiated within 6 months
&&
of deficiency onset [8 ] (Fig. 2). Extended periods of
deficiency (6 months) without repletion may have
permanent effects on growth and development.
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FIGURE 2. Erythematous dermatitis on the scrotum, penis,
and buttocks. Dermatitis rash resolved within 10 days of zinc
supplementation. Data from Leonard et al. [5].
Chronic zinc deficiency, if left untreated, can lead
to liver or kidney dysfunction.
&&
A review by Corbo and Lam [8 ] recommends
that children with acquired zinc deficiency receive
elemental zinc at 0.5–1 mg/kg per day to replenish
stores. Children with conditions leading to exces-
sive losses or suspected malabsorption issues will
most likely require higher doses, though exact doses
have not been specified. Therapy is administered for
3–4 months, but may be needed for up to 6 months
&&
[8 ]. Other studies show that acquired symptoms
typically improve with zinc sulfate supplementation
at 3–5 mg/kg per day of elemental zinc and patients
with acrodermatitis enteropathica may require sig-
&& &&
nificantly higher doses [6 ,12,19 ]. A case study
published by the Journal of Pediatrics proved that
supplementation of 4 mg/kg per day for a 9 month
old with low serum zinc levels resulted in symptom
resolutions. At 13 months of age, the patient was
weaned off breast feeding and supplementation was
discontinued, upon discontinuation erythematous
reoccurred. The symptoms persisted until zinc sul-
fate was supplemented at the level of 10 mg/kg per
&&
day [19 ]. Physicians and healthcare professionals
should be aware of the characteristic signs and
symptoms of zinc deficiency and recognize the need
for higher supplementation in acrodermatitis enter-
&&
opathica [19 ].
Recommendations from the American Society
of Clinical Nutrition conclude that zinc content in
TPN for preterm infants be 400 mg/kg per day
because of the limited tissue stores of zinc, low
albumin binding, increased catabolic state, and
& &&
increased urinary zinc losses [3 ,12,15 ,16 ]. Full-
&&
term infants require 200 mg/kg per day [12,16 ].
American Society for Parenteral and Enteral Nutri-
tion guidelines recommend 50 mg/kg per day to
maintain normal serum levels in older children
and up to 100 mg/kg per day for growth [12,26]. In
patients on exclusive TPN without gastrointestinal
losses, 3–4 mg should be given daily as a basic
requirement. In patients with fistulae, diarrhea,
drainage, or high ostomy outputs, 12 mg of zinc
Volume 26  Number 5  October 2014

should be added for each liter of loss [26]. Copper
and iron levels should also be assessed regularly
because of their close interaction with zinc. Plasma
zinc concentrations should be monitored regularly
for dosage adjustments [5].
TOXICITY
Zinc toxicity has been infrequently reported in child-
hood. Excessive acute intake has been associated with
nausea, vomiting, poor appetite, diarrhea, and head-
aches. A study in 2003 found that preschool children
had zinc intakes exceeding the dietary reference
intake, and 36% of the children in the study had
diets containing zinc exceeding the established upper
intake level [27]. In the USA, a combination of
increased availability of zinc-fortified foods coupled
with increased use of zinc supplementation could
possibly lead to excessive intakes among children
[25]. Zinc-induced copper deficiency has been
reported because of copper’s competition for the
&
same absorption site [15 ]. High oral zinc intake
induces the production of metallothionein, which
binds oral copper and excretes it from the body [26].
Zinc supplements can also adversely affect the
lipoprotein metabolism, including cholesterol, high-
density lipoprotein, and low-density lipoprotein
&
levels [14 ,28,29]. Triglycerides levels did not vary
significantly. Excessive zinc supplementation has
also been shown to lead to an impaired immune
response [29] and may interfere with a variety of
medications, including quinolone and tetracycline
antibiotics, penicillamine, and diuretics such as
thiazides.
CONCLUSION
Currently, there is insufficient evidence for regularly
recommending zinc supplementation for well-nour-
ished children. However, it is important to be able to
recognize the classic signs and symptoms of
deficiency and be mindful of the zinc status when
working with pediatric patients identified as at risk
for deficiency or malnutrition [25]. If a pediatric
patient has been diagnosed as zinc deficient utiliz-
ing a combination of serum zinc level, nutritional
intake via oral–enteral–parenteral routes, and pre-
senting signs and symptoms, oral supplementation
&
has been shown to be effective [12,15 ]. Zinc status
at baseline, dose given, growth rate, infections,
medication adherence, and other factors may affect
the efficacy of prescribed supplementation [12].
Acknowledgements
The authors would like to thank Bette Klein, MS, RD,
CSP, LD, Jenna Mastrobuono, MS, RD, CSP, LD, and
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Zinc deficiency and toxicity Willoughby and Bowen
Christina DeTallo, MS, RD, CSP, LD for their contri-
butions and review of this article.
Conflicts of interest
There are no conflicts of interest.
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