nutrients

Review
Pediatric Thermoregulation: Considerations in the
Face of Global Climate Change
Caroline J. Smith
Department of Health and Exercise Science, Appalachian State University, Boone, NC 28608, USA;
[email protected]




Received: 1 July 2019; Accepted: 16 August 2019; Published: 26 August 2019


Abstract: Predicted global climate change, including rising average temperatures, increasing airborne
pollution, and ultraviolet radiation exposure, presents multiple environmental stressors contributing
to increased morbidity and mortality. Extreme temperatures and more frequent and severe heat
events will increase the risk of heat-related illness and associated complications in vulnerable
populations, including infants and children. Historically, children have been viewed to possess
inferior thermoregulatory capabilities, owing to lower sweat rates and higher core temperature
responses compared to adults. Accumulating evidence counters this notion, with limited child–adult
differences in thermoregulation evident during mild and moderate heat exposure, with increased
risk of heat illness only at environmental extremes. In the context of predicted global climate
change, extreme environmental temperatures will be encountered more frequently, placing children
at increased risk. Thermoregulatory and overall physiological strain in high temperatures may be
further exacerbated by exposure to/presence of physiological and environmental stressors including
pollution, ultraviolet radiation, obesity, diabetes, associated comorbidities, and polypharmacy that
are more commonly occurring at younger ages. The aim of this review is to revisit fundamental
differences in child–adult thermoregulation in the face of these multifaceted climate challenges,
address emerging concerns, and emphasize risk reduction strategies for the health and performance
of children in the heat.

Keywords: thermoregulation; children; sweating; skin blood flow; heat stress; climate change;
pollution; ultraviolet radiation; hydration; environmental stressors

1. Introduction
Globally, increased variability in environmental extremes and rising average global
temperatures [1], coupled with increasing ultraviolet (UV) exposure [2] and pollution [3–6], are
greatly impacting human health and performance [7–9]. The very limits of human thermoregulation
may be tested, with multiple combined stressors of heat, dehydration, UV radiation, pollution, and
noise and disease transmission all exacerbating physiological strain [10,11]. This review aims to
address the topic of thermoregulation in the context of global climate challenges with emphasis placed
on children, who are considered an ‘at risk’ population for increased morbidity and mortality during
heat events and a range of environmental stressors.
Concepts in pediatric thermoregulation have been revisited and challenged over the past 20 years,
countering the argument that children possess inferior thermoregulatory capabilities [12], particularly
in mild and moderate environmental conditions. However, greater risk of adverse health events
compared to healthy adults is widely recognized in more extreme environmental conditions and during
physical exertion. Considering the rapidity and magnitude of predicted global climate change and
adverse environmental conditions, it is prudent to understand the effects on physiological function
resulting from high ambient temperatures, UV radiation [2,13,14], and pollution [4,15–18]. In addition,

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understanding the interplay between multiple environmental stressors and increasingly common
childhood diseases and comorbidities, including obesity and the onset of preventable ‘adult’ diseases in
children, is important in accurately predicting thermoregulatory responses and long-term health effects
in a rapidly changing environmental landscape. This review is not a comprehensive and exhaustive
review of thermoregulation in children, for which the reader is directed to other articles [19,20]. Rather,
the focus of the present review will be adult–child differences in thermoregulation, with an emphasis on
the adverse impact of projected environmental and climate change on thermoregulation, physiological
function, overall health, and precautions for risk reduction.

2. Thermoregulation
Humans regulate internal body temperature at ~37 ◦ C via complex autonomic control of skin
blood flow (SkBF) and sweating, with further local modulation [21]. Afferent inputs from central
and peripheral (skin) thermoreceptors are sent to the thermoregulatory control center in the preoptic
anterior hypothalamus (POAH) [22–24]. Inputs are integrated in the POAH before efferent sympathetic
signals elicit appropriate sudomotor and vasomotor adjustments to regulate core body temperature
(Tc ) [21]. Heat exchange and Tc responses are conceptually demonstrated via the human heat balance
Equation (1), with additional adjustments for respiratory heat losses:

S = M − W ± K ± R ± C − E. (1)

Metabolic energy (M) is either converted into external work (W; negligible in most conditions) or
thermal energy, which must be dissipated from the body to avoid an increase in heat storage (S). Heat
exchange (both losses and gains) occurs via dry heat loss mechanisms; conduction (K), radiation (R),
convection (C), in addition to evaporative heat loss (E), primarily from sweat on the skin surface but to a
minor extent via the respiratory tract. Rates of heat gain and dissipation must be equivalent to maintain
heat balance (S = 0) and a stable Tc [25]. Under normothermic conditions, cutaneous vasomotor
adjustments facilitate convective heat loss (or gain) at the skin surface to counter minor fluctuations in
body temperature. During exercise and/or exposure to high ambient temperatures, heat gains exceed
heat losses (S > 0), and increased Tc and skin (Tsk ) temperatures elicit more pronounced cutaneous
vasodilation and initiation of sudomotor responses [26–28]. SkBF can increase from ~0.25–0.30 L/min
during normothermic conditions to 6–7 L/min during extreme heat exposure. To facilitate increased
SkBF (and muscle blood flow during exercise in the heat), in addition to providing blood plasma as a
precursor for sweat production, cardiac output (Q) increases to meet demands. Notably, when ambient
temperature (Ta ) exceeds Tsk , a reversal of the temperature gradient prevents dry heat losses from
the body, and heat is gained, increasing thermal load. Evaporation of sweat is the greatest avenue of
heat loss from the body during exercise and heat exposure, varying with age, exercise intensity, and
hydration status. Thermoregulatory function is influenced by many factors, including cardiovascular
responses, sweating rate (SR), body surface area (BSA) to mass ratio, body composition, hydration
status, and nonthermal inputs. During hyperthermia, increased Tc and Tsk elicit thermoregulatory
responses to balance heat losses and gains and stabilize Tc (compensable conditions) [25]. If heat loss
mechanisms are not sufficient, conditions are said to be uncompensable and Tc will continue to rise,
with potential progression to heat-related illness and injury, including fatal heat stroke [29].
Adult–child differences in thermoregulatory responses to warm environments are evident, largely
owing to immaturity of their physiological systems, morphological, and neuroendocrine differences.
Children exhibit a lower Q [30], lower whole-body SRs [31–34], and greater increases in Tc during
passive exercise in the heat [33,35]. Children consistently show higher SkBF responses in warm
conditions compared to adults, directing a significantly greater proportion of their lower Q to the
skin. Combined with significantly lower SRs, children are reported to rely more heavily on dry heat
losses compared to adults [31,35]. Historically, these differences have led to the view that children
possess inferior thermoregulatory responses and poorer tolerance to heat compared to adults, defined
Nutrients 2019, 11, 2010 3 of 24

as an inability to maintain heat balance, resulting in an amplified Tc response that may progress to
serious heat illness without intervention [36]. This notion has been challenged [37], with accumulating
evidence of compromised thermoregulatory function only at environmental extremes. This warrants
further investigation with rising average global temperatures and increased frequency of heat events.
The concept of children being classified as “at risk” of heat-related illness relates to increased
vulnerability to the effects of heat stress, with increased morbidity or mortality versus a healthy adult
reference population [38]. Epidemiological evidence is mixed but does indicate a distinct age-related
variation in heat-related morbidity and mortality [38]. Age groups at greatest risk of health-related
morbidity and mortality include older adults (≥75 years) and “young children” (0–4 years) [38,39].
Death rates are lowest among children aged 5–14 years at 0.1 per million, with considerably higher infant
death rates at 4.2 per million, in part owing to infants and younger children being unable to operate locks
or being restrained in vehicles, in which ambient temperature is exacerbated [38]. Between 17–74 years
of age, a progressive, moderate increase in heat-related deaths occurs, with considerable increases with
more advanced age (≥85 years, 12.8 deaths per million). Prediction models of weather-related deaths
due to excessive natural heat exposure suggest an odds ratio of 4.4 in infants (<1 year), 1.9 in young
children (1–4) versus an odds ratio of 1.0 in the young adult reference population (25–34 years) [38].
Overall, the World Health Organization (WHO) predicts child mortality related to heat exposure at
>100,000 deaths per year by 2050, with greatest climate change related mortality occurring in South
Asia [40].

3. Global Climate Change

Climate fluctuations are recognized to increase the risk and exacerbate the impact of a broad range
of diseases, with extreme heat (and cold), pollution and UV exposure increasing human morbidity and
mortality [41,42]. Compelling evidence from predictive models of climate change indicate with virtual
certainty rising global temperatures and increasing heat wave frequency and severity, but the overall
impact of climate change on human health is not fully understood [43].
Climate change will disproportionally affect certain global regions, with extreme temperatures
occurring not only in traditionally warm countries, but also in regions not accustomed to high ambient
temperatures. A direct temperature–mortality relationship exists and varies by geographical region
and climate, with heat events causing significantly greater deaths in historically cooler areas. Predicted
heat-related illness and injury could be reduced with heat acclimatization and physiological adaptation,
improving the temperature–mortality relationship in cooler areas closer to that observed in warmer
geographical regions [44]. In areas frequently exposed to heat, increasing frequency and severity of
heat events will occur, with projected temperatures challenging the limits of human thermoregulation
and acclimatization [44–46]. In Europe, estimates for predicted heat-related mortality in the 2080’s
ranges from 60,000–165,000 in the absence of acclimatization or acclimation [44]. Notably, not only is
the increase in average global land and sea temperatures important, but close attention should be given
to the frequency, duration, and overall impact of heat events, during which fatalities dramatically
increase [44].
Global climate change has been evident for several decades, with anticipated increases in average
global temperatures of approximately 1.5 ◦ C (2.7 ◦ F) by 2100, with predictions ranging from 0.3 to
4.8 ◦ C (0.5–8.6 ◦ F) depending on varying emission scenarios predicted utilizing climate models [47,48]
(pp. 1037, 1065–1068). In the United States, predictive climate models indicate increases of 1.7–6.7 ◦ C
(3–12 ◦ F) by 2100, varying by the emission scenario. There will be an increased frequency and
intensity of heat waves and related events, with altered patterns and frequency of storms (both heat-
and cold-related) and precipitation [47]. Regional variation in severity of climate change will occur,
with amplified arctic warming at rates ~2.2–2.4 times greater than the global average [48] (pp. 1037,
1065–1068). Predicted heat events and extremes will continue to exceed prior records, causing hundreds
of thousands of additional deaths, crop destruction, and subsequent food shortages, altered disease
transmission, and significantly affected economic burden [41].
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Despite wide-scale scientific evidence associating greenhouse emissions and global climate change,
there is limited evidence of emission reductions. The accelerated rate of increase is unparalleled
in human history. Populations who are heat-sensitive or possess underdeveloped or compromised
thermoregulatory responses will be most at risk of heat-related morbidity and mortality. Particular
attention should be focused on the elderly, infants and children, individuals with cardiovascular,
renal, metabolic diseases and related comorbidities, and individuals using medications that alter or
limit mechanisms of heat dissipation. The limits of human thermal tolerance and ability to adapt to
increasing global temperatures, even in healthy populations, will be tested.

4. Adult–Child Differences in Thermoregulation during Heat Exposure

The American Academy of Pediatrics defines pediatrics as “the specialty of medical science
concerned with the physical, mental, and social health of children from birth to young adulthood.” [49].
Discrepancies in pediatric thermoregulation literature are therefore not surprising given the large
age range and developmental stages encompassed by this field. For the purposes of this review,
pediatric age categories follow US Food and Drug Agency (FDA) [50] and World Health Organization
(WHO) [51] guidelines for clinical pharmacology, reflecting the underlying principle of a liner
relationship between weight and growth. Based on these guidelines, pediatric subpopulations are
defined as (a) neonates, 0–1 month, (b) infants, 1 month to 2 years, (c) children, 2–12 years, and
(d) adolescents 12–16 years. If considering adolescent, further sub-classifications based on pubertal
maturational stage should be considered. Physiological responses to exercise and heat exposure differ
between infants, children, adolescents, and adults owing to differences in morphological, endocrine,
cardiovascular, metabolic, and thermoregulatory responses, yet guidelines are often modified from
adult data. Infants and children have traditionally been considered an ‘at risk’ group with greater
susceptibility to adverse physiological responses and health events during environmental extremes
owing to inferior thermoregulatory capabilities [12]. Over the past twenty five years, this notion
has been challenged, with limited physiological or epidemiological evidence of compromised or
insufficient thermoregulatory capabilities in a wide range of environmental conditions when compared
to healthy adults [19,37,52]. Many identified risk factors for heat illness in children, including hydration
status, clothing, training and recovery periods, are modifiable and thus largely preventable [52].
The importance of many of these factors in pediatric thermoregulation will be reviewed, with an
emphasis on recent advances and future challenges associated with climate change.

4.1. Morphology
Understanding alterations in thermoregulation in the context of growth and development is
complex and multifaceted. Not only do children grow and mature at differing rates, but the many
physical and physiological changes that impact thermoregulation during this time also occur at varied
rates and times, making the pediatric population challenging to assess. Understandably, as children and
adolescents grow and develop towards full maturity, adult–child differences become less pronounced.
During the 1990s, several investigators suggested that thermoregulation in children differed from adults
for physiological reasons beyond morphology [53–55], but this remains a prominent physical difference
with important consequences for thermoregulation. Children are smaller than adults, with associated
smaller total body surface area (BSA), lower total muscle mass, and metabolic heat production during
exercise [37,56]. Notably, children have a larger BSA to mass ratio, with more effective dry heat loss
and evaporative efficiency versus adults. This is advantageous in cooler and moderate conditions
when Ta < Tsk [32,57] but also provides a greater surface area to take on heat in hot conditions. Several
studies support the beneficial larger BSA:mass ratio in children during exercise in the heat [58], but this
may increase the risk of heat illness as global temperatures continue to rise.
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4.2. Body Composition

Obesity is widely recognized as a risk factor for heat-related illness and injury in both adults and
children [59–61]. The most recent nationally representative estimates from the United States indicate
that the prevalence of childhood obesity is continuing to increase: In 2015–2016, 35% of 2–19-year-olds
in the National Health and Examination Survey (NHANES) were overweight (BMI ≥85th CDC
percentile), and a further 24.5% obese (BMI ≥95th percentile) [62]. Globally, 50 (24–89) million girls
and 70 (39–125) boys aged 5–19 years are estimated to be obese (2SD above the WHO median) [63].
In the context of the increasing incidence of overweight and obesity in children both in the USA and
internationally, coupled with increasing average global temperatures, appropriate risk assessment
and safety guidelines for exercise in the heat are critically important [64]. The majority of data
regarding body composition and thermoregulation concerns adults, with considerable discrepancies
in the literature. Several studies indicate similar responses during passive heating [65] or exercise
in the heat [66], whilst others demonstrate blunted thermoregulatory (sweating) responses [67] and
increased thermal strain (Tc ) in obese versus normal weight individuals [67]. Notably, most studies
appear confounded by the effects of body mass and/or heat production introducing a systematic
bias owing to study design and not adiposity per se [68]. When metabolic heat production is fixed,
some of the differences are mitigated [69]. Several studies in children similarly demonstrate the
physiological disadvantage of higher adiposity during exercise in the heat [70–72]. Higher visceral
and subcutaneous fat deposits, combined with a typically lower BSA to mass ratio, may contribute
to hindered heat loss in obese versus lean children [73]. By contrast, a small number of studies
indicate similar heat tolerance of obese or overweight compared to normal weight children during
exercise in the heat [70,74]. This has been suggested by other authors to result in part from three
exercise heat acclimation sessions conducted prior to testing, which were not discussed in the studies
themselves [72]. Studies incorporating exercise/heat acclimation sessions prior to experimental testing
may reduce differences in thermoregulatory responses between groups but in applied terms have
important implications for reducing heat illness risk in obese children.
Importantly, total body mass is typically greater in obese compared to lean children, resulting in a
greater heat production and therefore evaporative requirement during similar absolute workloads.
In addition, obese children typically possess a lower maximal aerobic capacity, and therefore, when
exercising at the same intensity, obese children are achieving a higher absolute workload and heat
production [74]. Adipose tissue has a lower water content and lower specific heat compared to muscle
(2.97 kJ·kg−1 · ◦ C−1 versus 3.66 kJ·kg−1 · ◦ C−1 ), with less heat necessary to increase a specific mass
of adipose tissue a given temperature. It is logical to assume that both children and adults with
higher adiposity may therefore experience a greater Tc rise for a given heat production compared to
lean individuals. Notably, the physiological impact of adiposity on thermoregulation and practical
considerations for prescribing comparable workloads has recently been challenged [68]. In adults,
Dervis and colleagues [68] eloquently demonstrated that during exercise in the heat, overweight or
obese individuals experience a greater Tc increase versus those with lower body fat, independently of
differences in mass and metabolic heat production [68]. They further suggest that body fat percentage
has a relatively small influence on Tc , with independent influences on thermoregulatory function
during exercise only with large differences (>20%) between groups or individuals (e.g., obesity). Dervis
and colleagues calculated (based on another authors data [75]) that a 20% difference in body fat only
elicits a ~3%–5% difference in whole-body mean specific heat, perhaps explaining the similarities
between groups in some studies. Obese individuals pose a lower mean specific heat capacity compared
to lean individuals, which, coupled with blunted sudomotor responses, may explain the greater Tc
rise [68]. Prior studies have also suggested the insulative properties of adipose tissue may attenuate
heat loss at the skin [76], but this was not observed by Dervis et al. [68] and may only be relevant
in cool conditions when SkBF is minimal and subcutaneous fat is of greater importance. Many of
these biophysical principles may hold true in children but warrant further research to explore the
Nutrients 2019, 11, 2010 6 of 24

independent effects of adiposity on thermoregulation, with appropriate physiological adult–child

comparisons requiring workload adjustment for body mass and BSA to avoid systematic bias.
Body composition is an important factor for consideration in outdoor physical activity guidelines
for children, in addition to hydration, fitness level, acclimation status, disease, and medications, all of
which can modulate thermoregulatory responses and ultimately risk of heat-related illness and injury.
Although beyond the scope of this review, it is also pertinent to recognize that obesity is associated with
a multitude of risk factors for the development of cardiovascular disease, including insulin resistance,
dyslipidemia, and hypertension. Obesity is a proinflammatory condition that contributes to the
pathogenesis of obesity-linked diseases, including metabolic dysfunction, cardiovascular diseases, and
associated comorbidities [77]. In light of the growing incidence of childhood obesity [62,63], associated
comorbidities [78], and increased polypharmacy at increasing younger ages [79,80], development of
significant vascular dysfunction and cardiovascular disease in children and young adults is a sobering
reality [78,81,82]. This has serious implications for long-term cardiometabolic risk profiles [82,83],
in addition to thermoregulatory dysfunction contributing to increased heat illness risk [84–87],
exacerbated by a warming global climate.

4.3. Metabolic Heat Production

Children have less efficient locomotion than adults, producing more heat per unit body mass
during weight-bearing activities [88,89]. Metabolic heat production can be ~10%–15% higher in children
for a given workload [88], although is less pronounced during nonweight bearing activities including
cycling. Studies investigating the metabolic cost of locomotion in relation to individual biomechanical
variables have typically observed poor relationships. Rather, economy appears related to results from
the combined effects of a multitude of factors [90]. Frost and colleagues [91] investigated metabolic,
kinematic, and electromyographic responses of varying ages of children (7–8 years, 10–12 years, and
15–16 years) to 4 minute bouts of treadmill walking and running at increasing speeds. The best
predictor of both VO2 and efficiency was age, but specific growth-related factors that may influence
the metabolic cost of locomotion remain unclear [91]. Resting metabolic rate (per kg TBW) is higher
in children than adults, decreasing during childhood [92,93]. Differences in total mechanical work,
stride length [92], knee joint range of motion, gait efficiency [94], and higher respiratory frequency
(and a higher cost of ventilation) may all contribute to a greater submaximal VO2 in children versus
adults [92,93].
For children with disabilities or disease that affects mobility, low locomotion efficiency results
in large energy expenditure compared to healthy or typically developing children. For example,
cerebral palsy, the most common childhood disability in the United States, causes a high metabolic
demand on daily activates. Walking efficiency is three times higher in cerebral palsy children, affecting
participation in daily activities and overall quality of life [94]. Specific metabolic demands of activities
in children are important in the context of safe exercise practices and thermoregulation in extreme
environments, with important consideration and modifications to activities for children with disabilities
affecting movement.

4.4. Cardiovascular Responses

In comparison to adults, children produce a lower Q during similar absolute submaximal
workloads [30,95,96]. Several studies have reported similar Q during exercise in children and adults,
but an explanation for these discrepancies is not clear [97,98]. Lower Q in children results from a lower
stroke volume (SV), attributed to their smaller body size and therefore smaller heart (left ventricle)
compared to adults [95]. Partial compensation is provided by a higher heart rate, with more complete
compensation resulting from a greater arterial–venous O2 difference, ultimately providing similar
adult–child VO2 values despite a lower Q. Children therefore have an appropriate cardiovascular
response for their size during exercise. This is demonstrated when SV is scaled to body size, virtually
eliminating child–adult SV differences [95]. Similarly, Falk and Dotan calculated cardiovascular
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responses at fixed relative workloads corrected to provide a body mass specific Q (based on the data of
Turley and Wilmore [95]), with values that were in fact ~10% higher in children than adults.
Despite the lower, albeit size-appropriate exercise Q in children, differences in cardiovascular
responses associated with thermoregulatory challenges become apparent. Children possess a greater
(~20%) BSA compared to adults, shunting a greater proportion of Q to the skin to maximize dry
heat losses [31,33,35]. Higher SkBF responses are evident during exercise (50% VO2max ) in hot–dry
conditions [55] and for similar rectal temperature (Tre ) responses [31]. Notably, comparisons of
cardiovascular responses to heat are typically standardized to metabolic load (relative intensity). If
absolute workloads were utilized, group differences would be artificially exaggerated owing to factors
including differing locomotion and therefore greater physiological strain in children, differences in
body mass and size, and potentially greater SkBF responses for dissipation of additional heat [19].
The high SkBF response declines with increasing maturational development throughout adolescence.
Falk and colleagues [55] observed progressively lower SkBF responses in pre-, mid-, and late pubertal
boys (significant between all groups) during cycling at 50% VO2max in a hot–dry environment (42 ◦ C,
20% rh). Considering the proportionally higher SkBF responses in children, declines in performance
are understandable. Venous return and thus Q are compromised, coupled with relatively lower
muscle blood flow, presenting competing demands on the cardiovascular system during exercise in the
heat [99]. If conditions (heat and exercise intensity) are sufficiently extreme and exposure continues,
particularly without adequate rehydration, SkBF and sweating responses may decline, compromising
thermoregulatory function with potential development of heat illness [100].

4.5. Thermoregulatory Sweating

Many authors have reported lower local and whole-body SRs in children compared to
adults [31–34]. This is typically true regardless of normalization for BSA or per sweat gland, exercise
intensity, environmental conditions, and Tre [55–57]. Further, the significantly lower SRs in children
appear more pronounced in comparison to adults when exposed to greater environmental extremes,
higher workloads [20] or during hypohydration [101]. This leads to the widespread view that children
possess inferior thermoregulatory capabilities, a notion that was challenged by Falk and Dotan [37].
Despite lower whole-body SRs, Tc responses are often similar when workloads are adjusted or during
passive heating, leading some to suggest that children may actually possess greater thermoregulatory
efficiency during exercise and/or exposure to mild and moderate conditions [34,37]. This does not
hold true in extreme ambient conditions, with children displaying greater physiological strain and
increased heat illness risk.
The main focus on thermoregulatory sweating in children is typically whole-body sweating, with a
paucity of data regarding RSR. Regional SRs are widely recognized in adults [102–106], with differences
in children depending on maturational stage [34]. This was observed by Shibasaki and colleagues [34]
following passive heating of prepubertal boys (7–11 years) and young men (21–25 years) via lower
leg immersion in a 42 ◦ C water bath for 60 min. RSRs varied, with some sites significantly higher
than adults (forearm), some significantly lower (chest, thigh during latter 30 minutes only), and others
showing no differences (back) between groups. The sweating threshold (Tb ) was slightly higher in
boys, albeit nonsignificant (p < 0.10), regardless of body region. Heat-activated sweat gland density
(HASG) was higher in boys at all sites, but this is not surprising given their developmental stage and
smaller body size and surface area. The authors suggest regional variation in sweating associated
with maturational stage and argue a peripheral ‘underdevelopment’ at the level of the sweat gland
versus central drive [34]. This highlights the necessity for measuring RSR at multiple sites and the
need for more detailed regional sweating data in children and adolescents at varying maturational
stages. Notably, ambient conditions were 25 ◦ C, 45% rh, providing a favorable temperature gradient
for dry heat losses on which children typically rely more heavily. The authors focus on sweating in
relation to maturational age, but other heat loss mechanisms should be considered. Despite lower
RSR, change in Tre did not differ between groups, indicating that prepubertal boys could adequately
Nutrients 2019, 11, 2010 8 of 24

thermoregulate under mild to moderate passive heat stress in the specified conditions, relying on
differing mechanisms and perhaps displaying greater efficiency.
Greater evaporative efficiency can also be attributed to the lower sweat electrolyte concentration
in children [107] and serves to conserve body fluids. Children typically have higher Tsk , and thus
higher sweat temperatures, resulting in higher water partial pressure. The result is increased water
vapor pressure and higher sweat evaporation [37]. A greater evaporative efficiency and the ability
to conserve water may actually serve as an argument for thermoregulatory superiority in children
versus adults in mild and moderate conditions. Maximal SRs in children have never been established
for ethical reasons, but it is reasonable to assume that in the context of global climate change and
increasing heat waves, children may be unable to achieve sufficient sweating rates for heat balance
(maximal evaporation < required evaporation) more frequently. Maximal SRs may be improved
with heat acclimation, but in uncompensable conditions, children will be unable to thermoregulate
adequately, with the potential for progression to developing heat illness if precautionary measures are
not employed.

4.6. Heat Acclimation

Heat acclimation (HA) involves a series of beneficial physiological adaptations resulting from
repeated exposure to heat stress that facilitate a greater ability to deal with subsequent heat
exposure. Considering children are vulnerable to heat illness under extreme conditions, employing
HA strategies provides a feasible risk reduction strategy in the face of climate change. Differing
HA regimens may be utilized, with conditions closest to the anticipated exposure environment,
typically lasting 7–14 days [108–111] and often incorporating exercise to elicit a maximally heat
acclimated phenotype [112,113]. Physiological adaptations to HA have been extensively documented
in adults [104,114–120], including reduced cardiovascular strain (heart rate (HR) and Q) at a given
workload, a lower Tc threshold for sweating, increased thermosensitivity resulting in a higher SR for a
given Tc , and greater maximal SRs [111,116,119,121–125]. Children acclimate similarly to adults yet do
so more slowly, requiring several more days of exposure for complete HA [72]. The reduced sweating
onset threshold and HA-associated increases in SR are highly beneficial during subsequent exposure to
high ambient temperatures in a population that has significantly lower sweating responses compared
to adults. Children display lower sweat NaCl concentrations compared to adults [107], with reductions
in sweat Na+ and Cl− concentrations in both groups following HA [126,127]. Further acclimation
increases the responsiveness of the duct to aldosterone in adults [128], but this mechanism has not
been investigated in children.
A pertinent consideration with increasing prevalence of childhood obesity (Section 2.4. Body
Composition) is that obese children appear to possess a lower level of acclimation versus lean boys,
likely resulting from the partial acclimation acquired through training. Obese boys show higher resting
and exercise Tc , elevated HR responses, and lower SRs, indicating higher physiological strain [72].
Sedentary, obese children may therefore benefit most from carefully monitored HA regimens prior
to summer months. In the instance of athletes, similarly to adults, exercise intensity should be
progressively increased to emulate competition. A gradual increase in the number of training sessions
per day and progressive introduction of protective clothing that may hinder heat loss should be
adopted [129]. Considering the tendency for children to voluntarily dehydrate, special attention should
be given to rehydration strategies during HA to limit hypohydration and maximize cardiovascular
adaptations [130].
Ultimately, HA reduces cardiovascular strain, improves performance, and increases survivability
to extreme environmental conditions, making this a critical component in reducing heat-related illness
and injury in the pediatric population [72,111,116,119,121–125,129]. Most of the evidence available
indicates similar HA responses between children and adults, but further work is warranted if HA
regimens become widely adopted as ambient temperatures continue to increase, with additional
consideration for body composition, disease conditions, and medication use.
Nutrients 2019, 11, 2010 9 of 24

4.7. Sweat Composition and Fluid Intake

Fluid intake is of considerable importance in relation to thermoregulatory function, with
hypohydration considered a major risk factor in the development of heat illness [100,131–135].
In adults, even mild hypohydration (<2% body weight) impacts cardiovascular and sudomotor
responses, reducing SkBF [136,137], delaying both the vasodilatory and sweating onset thresholds, and
reducing sweating rates for a given Tc (reduced gain) [137,138], attenuating thermoregulatory function
and heat tolerance [137]. For extensive reviews regarding the physiology of water balance, hydration
assessment, strategies, and pathology, please refer to other reviews within this Special Issue. In the
context of this review, hypohydration in children with consideration for rising global temperatures
and concerns over predicted water shortages accompanying climate change are addressed.
In the pediatric population, voluntary dehydration is common, largely owing to children feeling a
limited need to replenish fluids even when intake is insufficient [139]. This increases susceptibility
to hypohydration and subsequent physiological and psychological impairments. Fluid intake and
euhydration are essential for physiological function and health, in addition to cognitive function and
mood in both children [140,141] and adults [142]. Hypohydration attenuates SRs in both populations,
with notable thermoregulatory impact on children due to their already lower sweating responses
for a given workload. Children experience a greater rise in Tc for a given level of hypohydration
versus their adult counterparts, increasing physiological strain and thus reducing tolerance to the
heat. Hypoydration is recognized as a major risk factor for heat-related illness and injury, including
progression to life threating heat stroke [52,101].
Both adults [143] and children [139] often hydrate inadequately, but the effects of chronic low
fluid intake and dehydration on health are not well understood. As global climate change progresses,
knowledge of the complex and multifaceted interplay of factors influencing thermoregulatory function
is important. Although speculative, consideration needs to be given to pediatric fluid intake as it
pertains to chronic health, with the mindset of encouraging “preventative” habits for long-term health
and risk reduction. In adults, fluid intake (typically self-reported) provides conflicting results regarding
cardiometabolic disease risk, in part due to failure of investigators to report plain water consumption
versus intake of other fluids, including sweetened beverages [144]. Evidence does indicate low fluid
intake is independently associated with developing hyperglycemia [145], type 2 diabetes mellitus [146],
and renal dysfunction including chronic kidney disease (CKD) [144], with inconsistent evidence of
cardiovascular disease risk. The putative link between hydration and long-term health in adults
remains controversial but certainly warrants consideration in children. This is particularly concerning
in light of climate change potentially exacerbating dehydration risk, coupled with the high incidence
of overweight and obese children in the western world, already at increased risk of cardiometabolic
disease. Limited research has assessed the relationship between fluid intake and childhood obesity,
but there is some indication that obese children are less hydrated compared to those of normal
weight. Maffeis and colleagues [144] determined significantly lower hydration in obese versus normal
weight children (7–11 years), based on average free water reserve over 48 h. In adults, Guelinckx
and colleagues [144] raise the concept of increased plain water intake as a mechanism to reduce renal
and metabolic dysfunction. Risk reduction for CKD and vascular dysfunction in adults has also been
observed with high water intake (>2.6 L/day) but not sweetened beverages [147–149]. In children,
albeit speculative, perhaps this approach serves to not only improve hydration and thermoregulatory
function but reduce or limit the risk of renal and metabolic dysfunction.
Appropriate replacement of both electrolytes and water should be achieved during exercise and/or
in warm conditions, yet limited data concerning sweat composition in children and adolescents are
available, with subsequent hydration guidelines for children derived from adult data. Maintaining
appropriate water balance is important, but beverage flavor and composition are of particular
significance when SRs are high. During exercise in the heat, children consume significantly more fluid
when beverages are flavored compared to plain water [150]. Bar Or and colleagues [150] observed that
voluntary dehydration was significantly reduced when chilled water (8–10 ◦ C) was grape-flavored
Nutrients 2019, 11, 2010 10 of 24

versus plain during 3 h of intermittent exercise in the heat (35 ◦ C, 40–45% rh). Further increases in fluid
consumption were observed when the beverage was not only flavored but also contained carbohydrates
(6%) and NaCl (18 mmol/L), resulting in mild overhydration (0.47% increase body weight). Physiological
and perceptual variables, including Tre , Tsk , HR, thirst, and stomach fullness did not differ between
conditions, which may be explained by the relatively minimal dehydration of only−0.65%, −0.32%,
and+0.47% of body weight for plain water, flavored water, and flavored carbohydrate/NaCl water,
respectively. Current guidelines by The American Association of Pediatricians [52] recommend
consumption of cooled, flavored beverages to mitigate dehydration in the heat, with the addition
of 15–20 mmol/L NaCl increasing ad libitum drinking by up to 90% versus plain water. Sweat
composition and optimal composition of fluid-replacement beverages has been extensively studied
in adults [150–154], but limited data are available in children, with an emphasis on pathophysiology,
specifically cystic fibrosis.
There are many individual factors that can influence sweat electrolyte losses and therefore
replacement, including age, physical fitness [155,156], and acclimation status [126,157]. Sweat
electrolyte concentrations are a function of SR [158], with higher sweat Na+ and Cl− concentrations
evident at higher SRs resulting from reduced reabsorption in the sweat duct [157,159]. Wide variation
in sweat lactate concentrations has been reported, with data indicating an inverse correlation with
SR [160,161], positive correlation [162], or no correlation [163]. Several studies have demonstrated
significantly lower sweat lactate concentrations with maturational age (pre- versus late-pubescent
boys) [164] and in children versus adults [160] during the initial stages of moderate exercise in the heat,
but not during subsequent bouts. Despite varying data concerning the relationship between sweat
lactate and SR, it has been proposed that sweat lactate is higher in children owing to their lower SR
compared to adults. However, sweat lactate tends to decrease with increasing exercise duration in the
heat [160], and the similarity in child and adult sweat lactate during latter stages of exercise cannot
be explained by SR. One proposed mechanism is the reliance on anaerobic metabolism in a sweat
gland during the initial stages of sweating, and an increasing reliance on oxidative phosphorylation
as exercise progresses [160]. Regardless of the mechanism, identifying sweat electrolyte losses and
adapting hydration strategies is vital.
Similarly to lactate, sweat NH3 is significantly higher during initial stages of exercise than adults,
which is thought to prevent further decreases in sweat pH through protonation of NH3 to NH4 + . This is
also reflected in the lower sweat pH observed in children during the initial stages of moderate exercise
in the heat (≤20 min) [160]. Further, an inverse correlation has been observed between sweat H+
and Na+ , thought to relate to acidification of sweat via tubular antiporters reabsorbing HCO− and/or
secreting H+ in exchange for Na+ reabsorption, potentially explaining the greater Na+ reabsorption
in children [160].
Understanding optimal fluid composition and replacement strategies should be a priority in
children, not only for performance but also overall health and safety. Hydration guidelines in
children are often based on adult data, yet adult–child differences in sweat electrolyte concentrations,
variation with intensity and duration, and marked differences in SR are evident. Coupled with
greater voluntary dehydration in children [101], beverage composition and hydration guidelines
need tailoring specifically to children and the intensity and environment in which they are exercising.
Drink palatability, including flavor and temperature, are also important when considering fluid
replacement in children. In the face of predicted rising average global temperatures, increased severity
and frequency of heatwaves, and predicted water shortages, tailored hydration strategies will be
increasingly important not only for those exercising in the heat, but for daily activates and prolonged
periods outside in the heat (i.e., summer camps).

5. Emerging Environmental Challenges: Effects on Thermoregulation and Health

The World Health Organization (WHO) first published an atlas outlining global environmental
challenges to children’s health in 2004, which has since been expanded and updated to highlight
Nutrients 2019, 11, 2010 11 of 24

emerging environmental stressors and strategies for exposure reduction [165]. Rising global
temperatures and heat waves are only one component of environmental hazards facing children,
with exposure to multiple physiological and psychological stressors influencing growth, development,
and long-term health. In the context of thermoregulation, stressors including pollution, UV exposure,
and water shortages may not only directly affect physiological function, but a complex interplay of
multiple stressors may plausibly modulate thermoregulatory function in children (e.g., via impacts on
the cardiovascular system), potentially increasing risk associated with heat-related illness and associated
complications. Currently, little is known about the effects of multiple stressors on thermoregulatory
function in children.

5.1. Pollution
Acute exposure to pollutants and toxic substances can impair thermoregulatory responses [166],
with chronic exposure resulting in a multitude of long-term health complications. Children are
reported to spend significantly greater periods of time outdoors compared to adults, potentially
increasing their likelihood for exposure to toxicants. It is widely recognized that high ambient
temperatures increase the uptake of many pollutants and play a critical role in increasing toxicity [167],
which may be further compounded by exercise in the heat [167]. Pollutants and toxins that alter
metabolism, SkBF, and/or sweating responses may have a profound effect upon thermoregulation
responses of both children and adults [168]. In rodents, an acute, protective hypothermia followed
by a rebound, sustained hyperthermia is observed following dosing with many toxic substances,
including insecticides. Humans do not typically experience the magnitude of hypothermia observed
in rodents following toxicant exposure, although marked hypothermia has been observed in specific
instances [169]. More common is a hyperthermic or fever response that may persist for several days
after exposure to a toxic agent [167]. Importantly, Tb affects both uptake and toxicity of substances,
which in turn impacts Tb regulation. Based on increasing levels of pollution from vehicles, insecticide
use, and byproducts from industry, an understanding of routes of absorption, toxicity, modulation of
physiological responses, including temperature regulation, and long-term health effects is necessary.
Increasing interest in the complex interplay among pollutants, mortality, and heat stress in older
individuals is evident [17,170], which should be extended to other vulnerable populations.
The WHO estimates the global cost resulting from pollution at 1.7 million children deaths per
year [171]. High ambient temperatures and airborne pollutants independently increase morbidity
and mortality, but few studies have investigated the interplay between both stressors [172,173]. A
limited number of studies have attempted to do so, yielding mixed results. Several studies indicate an
interaction effect, with pollution effects being greater on days with higher ambient temperature [17],
whilst others found limited or no interaction [172]. Toxicity of air pollutants can be modified by
atmospheric transformations, with greater primary pollutants forming toxic secondary products under
conditions of higher temperature, greater sunlight exposure, and in the presence of copollutants [174].
Considering predicted elevations of both stressors in the future, and limited current knowledge
of how their interactions affect thermoregulation and overall health, further research is urgently
needed. The physiological strain associated with exposure to high ambient temperatures may alter the
physiological response to pollutants and other chemicals, increasing susceptibility to the negative health
effects [172,173]. A further plausible consideration is the deleterious cardiovascular and respiratory
effects of airborne pollution that may lead to compromised thermoregulatory function both in children
and later in life, raising health risks in an already vulnerable population during extreme heat exposure.
An increasing number of studies have elucidated an association between residential proximity
to high traffic roads and, thus, airborne vehicle pollution and a multitude of adverse health events
and conditions. Impacts on the respiratory system have been widely studied [175], and increasing
literature is indicating a concerning impact on the cardiovascular system.
Air pollution has been implicated as proatherogenic, increasing likelihood of cardiovascular
events [176]. Vehicle emissions are a major contributor to outdoor pollution, accounting for up to 90% of
Nutrients 2019, 11, 2010 12 of 24

pollutants, including carbon dioxide (CO2 ), carbon monoxide (CO), oxides of nitrogen (NOx ), particulate
matter (PM), ozone (O3 ), volatile organic compounds (VOCs) including benzene and formaldehyde,
and other byproducts. Many of these pollutants are linked to numerous adverse health conditions and
events, particularly relating to respiratory function [177] and cancer risk [178]. Specifically, PM from
vehicle exhaust emissions has been linked to adverse cardiovascular events [179,180]. Of concern to
climate change, higher ambient temperatures are linked to greater respiratory uptake of pollutants
such as O3 and greater toxicity [167].
In adults, literature is varied, with some evidence that long-term exposure to urban pollution may
increase arterial stiffness and carotid intima–media thickness, regardless of pre-existing Cardiovascular
disease (CVD) [181]. Potential mechanisms include signaling cascades stimulating pro-inflammatory
cytokine release, ROS production, endothelial dysfunction, and vascular smooth muscle remodeling,
ultimately attenuating vascular function and promoting atherogenesis [182,183]. Children are at
greater risk of negative health effects associated with pollution, owing to a complex interplay of factors,
including immature immune responses, small lung volumes, higher respiratory rates, tendency for
mouth breathing, and longer time periods spent outside [184]. Children exposed to urban air pollution
show increased markers of oxidative stress, inflammation, and endothelial dysfunction [16,185].
Notably, this an understudied area of toxicology and physiology, with only one study indicating that
long-term urban residency of children living in close proximity to a major road (30–300 m) was linked
to increased carotid arterial stiffness versus those living further away.
Armijos and colleagues [186] observed that long-term residency in close proximity to a high traffic
road (<100 m), and thus airborne pollution, stimulates arterial remodeling (carotid intima–media
thickness) in children aged 7–12 years versus those living further away (>200 m), with control for
covariates and risk factors for atherosclerosis [186]. Many factors can influence inflammation and CVD
risk, but there is a need for long-term, longitudinal, epidemiological studies to determine the cumulative
effects of pollution on cardiovascular health, with putative implications for thermoregulatory function
and exercise capacity. Exposure to proatherogenic environmental factors may cause early progression
to clinical disease, rendering current knowledge of vascular responses in children inaccurate with the
potential for overestimating heat loss potential in certain conditions. Whilst currently speculative,
elucidating if pollution has functional consequences for thermoregulation in children is vital in the
face of multifaceted physiological stressors, including climate change and increasing prevalence of
noncommunicable diseases.

5.2. Ultraviolet Exposure

Exposure to UV radiation can have beneficial or detrimental effects depending on a complex
interplay of factors, including the wavelength of UV radiation, extent of exposure, skin pigmentation,
and other individual factors [2]. Depletion of protective stratospheric ozone has led to increased UVB
(315–400 nm) levels reaching the earth’s surface [187] and is therefore of concern to human health.
The epidermis absorbs the majority of UV that irradiates the skin, with only longer wavelengths
transmitted deeper into the dermis. UVB has therefore been the predominant focus of research, but
interest is growing in the effects of the UVA waveband (315–400 nm). Environmental change coupled
with lifestyle choices in recent decades, including increased leisure time, popularity of beach/sunshine
vacations, poor sunscreen habits, use of tanning beds, and fewer clothes worn outdoors, places
individuals at risk of irradiation. This has pertinence to both adults and children; however, some
evidence indicates that UV radiation exposure during childhood may be of greater importance for
both beneficial and detrimental effects compared to exposure later in life [188].
Despite the largely negative literature surrounding UV exposure, it is important in many
physiological processes, with skeletal disease and vitamin D insufficiency associated with inadequate
exposure. Some evidence indicates a regulatory role in blood pressure via calcium homeostasis
and vitamin D3 , with artificial UVB exposure lowering blood pressure in mild, unmedicated
hypertensives [189]. Photoimmunology, an emerging field of study regarding how UV radiation
Nutrients 2019, 11, 2010 13 of 24

impacts immune function, is a reminder of how limited current knowledge is on topics such as UV
and effects on many physiological processes. UV radiation is typically immunosuppressive, yet
increasing evidence suggests a protective role of UV radiation in autoimmune diseases, including
Type 1 diabetes, rheumatoid arthritis, and multiple sclerosis [14]. This occurs via multiple signaling
mechanisms, including local and systemic immunosuppression, the immunomodulatory effects of
vitamin D (1,25-dihydroxycholecalciferol), and suppression of melatonin secretion and subsequent
T cell responses [190–193]. Overall, it appears that UV radiation exerts immunomodulatory effects,
primarily via suppression of helper T cell type-1 mediated responses thorough multiple mechanisms.
This may be beneficial in specific circumstances, including autoimmune diseases, but requires further
investigation in humans.
Excessive exposure to UV radiation is associated with many negative health effects, including
increased skin cancer risk [13,194,195], eye damage, and suppressed immune function [196], with further
deleterious health effects becoming more apparent. In instances of sunburn, skin injury results from
penetration of UVB into the dermal and epidermal layers, causing damage to cutaneous blood vessels
and eccrine sweat glands [197]. Mild artificial sunburn appears to attenuate SRs and sensitivity for at
least 24 h, with potential for impaired thermoregulatory function if this occurs over a large body surface
area [197]. Greater time spent outdoors by children compared to adults, poor sunscreen habits, and
increasing UVB levels increase the likelihood of sunburn in a pediatric population, with potential for
thermoregulatory dysfunction. Specific dermal conditions have been shown to impair thermoregulation
and reduce heat tolerance [198]. Evidence is currently limited with regard to sunburn and thermal
tolerance, but further studies examining the acute and chronic effects on eccrine sweat gland function
and vascular responses are necessary in light of changing environmental conditions. Evidence of
UVB-induced alterations in cutaneous vasodilation have recently been reported in adults but, as an
important component of the thermoregulatory response, may have relevance for thermoregulation
in both children and adults. Children rely more heavily on cutaneous vasodilation and ‘dry’ heat
losses for thermoregulation compared to adults, making decrements in this response potentially more
problematic. Nitric oxide (NO) is a potent vasodilator, produced from the substrate L-arginine via
nitric oxide synthase (NOS) isoforms, and is necessary for full expression of the cutaneous vascular
response to both local [199–201] and whole-body heating [202]. Recent work by Wolf et al. [203,204]
indicates deleterious effects of acute UV radiation exposure on cutaneous microvascular function.
Specifically, an acute dose of UVB radiation (300 mJ.cm2 , 75 s) was shown to attenuate NO-dependent
vasodilation on the ventral forearm, likely via its putative degradation of 5-methyltetrahydrofolate
(5-MTHF) and subsequent reactive oxygen species (ROS) signaling [203]. A further study by this
group [204] indicated attenuated NO-dependent skin blood flow responses to a local heating protocol
(42 ◦ C) following acute broad spectrum UV radiation exposure (450 mJ.cm−2 , 75 s) versus control
(non-exposure). UV radiation-mediated reductions in NO-dependent vasodilation were prevented
with application of SPF 50 sunscreen or ‘simulated sweat’. Notably, this was conducted under very
acute conditions (60–75 s) in a young, healthy adult population, but consideration must be given to
implications in children and adolescents. Children often spend greater time outdoors than adults, and
rely more heavily on dry heat losses, shunting a greater proportion of Q to the skin during passive and
exercise heat exposure. Whether long-term effects of chronic, repeated UV exposure on cutaneous
vascular reactivity translate to meaningful physiological outcomes and compromised thermoregulatory
function is currently unknown. As average global temperatures rise and broad spectrum UV radiation
exposure increases, in part due to decreasing atmospheric ozone [187], understanding if these factors
modulate cutaneous vascular responses, and thus thermoregulation, is certainly warranted.

6. Child Health, Safety, and Risk Reduction

Based on global climate predictions, awareness of the factors increasing risk of heat-illness in
children is important in prevention, with particular emphasis on dehydration, current or recent illness,
chronic conditions, and specific medications [52]. In particular, illness involving gastrointestinal distress
Nutrients 2019, 11, 2010 14 of 24

(particularly vomiting and diarrhea), and conditions and medications that affect thermoregulation,
exercise tolerance, and water–electrolyte balance should be addressed. Common examples include
type 2 diabetes [205–207], obesity [72,208], cystic fibrosis [209], diabetes insipidus, anticholinergic
medications, diuretics, dopamine [210], and serotonin uptake inhibitors.
A second important step in the prevention of heat-related illness and injury is understanding
and implementing HA. Children acclimate to heat more slowly than adults [72] but will beneficially
increase sweat capacity, reduce the onset threshold for sweating, and reduce overall physiological
strain [72,208]. Obese children possess lower levels of acclimation and therefore should be acclimated
more progressively during summer months [72]. When exercising in the heat, children should follow
appropriate hydration and exposure guidelines for the ambient conditions, with special consideration
and awareness of their propensity for greater voluntary dehydration [101]. Hypohydration compromises
thermoregulatory function to a greater extent in children compared to adults, making it an import
factor to mitigate health risks during exposure. The American Academy of Pediatrics position stand
addressing “Climatic Heat Stress and Exercising Children and Adolescents” [52] recommends multiple
risk reduction strategies, including but not limited to:

1. Increasing rest periods. Activities lasting >15 min should be reduced in conditions of high solar
radiation, high humidity, and ambient temperatures above critical limits.
2. When beginning a strenuous exercise program or travelling to a warmer climate, HA over
10–14 days should be planned with reduced exercise intensity, duration, and protective clothing.
3. Ensure adequate hydration prior to extended exercise in the heat. Intermittent drinking
periods should be enforced, regardless of thirst (100–250 mL every 20 min). Weighing a
child pre/post-exercise can assist with verifying hydration.
4. Lightweight, light-colored, single-layer clothing should be worn that is absorbent. Sweat-soaked
garments should be replaced.
5. Child education on heat illness and hydration practices should be adopted to help raise awareness
of prevention, and recognition of the signs and symptoms of heat-related illness and injury.
Trained staff should be present, and an emergency plan should be in place.

Considering the increasing incidence of a multitude of childhood diseases, awareness of diseases

that alter thermoregulatory responses, recent illness, specific medications, and mental retardation (for
example, a compromised ability to recognize dangers of heat, not rehydrating) are also important.
Education surrounding behavioral thermoregulation is vital, including seeking shade, requesting
help when needed, and using cool water and damp towels to help to reduce body temperature
during hyperthermia. Sunscreen should be applied to reduce acute effects of UV radiation on
cutaneous vascular responses in the heat and avoid sunburn. Clothing insulation and requirements
in children in varying environmental conditions are beyond the scope of this review but are an
important consideration. Readers are directed to other excellent reviews [211]. Emerging evidence
highlights the complex interplay between multiple stressors, modulating physiological responses,
and, therefore, morbidity and mortality risk. Exposure to increasing global temperatures necessitates
consideration of heat stress in cumulative risk assessment [43], due to potential temperature-related
modulation of toxicity of air pollution and other abundant chemicals, for example, pesticides [174],
exacerbating health effects. Children are exposed to many physical and chemical stressors, including
heat, UV radiation, sunlight, noise, infection, psychosocial stressors, and pollution. Long-term
exposure may facilitate earlier progression to clinical disease, altered physiological responses versus
those observed in healthy children, and ultimately premature mortality. The long-term impact
of multiple environmental–physiological factors on physiological function are currently not fully
understood. Combined efforts between thermal physiologists, epidemiologists, climate physiologists,
and regulatory bodies/policymakers are necessary to produce more comprehensive heat protection
policies, incorporating technology, clothing, and behavioral adaptations as global climate change
advances and limits of human tolerance are reached [45].
Nutrients 2019, 11, 2010 15 of 24

7. Summary
Understanding physiological responses to heat exposure is of increasing importance in the face
of extraordinary environmental and climate change facing humans. In particular, emphasis should
be placed on ‘at risk populations’, including children and infants, the elderly, and individuals with
obesity and chronic pathologies, including cardiovascular, renal, and metabolic diseases. Many
physiological differences exist between adults and children of varying developmental stages in their
responses to exercise and exposure to environmental extremes, including morphological, endocrine,
cardiovascular, metabolic, and thermoregulatory responses. The classic notion that children possess
inferior thermoregulatory capabilities and reduced thermal tolerance has been vigorously challenged
over the past 25 years and may only hold true in extreme conditions. Of course, this is particularly
relevant in light of global climate change where ‘extremes’ are more likely to be encountered, evidenced
by patterns of increasing average global ambient temperatures, increased frequency and severity of
heat waves, and increased pollution and UV exposure. The complex interplay between increasing
environmental stressors should be carefully considered when coupled with concerning health statistics
that negatively affect thermoregulation in children, including prevalence of inactivity, childhood obesity,
and the earlier onset of preventable ‘adult’ diseases, including type 2 diabetes and dyslipidemia.
The long-term impact of multiple environmental–physiological stressors, including heat, UV exposure,
and pollution on physiological function in children, is not fully understood and warrants further
investigation as a significant future global health challenge.

Funding: This research received no external funding.

Conflicts of Interest: The authors declare no conflict of interest.

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