Exposure Under Pressure
Lead Linked to Release of Cortisol in Children
Lead exposure is linked to cognitive deficits, cardiovascular
disease risk, and behavioral problems, outcomes that potentially follow
dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis. In
animal studies, lead exposure has heightened the release of
corticosterone, the counterpart to the human stress hormone cortisol.
New research now reveals for the first time a similar response in
children with blood lead levels below 10 µg/dL, the action level
established by the Centers for Disease Control and Prevention
[
EHP 116:249–255; Gump et al.]. This finding corroborates concerns that there is no safe level of lead exposure.
The researchers interviewed 1,060 children diagnosed within the
prior 6 months and 1,681 control children. When analyzing the data on
the children, the team controlled for other factors that may alter a
child's risk of getting cancer, including family cancer history and
whether the child was breastfed. The children with cancer were part of
the French National Registry of Childhood Blood Malignancies, begun in
1990, which documents all children in the country under age 15 year who
have had hematopoietic tumors.
The researchers drew their study population from the ongoing Oswego
Children's Study, a longitudinal study at the State University of New
York at Oswego's Center for Neurobehavioral Effects of Environmental
Toxics. Of the 169 children in the current study, blood lead levels
were known for 154 prenatally (≥ 1–6.3 µg/dL) and for 120 during
infancy or toddlerhood (1.5–13.1 µg/dL). At the time of their
participation in the current study, children were 9.5 years old.
Cortisol levels vary diurnally, rising quickly
after awakening and then declining steadily thereafter. To help control
for this diurnal variation, tests always occurred in the late
afternoon. Beginning with a brief rest period, each child's session
involved submerging an arm in ice water for 1 minute and completing a
series of simple tasks with intervening rest periods—a standard
protocol to assess neuroendocrine response to acute stress. Saliva was
collected for cortisol measurements during the first rest period and at
21, 40, and 60 minutes after the cold stressor test.
The researchers controlled for numerous
potentially confounding factors, including demographics, socioeconomic
status, and the health, nutrition, and substance use of mothers and
children. They also tested for the presence of other neurotoxicants
such as polychlorinated biphenyls, DDE, and hexachlorobenzene in
children's blood, as well as maternal mercury exposure.
Pre- and postnatal blood lead were not associated
with any variation in baseline cortisol levels. However, increasing
blood lead levels were independently and significantly associated with
increasing cortisol responses to stress. Curiously, cortisol levels
remained elevated throughout the test period instead of tapering off as
expected. The authors suggest that the children may have already been
stressed when the test began or that 60 minutes was insufficient for
cortisol levels to return to baseline.
The precise mechanisms of lead's effect on the
HPA axis are unclear. However, given the effects they found at
relatively low lead exposures, the authors suggest that cortisol
reactivity be considered in future studies as a potential mediator of
lead-induced disorders.
Julia R. Barrett
originally published at http://www.ehponline.org/docs/2008/116-2/ss.html
