How can our regulatory system more effectively protect the health of the developing fetus?
This essay is in response to: How is the developing fetus vulnerable to toxic chemical exposures, and how can our regulatory system more effectively protect our health in the prenatal period?
There is a growing concern regarding the vast number
of environmental exposures that can negatively impact the health of children
through pre-conceptual and prenatal exposures to the mother and father. Common
exposures to toxins such as pesticides and heavy metals such as methylmercury
(MeHg) impact critical windows of growth and development in the fetus and may result in life-long adverse health effects.
Despite our increasing knowledge about the
untoward effects of environmental exposures on the long-term health of children,
the regulatory system does little to protect mothers, fathers, and ultimately, children.
One example of a common yet unregulated exposure is methylmercury
(MeHg) found at varying levels in fish. Mercury, a potent neurotoxin, crosses the placenta,
with levels substantially higher in the umbilical cord blood than in the
maternal blood supply. Historically, research findings indicate that prenatal exposure to
MeHg can cause lifelong adverse developmental and cognitive effects, even at
low doses.1-3 Children who are exposed in-utero through mother’s
consumption of fish contaminated with MeHg are at increased risk of poor
performance on neurobehavioral tests such as those measuring attention, fine
motor function, and language skills. There is some evidence that early life exposure may
also affect cardiovascular, immune, and reproductive health.4-9
Severe health effects as a result of high poisoning
events include cerebral palsy, mental retardation, deafness, and blindness,
which were evidenced in the sentinel case that occurred in the 1950s in
Minamata Bay, Japan. 10-11
Underscoring these findings are estimates that over 600,000 U.S. children
could be exposed to unsafe levels of MeHg as a result of prenatal exposure and that
of women who eat any fish at all, 50% consume more than safe levels.12 Despite these and other disturbing research results, and until
very recently, there has been little political will to actively protect children
from the potentially harmful health effects associated with fish consumption
and MeHg exposure through regulatory mechanisms.
Two encouraging exceptions bring hope to this
discussion. The first is the landmark Mercury and Air Toxic Standards that will protect children by limiting emissions of
mercury and other air toxics from power plants. It is estimated that by 2016 130,000 cases of asthma
among children will be prevented annually. This ruling has significant implications in
protecting children prenatally as well, as reductions in mercury emissions will
eventually lead to reductions in MeHg found in the fish childbearing women
The second example is work currently conducted
by the Children’s Health Protection Advisory Committee under the guidance of
the Office of Children’s Health Protection (OCHP) of the Environmental
Protection Agency (EPA). Last year, CHPAC advised the Administrator on criteria for identifying chemicals of concern for children.
More recently, a workgroup of the CHPAC was
convened to specifically explore and advise on environmental exposures in the
prenatal period. Areas identified as important for EPA to consider include the
development of policies and practices that address the prenatal period (e.g.,
expanding bio-monitoring to include prenatal period); incorporating social
determinants of health and environmental justice into existing programs and
policies; developing a national agency-wide campaign to educate the public
about prenatal hazards and prevention; and funding research that addresses the
prenatal period including key outcomes and mechanisms.
These recommendations will provide a framework
for action that can begin to address a stage of human development that has been
all but ignored from a regulatory perspective. The potential for serious, long-term
health impacts in children resulting from a wide range of pre-conceptual and
prenatal environmental exposures is a legitimate concern based on evidence. It
is essential that our government address them through innovative strategies
that support expanded research for the preconceptual/prenatal
period, collaboration between federal agencies, and improved regulatory
mechanisms informed by the evidence, to protect the health of future
1. Environmental Protection Agency (2012). Mercury: Human Exposure, Retrieved January 20, 2012.
2. Chalupka, S. & Chalupka, A. (2010). The impact of
environmental and occupational exposures on reproductive health. JOGNN, 39,
3. Sakomoto, M., Kubota, M., Liu, X. J., Murata, K., Nakai, K.,
& Satoh, H. (2004). Maternal and fetal mercury and n-3 polyunstaurated
fatty acids as a risk and benefit of fish consumption to fetus. Environ Sci
Tech, 38(14), 3860-3863.
4. Myers, G. J., & Davidson, P. W. (1998). Prenatal
methylmercury exposure and children: Neurologic, developmental, and behavioral
research. Environ Health Perspect, 106 Suppl 3, 841- 847.
5. Goldman, L., & Shannon, M. (2001). American Academy of
Pediatrics and the Committee on Environmental Health: Technical Report--Mercury
in the environment: Implications for pediatricians. Pediatrics,
6. Landrigan, P., Kimmel, C., Correa, A., & Eskenazi, B.
(2004). Children's health and the environment: Public health issues and
challenges for risk assessment. Environ Health Perspect, 112(2), 257-265.
7. Davidson, P. W., Myers, G. J., Cox, C., Axtell, C., Shamlaye,
C., Sloane-Reeves, J., et al. (1998). Effects of prenatal and postnatal
methylmercury exposure from fish consumption on neurodevelopment: outcomes at
66 months of age in the Seychelles Child Development Study. JAMA,
8. Salonen, J.T., Nyyssonen, Salonene, R. (1995). Fish intake and
the risk of coronary disease. N Engl J Med, 333 (14), 937.
9. Laks, D.R. (2009). Assessment of chronic mercury exposure
within the U.S. population, National Health and Nutrition Examination Survey,
10. Harada, M. (1995). Minamata disease: methylmercury poisoning
in Japan caused by environmental pollution. Crit Rev Toxicol, 25(1), 1-24.
Morikawa, N., Atsumoto, H., & Shiraishi, Y. (1962). A pathological study of
Minamata disease in Japan. Acta Neuro, 2(1), 40-57.
12. Mahaffey KR. Update on recent epidemiologic mercury
Proceedings of the 2004 national forum on contaminants in fish; 2004 Jan 25–28;
San Diego: National Service Center for Environmental Publications, U.S.
Environmental Protection Agency; 2004. p. 31-4.
Comments Leave a Comment