Environmental contaminants, including pesticides, industrial chemicals,
and heavy metals are ubiquitous. Their long lasting, background
presence in foods, soil, and dust results in ongoing consumption and exposure
of virtually everyone, even long after use of a particular contaminant
(e.g. DDT) has been discontinued. Concerns have been raised about
the possible effects of these environmental contaminants on growth, sexual
maturation, behavior and development, immunologic competence,
and carcinogenic potential in the developing fetus, infant and child.
Little is known about levels and trends of environmental contaminants
in breastmilk in the US Studies available from the US are geographically
limited, based on small groups, and thus are not represent ative
of the general population. Based upon studies from other countries,
it appears that the concentration of some contaminants in breastmilk
such as dioxin have declined worldwide since the 1970’s. Fortunately,
maternal exposure to environmental contaminants in the US is low except
in women at specific occupational risk (pesticides in farm workers),
women living in contaminated housing (lead in northeastern cities), accidental
massive contamination of the food chain (PCB exposure via
cow’s milk and beef in Michigan in 1970’s) or chronic ingestion of fish
taken from waters with high levels of industrial contaminants (mercury or PCB in Lake Ontario, Hudson River).
Lipophilic, organochlorine contaminants, such as DDT compounds
and PCB, are stored in body fat and accumulate over time. Exposure
of the breastfeeding infant begins before birth by transfer of
maternal contaminants present in maternal blood across the placenta.
These contaminants, especially those stored in maternal fat (DDT,
PCB), continue to be released into human milk throughout lactation.
Maternal stores of these compounds are depleted as maternal fat is mobilized
and the compounds are released into milk, thus transferring the
contaminants from mother to the breastfeeding infant. Breastmilk levels
of environmental contaminants decline substantially over the duration
of breastfeeding and decrease with subsequent pregnancies, presumably
reflecting the gradual depletion of maternal stores via breastfeeding. In
general, larger amounts of contaminants are transferred postnatally via
breastmilk than are transferred antenatally via the placenta. Despite
this, the adverse physiologic effects of various contaminants appear to
be greater with transplacental compared to lactational exposure in both
humans and experimental animals. This greater susceptibility of the
fetus may relate to the immaturity of affected systems at the time of
In experimental animals, organochlorine compounds (e.g., PCB, DDT) interfere with normal hormonal balance. Effects are variable and onflicting, depending upon the species, gender, age and immaturity of the nimal studied. Nevertheless, estrogenic, androgenic and anti-estrogenic ffects have all been associated with exposure to DDT and PCB compounds.
These effects include acceleration or delay of puberty, decreased irthweight, and increased weight at puberty. There are few studies in uman infants and children relating to low, background level exposure to nvironmental contaminants. Recently, Gladen, et al reported the effects f transplacental and lactational exposure to DDE, a DDT metabolite, and CB on growth at puberty in a large cohort of normal, healthy children born in North Carolina in 1978-1982 and followed longitudinally from birth to puberty.
In this study the authors calculated the theoretical transplacental nd lactational exposure of the fetus and infant based upon maternal serum and breastmilk levels of DDE and PCB and the duration of breastfeeding. No effects of either antenatal or postnatal DDE or PCB
exposure were seen in the first year on either birthweight or growth. At
puberty, however, transplacental DDE exposure was associated with significantly
increased height and weight of boys. This effect was doserelated.
No effect of DDE exposure was seen on growth in girls. The age
of puberty was not affected in either sex. Although the calculated
amount of PCB and DDE ingested via breastmilk was much higher
than the amount acquired antenatally across the placenta, no effect of
lactational exposure was found in either sex on growth or puberty.
The authors concluded that body size at puberty may be affected by prenatal,
but not lactational, exposure to background levels of these environmental
contaminants. Additional studies (Darvill, et al) have shown a
dose-related, adverse effect of prenatal PCB exposure, as determined by
umbilical blood levels, on infant performance on the Fagan test of visual recognition at 6 and 12 months of age. Again, there was no adverse
effect associated with PCB breastmilk levels.
In conclusion, despite concerns about the adverse biologic effects
of environmental contaminants, thus far there is no evidence
that, under ordinary circumstances, the low level of exposure to
these contaminants in breastmilk adds to potential risks incurred
from antenatal or subsequent postnatal exposure. The many benefits
of breastfeeding far outweigh the theoretical risks of exposure
to environmental contaminants.
DDT: organochlorine pesticide banned in the US since 1970’s
DDE: dichlorodiphenyl dichloroethane (primary metabolite of pesticide DDT)
Dioxin: contaminant in defoliant, Agent Orange
PCB: polychlorinated biphenyls (organochlorine industrial chemical; used in