The efficiency of maternal transfer of lead and its influence on plasma IgE and splenic cellularity of mice.
Exposure to the well known environmental toxicant lead is typically assessed by blood and/or bone levels and has been implicated in the onset of a variety of diseases affecting multiple human systems. However, there are conflicting data regarding the efficiency of in utero versus lactational transfer of lead to offspring, and the immunomodulatory effects of lead in early life have not been well defined. Pregnant BALB/c mice were exposed to lead acetate in their drinking water beginning at approximately day 15 of gestation, and cross-fostering of exposed/nonexposed litters was performed at parturition. Significant increases of blood lead levels of all exposed offspring were found at 1 week of age with evidence for both transplacental and lactational transfer. Additionally, mice exposed to lead continuously beginning at approximately 6 days prior to birth showed significant decreases in their blood lead levels 2 weeks after weaning, despite continued exposure as adults. This result suggests maternal transfer of lead is more efficient than oral adult exposure and that substantial lead transfer occurs both transplacentally and lactationally. The incidence of childhood atopic responses including asthma has risen considerably in recent years, particularly within areas containing higher levels of environmental pollutants. Plasma IgE levels of 2-week-old neonates exposed to lead before and/or after birth were measured as an index of atopy. Neonates exposed to lead transplacentally and/or lactationally had significantly higher plasma IgE levels, a biomarker of atopy, and lower splenic white blood cell numbers than age-matched controls. These results resemble the lag in immunocompetency and increase in serum IgE noted in atopic children and suggest a role for environmental toxicants and non-allergen-specific immunology in the prevalence of atopy and asthma in children.
Snyder
J E
JE
Wadsworth Center, New York State Department of Health, P.O. Box 509, Albany, New York 12201-0509, USA.
Filipov
N M
NM
Parsons
P J
PJ
Lawrence
D A
DA
D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D000833:Animals, Suckling; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D007073:Immunoglobulin E / Q000097:blood*; D015847:Interleukin-4 / Q000097:blood; D007854:Lead / Q000097:blood / Q000493:pharmacokinetics* / Q000633:toxicity*; D008431:Maternal-Fetal Exchange / Q000502:physiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008892:Milk / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D013154:Spleen / Q000166:cytology* / Q000187:drug effects; D013601:T-Lymphocytes / Q000187:drug effects
D015847:Interleukin-4; D007854:Lead; D007073:Immunoglobulin E