
Photo Credit: Sugarsnap Photography
- A Polluted World Affects All Kinds of Infant Feeding
- Toxins In Human Breast Milk
- How These Substances Reach the Milk
- Immunologic Factors Over Time
- Anti-Bacterial Factors
- Anti-Viral Factors
- Anti-Parasite Factors
Toxins
A POLLUTED WORLD AFFECTS ALL KINDS OF INFANT FEEDING
There’s no reason to worry or *panic* about the toxins possibly found in breast milk.
We hear a lot of sensational news about the toxins that can pass through breast milk, but it seems a lesser-numbered crowd will linger much on the fact that the other option, formula, has toxins (and pesticides) too, often in much higher amounts. (Read about the toxins in formula in this section). Perhaps not so surprising, after all it is an entirely processed food even before possible contaminants.
I’ve read various aggressively-written articles and scare-tactic ‘research’ that claim breastfeeding is bad because of toxins found in collected samples. First consider who might profit from a campaign against free infant feeding. Is full disclosure a priority in these articles? It would serve to question an authorial hidden agenda or connection to formula industry lobbying. Remember that breastfeeding advocates and current infant feeding guidelines don’t have a fat wallet to gain from advocating for breastfeeding.
Unfortunately we do live in a porous, imperfect world, and there is no ‘perfect’ option for feeding ourselves, our babies, our dogs, or our backyard garden shrubbery — still, breastfeeding remains the best option for our children.
Your average modern human is both at the top of the food chain and a highly toxic creature. Many hold to the idea of mixing up a bottle of chemically-engineered and therefore ‘perfect’ commercial formula to detour the passage of body-accumulated toxins to their babies. He, she, and we are responsible for attempting to give our children the best possible food, which can be easily accomplished by cleaning up our family lifestyles, not by defaulting to a product for this flawed reasoning alone. Pesticides hurt both breast milk and formula, and they can also hurt anyone who consumes either.
“Breastfeeding is still recommended despite the presence of chemical toxins. The toxicity of chemicals may be most dangerous during the prenatal period and the initiation of breastfeeding. However, for the vast majority of women the benefits of breastfeeding appear to far outweigh the risks. To date, effects on the nursing infant have been seen only where the mother herself was clinically ill from an toxic exposure.” – U.S. Centers for Disease Control
IN HUMAN BREAST MILK
Bifidobacterium in breast milk can protect against chemicals in it, as discovered in this study that finds infants of breastfed mothers tested lower for toxic perchlorate than formula-fed babies (even though the toxin level was higher in the breast milk itself than the formula).
Notes from the reference text “Chemical Compounds in Human Milk”:
“Dietary intake of contaminants during lactation is not a significant source of contamination in breast milk; the contaminants come from the mobilization of adipose tissue into the lipids in human milk. During pregnancy, however, dietary intake may significantly affect maternal contaminant levels because of an increase in adipose tissue in conjunction with weight gain, as well as development of key organ systems in the fetus itself.”
“Contaminant levels are also dependent on personal exposure from a woman’s location in the environment. There are higher levels of persistent organochlorines in women living in coastal regions, presumably from eating more readily available fish. However, women who consume great quantities of beef and dairy products should also be aware of concerns.”
“There are lower levels of DDT and DDE in the milk of vegetarian mothers, but stable PCB levels indicate that contaminant sources other than food are involved, for example air pollution outdoors and indoors.”

Via permaculturenews.org
From “Pesticides and Breastfeeding” by Betty Crase, LLLI Breastfeeding Reference Library & Database:
“The February 1994 issue of Pediatrics takes an extensive look at the lead crisis in infants in general, including the continuing controversy over the new lower blood lead concentration limit recently set.
Cadmium levels in breast milk are about the same as in cow’s milk. Please note, however, that cadmium and DDT levels are higher in the breast milk of smokers.
Mercury levels typically are lower in human milk than those of lead and cadmium. The highest levels have been found in the milk of fish eaters, particularly sport fish. Concern is also raised from time to time about the contribution of mercury to human milk from silver amalgam dental fillings.”
HOW THESE SUBSTANCES REACH THE MILK
“Our bodies have several systems that regulate what gets into our milk, and it’s worth understanding how it works in this context.
In order for a substance to get into breastmilk, it must pass through a number of ‘screens.’ Some things we ingest are destroyed in our digestive system, eliminated from our bodies, or held in our livers before they even enter our bloodstream, which is where they may transfer into milk.
And not everything that enters our bloodstream makes it into our milk, either. Only substances that are small enough in molecular weight to squeeze in between our milk making cells, or fat-soluble enough to ‘hitchhike’ through the cell walls, make the cut.
And (in an act I consider to be just a little bit miraculous) once the level in our bloodstream declines, some substances that make it into milk actually move out of the milk, back into our bloodstream. Even when something harmful does make it into your milk, your baby’s gut may destroy it or poop/pee it out before it can enter her bloodstream.
Of course, these systems are not foolproof, and it’s important to emphasize that some harmful substances can enter milk can pose a threat to your baby.” – Tanya Lieberman, IBCLC
Links:
- “Breastfeeding Remains the Best Choice in a Polluted World” by Mary Hurt, LLLI Public Relations Associate
- “Environmental Contaminants and Human Milk” by Elizabeth Bauchner
- “Searching for the truth about toxins in breast milk” – The Alpha Parent
- “Toxins and Infant Feeding” – International Breastfeeding Centre
Visual Aids: The Good Factors
Concentration of Immunologic Components in Human Milk
Average Concentration, mg/ml |
||||||
2-3 days
|
1 mo
|
6 mo
|
12 mo
|
13-15 mo
|
16-24 mo
|
|
Lactoferrin |
5.3
|
1.9
|
1.4
|
1.0
|
1.1
|
1.2
|
Secretory IgA |
2
|
1
|
0.5
|
0.8
|
1.1
|
1.1
|
Lysozyme |
0.09
|
0.02
|
0.25
|
0.196
|
0.244
|
0.187
|
Sources: http://kellymom.com/nutrition/milk/immunefactors/ |
Anti-Bacterial Factors
Factor | Shown in vitro to be active against |
---|---|
Secretory IgA | E. coli (also pili, capsular antigens, CFA1) including enteropathogenic strains, C. tetani, C. diphtheriae, K. pneumoniae, S. pyogenes, S. mutans, S. sanguins, S. mitis, S. agalactiae (group B streptococci), S. salvarius, S. pneumoniae (also capsular polysaccharides), C. burnetti, H. influenzae, H. pylori, S. flexneri, S. boydii, S. sonnei, C. jejuni, N. meningitidis, B. pertussis, S. dysenteriae, C. trachomatis, Salmonella (6 groups), S. minnesota, P. aeruginosa, L. innocua, Campylobacter flagelin, Y. enterocolitica, S. flexneri virulence plasmid antigen, C. diphtheriae toxin, E. coli enterotoxin, V. cholerae enterotoxin, C. difficile toxins, H. influenzae capsule, S. aureus enterotoxin F, Candida albicans*, Mycoplasma pneumoniae |
IgC | E. coli, B. pertussis, H. influenzae type b, S. pneumoniae, S. agalactiae, N. meningitidis, 14 pneumoccoccal capsular polysaccharides, V. cholerae lipopolysaccharide, S. flexneri invasion plasmid-coded antigens, major opsonin for S. aureus |
IgM | V. cholerae lipopolysaccharide, E. coli, S. flexneri |
IgD | E. coli |
Analogues of epithelial cell receptors (oligosaccharides and sialylated oligosaccharides***) |
S. pneumoniae, H. influenzae |
Bifidobacterium bifidum growth factors (oligosaccharides, glycopeptides) Other Bifidobacteria growth factors (alpha-lactoglobulin, lactoferrin, sialyllactose) |
Enteric bacteria. Two infant Bifidobacteria species provide a lipophilic molecule which kills S. typhimurium. B. bifidum produces Bifidocin B which kills Listeria. B. longum produces protein BIF, which stops E. coli. |
Carbohydrate | E. coli enterotoxin, E. coli, C. difficile toxin A |
Cathelicidin (LL-37 peptide) | S. aureus, group A streptococcus, E. coli |
Casein | H. influenzae |
kappa-Casein ** | H. pylori, S. pneumoniae, H. influenzae |
Complement C1-C9 (mainly C3 and C4) |
Killing of S. aureus in macrophages, E. coli (serum-sensitive) |
β-defensin-1 or -2 or neutrophil-α-defensin-1 or α-defensin-5 or -6 |
E. coli, P. aeruginosa, (some Candida albicans *) |
Factor binding proteins (zinc, vitamin B12, folate) |
Dependent E. coli |
Free secretory component** | E. coli colonization factor antigen 1 (CFA I) and CFA II, C. difficile toxin A, H. pylori, E. coli |
Fucosylated oligosaccharides | E. coli heat stable enterotoxin, C. jejuni, E. coli |
Ganglioside GM1 | E. coli enterotoxin, V. cholerae toxin, C. jejuni enterotoxin, E. coli |
Ganglioside GM3 | E. coli |
Glycolipid Gb3 | S. dysenterae toxin, shigatoxin of shigella and E. coli |
Glycoproteins (mannosylated) | E. coli, E. coli CFA11, fimbrae |
Glycoproteins (receptor- like)+ oligosaccharides |
V. cholerae |
Glycoproteins (sialic acid -containing or terminal galactose) |
E. coli (S-fimbrinated) |
alpha-Lactalbumin (variant) | S. pneumoniae |
Lactoferrin** | E. coli, E. coli/CFA1 or S-fimbriae, Candida albicans*, Candida krusei*, Rhodotorula rubra*, H. influenzae, S. flexneri, Actinobacillus actinomycetemcomitans |
Lactoperoxidase | Streptococcus, Pseudomonas, E. coli, S. typhimurium |
Lewis antigens | S. aureus, C. perfringens |
Lipids | S. aureus, E. coli, S. epidermis, H. influenzae, S. agalactiae, L. monocytogenes, N. gonorrhoeae, C. trachomatis, B. parapertusis heat-labile toxin, binds Shigella-like toxin-1 |
Lysozyme | E. coli, Salmonella, M. lysodeikticus, S. aureus, P. fragi, growing Candida albicans* and Aspergillus fumigatus* |
Milk cells (80% macrophages, 15% neutrophils, 0.3% B and 4% T lymphocytes) |
By phagocytosis and killing: E. coli, S. aureus, S. enteritidis By sensitised lymphocytes: E. coli By phagocytosis: Candida albicans*, E. coli Lymphocyte stimulation: E. coli K antigen, tuberculin Spontaneous monokines: simulated by lipopolysaccaride Induced cytokines: PHA, PMA + ionomycin Fibronectin helps in uptake by phagocytic cells. |
Mucin (muc-1; milk fat globulin membrane) |
E. coli (S-fimbrinated) |
Nonimmunoglobulin (milk fat, proteins) |
C. trachomatis, Y. enterocolitica |
Phosphatidylethanolamine | H. pylori |
(Tri to penta) phosphorylated beta-casein | H. influenzae |
Sialyllactose | V. cholerae toxin, H. pylori |
Sialyloligosaccharides on sIgA(Fc) |
E. coli (S-fimbrinated) adhesion |
Soluble bacterial pattern recognition receptor CD14 | Bacteria (or LPS) activate this to induce immune response molecules from intestinal cells |
Sulphatide (sulphogalactosylceramide) | S. typhimurium |
Unidentified factors | S. aureus, B. pertussis, C. jejuni, E. coli, S. typhimurium, S. flexneri, S. sonnei, V. cholerae, L. pomona, L. hyos, L. icterohaemorrhagiae, C. difficile toxin B, H. pylori, C. trachomatis |
Xanthine oxidase (with added hypoxanthine) |
E. coli, S. enteritidis |
Anti-Viral Factors
Secretory IgA | Polio types, 1,2,3*. Coxsackie types A9, B3, B5, echo types 6,9, Semliki Forest virus, Ross River virus, rotavirus*, cytomegalovirus, reovirus type 3, rubella varicella-zoster virus, rhinovirus, herpes simplex virus, mumps virus, influenza, respiratory syncytial virus, human immunodeficiency virus, hepatitis C virus, hepatitis B virus, hepatitis E, measles, sin nombre hantavirus, SARS virus, Norwark and noroviruses. |
IgE | Parvovirus B19 |
IgG | Rubella, cytomegalovirus, respiratory syncytial virus. rotavirus, human immunodeficiency virus, Epstein-Barr virus, sin nombre hantavirus, West Nile virus. |
IgM | Rubella, cytomegalovirus, respiratory syncytial virus, human immunodeficiency virus, sin nombre hantavirus, West Nile virus. |
Bifidobacterium bifidum** | Rotavirus (by increasing mucin) |
Chondroitin sulphate (-like) | Human immunodeficiency virus |
β defensins (1-3) | Herpes simplex virus, vesticular stomatitis virus, cytomegalovirus, influenza, human immunodefiency virus |
β-defensin 1 or α-defensin-5 |
Adenovirus |
Haemagglutinin inhibitors | Influenza, mumps. |
Lactadherin (mucin-associated glycoprotein) | Rotavirus* |
Histo-blood group carbohydrates | Norwalk virus |
Lactoferrin | Cytomegalovirus, human immunodeficiency virus and reverse transcriptase, respiratory syncytial virus, herpes simplex virus type 1, herpes simplex virus type 2, hepatitis C, hepatitis B, poliovirus type 1, adenovirus 2 and Friend retrovirus. Also binds to the virus receptors, low density lipoprotein receptor, and heparin sulphate proteoglycans. Hepatitis G***, rotavirus*** and Seoul hantavirus***. |
Lipid (unsaturated fatty acids and monoglycerides) | Herpes simplex virus, Semliki Forest virus, influenza, dengue, Ross River virus, Japanese B encephalitis virus, sindbis, West Nile, Sendai, Newcastle disease virus, human immunodeficiency virus, respiratory syncytial virus, Junin virus, vesticular stomatitis virus, cytomegalovirus, mumps, measles, rubella, parainfluenza viruses 1-4, coronavirus, bovine enterovirus (C12), poliovirus (C18), African swine fever virus. |
Lysozyme | Human immunodeficiency virus, ectromelia |
alpha2-macroglobulin (like) | Influenza haemagglutinin, parainfluenza haemagglutinin. |
Milk cells | Induced gamma-interferon: virus, PHA, or PMA and ionomycin Induced cytokine: herpes simplex virus, respiratory syncytial virus. Lymphocyte stimulation: rubella, cytomegalovirus, herpes, measles, mumps, respiratory syncytial virus, human immunodeficiency virus. |
Mucin (muc-1; milk fat globulin membrane) | Human immunodeficiency virus, pox virus |
Non-immunoglobulin macromolecules | Herpes simplex virus, vesicular stomatitis virus, Coxsackie B4, Semliki Forest virus, reovirus 3, poliotype 2, cytomegalovirus, respiratory syncytial virus, rotavirus*. |
Neutrophil-derived α-defensin-1 (HNP-1) | Herpes simplex virus 1 |
Ribonuclease | Murine leukaemia, human immunodeficiency virus |
Secretory leukocyte protease inhibitor | Human immunodeficiency virus, sendai, influenza |
Sialic acid-glycoproteins | Adenovirus 37 |
slgA + trypsin inhibitor | Rotavirus |
Sialylated glycans | Enterovirus 71 |
Soluble intracellular adhesion molecule 1 (ICAM-1) | Rhinoviruses (major-group) 3, 14, 54; Coxsackie A13 |
Soluble vascular cell adhesion molecule 1 (VCAM-1) | Encephalomyocarditis virus |
Sulphatide (sulphogalactosylceramide) | Human immunodeficiency virus |
Vitamin A | Herpes simplex virus 2, simian virus 40, cytomegalovirus |
Factors | Shown in vitro to be active against |
---|---|
Prostaglandins E2, F2 alpha | Parainfluenza 3, measles |
Prostaglandins E1 | Poliovirus, encephalomyocarditis virus, measles |
Gangliosides GM1-3 | Rotavirus, respiratory syncytial virus, adenovirus 37 |
Gangliosides GD1a, GT1b, GQ1b | Sendai virus |
Glycolipid Gb4 | Human B19 parvovirus |
Heparin | Cytomegalovirus, respiratory syncytial virus, dengue, adenovirus 2 and 5, human herpesvirus 7 and 8, adeno-associated virus 2, hepatitis C |
Anti-Parasite Factors
Factor | Shown in vitro to be active against |
---|---|
Gangliosides | Giardia lamblia, Giardia muris |
IgG | Plasmodium falciparum Strongyloides stercoralis (threadworm) |
Lactoferrin (or pepsin-generated lactoferricin) | Giardia lamblia, Plasmodium falciparum |
Lipid (free fatty acids and monoglycerides) |
Giardia lamblia Entamoeba histolytica Trichomonas vaginalis (protozoa) Eimeria tenella (animal coccidiosis) |
Macrophages | Entamoeba histolytica |
Oligosaccharides | Entamoeba histolytica |
Secretory IgA | Giardia lamblia (protozoa) Entamoeba histolytica (protozoa) Schistosoma mansoni (blood fluke) Cryptosporidium (protozoa) Strongyloides stercoralis (threadworm) Toxoplasma gondii Plasmodium falciparum (malaria) |
Unidentified | Trypanosoma brucei rhodesiense |