Pesticide Carcinogens in Mothers’ Milk and Total
Diet; An Issue of Motherhood; A Toxicology
Review. Aug. 1997. File: mmkpescarcs.htm
Jorma Jyrkkanen Home Page
Abstract
In a literature review I assessed the
carcinogenicity of pesticide and chemical residues found
in mothers’ milk by various researchers, and
determined their probable contamination route, source
and carcinogenic effects. It was concluded that
carcinogens were present and these were probably
causing cancers in humans. The main source of
exposure in women was diet but occupational exposure
may play a role for many. The primary candidate
cancers for pesticidal origin are melanoma,
lymphatic cancers, blood cancers and multiple myeloma.
Other cancers also have a highly suggestive
correlation with pesticide carcinogenesis, including
breast cancer. Articles were discussed which
suggest that synergism and immune system compromise
may increase mortality. The concept of safe level
was found to be based on erroneous arguments,
which do not represent the real world. Inerts and
their contaminants have a potential to explain a
large component of carcinogenicity but have not been
researched because they have been in use
covertly. Epidemiology is largely after the fact of
exposure and can lead to the conclusion that a product
is unsafe after it has been used for a long time,
thereby endangering many populations. It was
found that most carcinogens in Mother’s Milk were
also endocrine and reproductive disruptors with
hormonal impacts and involvement in development and
carcinogenesis. Banning carcinogens at the source
and using alternatives to pesticides are
discussed as options to use of carcinogenic pesticides.
Key Words: breast cancer, carcinogens, childhood
cancers, contaminants, covert, endocrine,
epidemiology, exposure, disruptors, hormonal, inerts,
leukaemia, lymphoma, melanoma, Mother’s milk,
multiple myeloma, pesticides, reproductive, residues,
synergism, toxicology
Clean Milk/A Broken Trust
The International Agency for the Research of
Cancer (IARC, 1979) recognized that animal
carcinogens are a cancer risk to humans and
stated that for practical regulatory purposes
they should be treated as if they are human carcinogens.
Additionally, Uma Ram Nath (1978) of the World
Health Organization (WHO) raised an alarm over
their concern over chemicals in breast milk. In his
report, he cites food as the main source of
toxins, and environment as another; that the
contamination poses an unkown risk to babies, and in some
cases, breast feeding should be discontinued;
that experts recommend alternative preventative
measures for reducing environmental pollution.
Keeping these comments in mind, I decided in 1989
to have a look at published literature worldwide
to see how many pesticide residues were in
Mothers’ Milk and how many of them were considered to
be cancer causing. I did a rudimentary update of
this in 1998.
This exploration uncovered many surprises.
Publishing in Residue Reviews, Volume 89, author
Allan Astrup Jensen (1983) reports on a worldwide
survey in an article titled “Chemical
contaminants in human milk”.
The list of findings is substantial. I assessed
the carcinogenicity from available peer reviewed
literature (Saks, I., 1981) of the most common
residues and found the following associations of
pesticide to its reported carcinogenicity [published
cancer causing ability] (see Tables I & II).
The Breast Feeding Infants Diet
Table 1.
Carcinogenicity of Residues Found in Human Milk
EXPOSURE SPECIES CARCINOGENICITY
PESTICIDE ROUTE TESTED FINDING
DDT(r)(Linked to breast cancer); oral-mouse(mus)-conclusive
(concl) carcinogen (carc),
subcutaneous(scu)-mus-concl, animal (anim)-suspected(susp)- International
Agency for Research on Cancer(IARC)
PCB’s(r); conclusive human and mouse liver
carcinogen
DDE(r); oral-mus-concl, etc.etc.
hexachlorobenzene (HCB)(r); oral-hamster
(ham)-concl
hexachlorocyclohexanes (HCH)(r); (includes
Lindane)-oral-mus-concl, anim-positive (pos)-IARC(Linked to breast cancer)
dieldrin(r); oral-rat-suggest (sugg),
oral-mus-concl, anim-pos-IARC
heptachlor epoxide(r); oral-mus-concl-potent
experimental carc
aldrin; mus-National Cancer
Institute(NCI)-bioassay-pos,
oral-rat-suggestive (sugg)
heptachlor(r); oral-mus-concl
DDD (TDE); oral-rat-sugg, oral-mus-sugg,
questionable (quest), anim-pos-IARC, NCI bioassay;
results indefinite (indef)
mirex(r); oral-mus-concl, anim-pos-IARC
oxychlordane(r); oral-mus-concl
trans-nonachlor(r); no references in Sax (1981)
pentachlorobenzene; “benzene is a high volume
chemical and presents a serious and imminent threat to
public health”Sax.
PCT; oral-mus-concl
PBB; oral-rat-quest, indef-IARC
TCDD(r); Discussed below
hexachlorophene; negative (neg)
perchloroethylene; oral-mus-concl, NCI
bioassay-mus-pos
halothane; note-1,2-dibromoethane used as a
fumigant for apples-oral-rat-concl,oral-mus-concl,
IARC-pos, also related 1,2-dichloroethane-mus-concl,
rat-concl,
bioassay-pos
carbon disulphide; note that bisdiethylthiocarbamoyl,
disulfide is oral-mus-concl, scu-mus-sugg,
NCI bioassay-neg
nicotine; oral-rat-sugg, intraperitonially
(ipr)-mus-sugg, scu-ham-sugg, ipr-mus-concl, human
suspected (susp)
(r)Reproductive and endocrine disrupters as of
1995. Clearly this is a diet that has the potential
to alter masculinity and feminity and
reproduction potential.
Pellizzari et al.(1982) found several hundred
volatile chemicals in Mother’s’ milk from four
different areas of the USA indicating a much broader
contamination than expected. His list included the
following chemicals.
Volatile Organics in Mothers’ Breast Milk
I mention that numerous purgeable organic
compounds have been found in Mother’s’ milk.
The carcinogenicity and endocrine disruptivity
of these is of great interest due to the
widespread nature of the contamination, and the potential
ramifications of this to nursing infants later in
life, as well as to the contaminated parents.
Exposure to multi-chemical carcinogens through
nursing can be expected to induce mutations which
may contribute to increased cancer incidence at a
later date.
Toxic chemicals can of course have other effects
including neurological, reproductive,
immunological, behavioural, developmental and cognitive. The
list is long but I will grind through it for the
sake of science to show that multi-chemical
exposure is highly multi, when taken together with the
multitude of pesticides, thousands of inerts and contaminant residues I
also mention and don’t mention in this review article.
26 HALOGENATED cpds; chlorodifluoromethane,
chlorotrifluoromethane, dichlorodifluoromethane,
chloromethane, chloroethane, trichlorofluoromethane,
dichloroethylene, Freon 113, methylene chloride,
chloroform, 1,1,1-trichloroethane, carbon
tetrachloride, tetrachloroethylene, chloropentane,
dibromochloromethane, tetrachloroethylene,
dichloropropene, chlorobenzene, chlorohexane, iodopentane,
3-methyl-1,1-iodobutane, chloroethylbenzene,
dibromodichloromethane, dichlorobenzene, chlorodecane,
trichlorobenzene.
This class of compounds tends to be carcinogenic
and many induce cancers of the stomach, blood
vessels, skin, breast, lung, uterus, liver and
biliary tract in experimental animals. Some have
proven to be human carcinogens of the lung, skin,
liver and blood forming tissues. (N. I. Sax, 1983}.
17 ALDEHYDES; acetaldehyde, methyl propanal,
n-butanal, methylbutanal, **Crotonaldehyde
{Insecticide and CHEMICAL WARFARE AGENT (CAS:
4170-30-3)}, n-pentanal, n-hexanal, Furaldehyde
{Insecticide, fungicide, germicide, irritates mucous
membranes and acts on CNS, lacrimation and acts on eyes},
n-heptanal, benzaldehyde, n-octanal, phenyl
acetaldehyde, n-nonanal, methyl furaldehyde,
n-decanal, n-undecanal, n-dodecanal.
20 KETONES; acetone, methyl ethyl ketone, methyl
propyl ketone, methyl vinyl ketone, ethyl vinyl
ketone, 2-pentanone, methyl pentanone, methyl
hydroxyfuranone, 2-methyl-3-hexanone, 4-heptanone,
3-heptanone, 2-heptanone, methyl heptanone
{narcotic in high doses}, furyl methyl ketone, octanone,
acetophenone, 2-nonanone, 2-decanone, alkylated
lactone, phthalide.
26 other OXYGENATED cpds; C4H6O, C4H8O, C5H10O,
C6H8O, C6H10O, C4H6O2, C6H12O, C7H12O, C7H10O,
C7H14O, C6H6O2, C8H14O2, C8H16O, C7H8O2, C7H10O2,
C9H18O, C8H6O2, C10H12O2, C10H14O, C10H16O,
C10H18O, C10H20O, C10H.22O, C9H8O2, C11H20O, C10H10O2;
{Note: C4H6O can be either vinyl ether, an
explosive anesthetic, or methyl vinyl ketone, an
alkylating agent, plastic, steroid and vitamin A
precursor, with high absorbtion, irritancy to mucous
membranes and respiratory system (Asthma link?),
and high general systemic toxicity in mammals, or
Crotonaldehyde which is already confirmed is a chemical
warfare agent}.
10 ALCOHOLS; methanol, isopropanol,
2-methyl-2-propanol, n-propanol, 1-butanol, 1-pentanol,
alpha-furfuryl alcohol, 2-ethyl-1-hexanol phenol,
2-ethyl-1-hexanol phenol,
2,2,4-trimethylpenta-1,3-diol, alpha terpineol.
2 ACIDS; acetic acid, decanoic acid. 4 SULFUR
cpds; sulfur dioxide {Linked to increased heart
disease, many cancers but especially lung cancer,
respiratory diseases including asthma, infant
mortality} carbon disulfide, dimethyl disulfide,
carbonyl sulfide.
7 NITROGEN cpds; nitromethane {solvent, rocket
fuel, coating industry}, C5H6N2 {this is either
alpha or beta aminopyridine [Dye or anithistaminic]
or Glutaronitrile [trimethylene cyanide]},
C5H8N2, C4H4N2O, methyl acetamide, benzonitrile, methyl
cinnoline.
6 ESTERS; vinyl propionate, ethyl acetate,
ethyl-n-caproate, isoamyl formate, methyl decanoate,
ethyl decanoate.
2 ETHERS; dimethyl ether {refridgerant},
dihydropyran.
1 EPOXIDES; 1,8-cineole.
14 FURANS; furan {vapors anesthetic, absorbed
through skin}, methyl furan, tetrahydrofuran,
methyltetrahydrofuran, ethylfuran, dimethylfuran,
2-vinylfuran, furaldehyde, 2-n-butylfuran,
2-pentylfuran, methylfuraldehyde, furyl methyl ketone,
alpha-furfuryl alcohol, benzofuran.
13 ALKANES; C3H8, C4H10, C5H12 {pentane or
neopentane}, C6H14, C7H16, C8H18, C9H20, C10H.22,
C11H24, C12H26, C13H28, C14H30, C15H32. 12 ALKENES;
C3H6 {cyclopropane [explosive anesthetic],
propylene [plastic, simple asphyxiant [asthma?] and
anesthetic at high concs]} , C4H8, C5H10, C6H12,
C7H14, C8H16, C9H18, C10H20, C11H.22, C12H24, C13H26,
isoprene {skin and mucous irritant, and in high
concentrations, narcotic}.
7 ALKYNES; C5H8 {isoprene again??}, C6H10
{Norcarane}, C7H12, C8H14, C9H16, C10H18, C12H.22,
11 CYCLIC cpds; cyclopentane, methyl
cyclopentane, cyclohexane, ethyl methyl cyclohexane, C10H14
isomers, C10H16 isomers, limonene, methyl
decalin, alpha pinene, camphene, Camphor {plasticiser,
pyrotechnics, moth repellents, preservative in
pharmaceuticals and cosmetics, topical
anti-infective, topical antipruritic, internally as stimulant
and carminative, counter-irritant and antiseptic:
causes nausea, vomiting, vertigo, mental
confusion, delerium, clonic convulsions, coma,
respiratory failure, death}; benzene {leukemia}, toluene
{cancer promoter}, ethyl benzene, xylene, phenyl
acetylene, styrene, benzaldehyde, C3 alkylbenzene
isomers, C4 alkylbenzene isomers, C5 alkylbenzene
isomers, C6 alkylbenzene isomers, methyl styrene
{styrene is a carcinogen}, dimethyl styrene,
napthalene.
Clearly, Pellizzarri et al. has much to tell us
about how we are getting our pollutants into
human tissues and into our children, pollutants which
will do virtually nothing to improve health and
almost everything to degrade it.
He cites (IARC) 1979 and mentions that some of
the most often detected contaminants seem to be
carcinogenic or cocarcinogenic in laboratory
animals. This concurs with these findings on the above
chemicals. It cries out for action. Lance A.
Wallace et al. (1989) followed this work up and the
interested reader might find their work helpful.
Infants and Fetus at Higher Risk
” Jensen, says that “…In general, newborns are
particularily sensitive to toxic chemicals citing
Quinby et.
al. (1965) .. because their kidneys, liver enzyme
systems,
and blood -brain barriers are not fully developed
(Knoll and
Jayarman 1973 a and b). “
“..Furthermore, the newborn has very little body
fat for storage; consequently, the fat soluble chemicals
are circulated in the blood throughout the body for a
longer period and may interfere more intensely with the
normal enzyme activity (Kroger 1974). “
Jerry M. Rice (1982) in his paper on exposure to
chemical carcinogens during pregnancy and the
consequences for mother and conceptus, says that
transplacental transfer of carcinogens can cause
cancer in the developing infant.
The developing fetus is apparently exposed to
pesticide residues in utero as well as at the
breast.
The BC Province Newspaper ran a story, Dec. 20,
1987, on Arnold Schecter, New York Scientist, who
analysed the cancer risk to infants from just one
of these compounds, tetrachlorodibenzo-p-dioxin
(TCDD), one form of dioxin.
Schecter is purported to have said; ” We have
calculated
that the current exposure of nursing infants are
27 times greater than EPA’s one in a million cancer risk
level.” But Schecter added that the lifetime risk is much
higher.
He said; ” If it is assumed that infants in the
United States nurse for one year, then during this year
the child will have consumed 189 to 858 times the lifetime
(70 yr ) Environmental Protection Agency (EPA)
recommended intake.” [1300 x in another source]
This leads naturally to the question of what
happens when you add the risk from all of the other
chemicals and pesticides, taken singly and in
combination? But first, lets look at routes or
exposure and quantities.
Routes of Exposure
So where are these contaminants coming from and
how is it getting into the milk?
A report at the Third International Conference on
Pesticides held in Helsinki, 3-9th July 1979 which made the
link clear.
V. M. Adamovic, et al. (1979) gave a report
titled ” Daily Pesticides Intake through food in the Population
of Serbia”.
He reported finding DDT, alpha BHC, gamma-BHC and
Dieldrin. Thus food is one avenue of
contamination.
Linda R. Pim (1981) cites H.F. Kraybill (1969)
who was writing in the Canadian Medical Association
Journal about pesticide exposure in the general population.
Kraybill estimates that 30 mg of DDT and DDE are
absorbed from food, 4.96 mg are inhaled and 0.03
mg are absorbed from air and 0.01 mg from water, per
annum.
He says that 90% of the contamination is from
food. He estimated that average daily intake of
chlorinated organic pesticides was .0013 mg/kg body weight per day in
the general population in the period 1965-67.
2,4-D, 2,4,5-T, (Agent Orange was a mixture of
these two) PCP, MCP, and others amounted to 0.00013
mg/kg/day of which 2,4-D formed 1/3 while MCP and PCP formed
1/2. 2,4,5-T isn’t legally sold anymore but many
related isomers are still on the market covertly
as Inert ingredients.
Organophosphates (OP’s), chiefly malathion, but
also parathion, diazinon, ethion, ronnel formed .00013 mg/kg body
wt/ day.
Carbamate daily dietary intake was .0009 mg/kg
Body weight.
Adipose tissue retained 6 ppm DDT and 8.6 ppm
DDE. Though banned in Canada and the USA, DDT is
widely used in tropical regions.
Meats, fish, poultry and dairy products were the
Main sources of persistent pesticides.
Hair dressing, lipstick, hair lotion and sprays,
and eye shadows provided 3.5 mg/person/year.
White Americans averaged 8 ppb while non-whites
Averaged 16 ppb, indicating greater exposure in
non-whites.
His most important statement was that chlorinated
organic pesticides have been found in all diet
samples and all food classes within samples. That was in
1965-1967.
Of course the variability could be very large
depending on what a person ate, what their occupation was, and
where they lived, and so on.
Pesticides in the Canadian Diet
Pesticide residues in the total diet in Canada
Were reported by Harry A. McLeod et. al. (1980).
His list included along with average daily
Dietary intake in micrograms/kg (ug/kg) during the period
1976-1978, the following 24 different residues
at that time representing organochlorines (OC’s), OP’s,
sulfur, nitroanaline, phthalonitrile, and carbamate
compounds.
He reported for the first time; chlordane,
methidathion, phosalone, toxaphene, chlorothalonil, dichloran,
quintozene, sulfur, chlorpropham, and PCB (see Table II).
Many could have been missed due to crude
detection limits or by limiting the scope of the
assay.
Table II.
Carcinogenicity of Pesticide Residues in the
Canadian Diet
EXPOSURE SPECIES CARCINOGENICITY
PESTICIDE ROUTE TESTED
FINDING
=(avg Intake in ppb/day)
INSECTICIDES
BHC(r)=.01; oral-mus-concl, anim-pos-IARC
(benzene
hexachloride). Contaminant of corn, oats, rice.
Chlordane(r)(Linked to breast cancer)=<.001; oral-mus-concl.,
hepatocellular
carcinomas (technical grade has 3 isomers incl.
heptachlor).
Garden fruits.
DDT(r)=.023;
oral-rat-sugg/or-mus-concl/scu-mus-concl/anim-susp-IARC, NCI-bioass-neg. Wide
range of foods.
Diazinon=.001; NCI-neg: final. Cereals.
Dieldrin(r)=.002;
oral-rat-sugg/or-mus-concl/anima-
pos/NCI bioassay-neg:final. Wide range of foods.
Endosulfan(r)(Linked to breast cancer)=.007;
oral-mus-sugg/NCI-neg:final
Fruits, veggies.
Endrin=.001; EPA Farm Worker Field
Re-entry/NCI-neg
Ethion=<.001; no data; Fruits.
Heptachlor(r) epoxide=<.001;
oral-mus-concl/potent
experimental carc in animals; Dairy products.
Malathion(r)=.012; oral-rat-quest/ NCI-neg/neg;
Cereal contam.
Methidathion=.012; No data; Regist. for
potatos only
Canada, contaminant on citrus fruits and apples
imported from S. Africa, Chili, NZ, Australia,
USA.
Parathion=.003; oral-rat-quest/farm
worker field
re-entry NCI-Indefinite; Leafy vegetables
and fruits.
Parathion methyl; farm worker field
re-entry/NCI-neg
Phosalone=.007; (Zolone) No data;
Winnipeg, Vancouver,
Fruits.
Toxaphene(r)=.012; oral-rat-quest,
oral-mus-concl/oral-mus-concl/oral-mus-concl/NCI-bioassay-pos-mus;
Halifax-leafy vegetables and legumes.
FUNGICIDES
MITICIDE Captan=.004;
oral-mus-sugg/scu-mus-sugg/NCI-mus pos
(Orthocide); Fruits.
Chlorothalonil=<.001; oral-rat-sugg/NCI-
rat pos
(Daconil-2787, Bravo, Termil, Bravo-w-75); Garden
fruits-Montreal.
Dichloran=.01; (Dichloramine??)-intravenous
(intrav)-rat-conc/skin-mus-quest/IARC-indef. (Batran); Not
registered for
fruits in Canada, USA. Minor foods pest use
contaminant.
Folpet; scu-mus-sugg (phaltan)
HCB(r)=<.001;
oral-mus-sugg/oral-ham-sugg/oral-ham-sugg; Dairy, meats, potatos, oils and fats.
Quintozene=<.001; oral-mus-concl/skin-mus-
sugg/IARC-anim-pos/NCI bioassay-neg; Leafy veggies.
Sulfur=<.001; (Orthoflotox, Magnetic 6) No data
Chlorobenzilate=.006;
oral-rat-quest/oral-mus-concl/oral-mus-concl
IARC-anim-pos/NCI- mus-pos; Fruit.
Dicofol(r)=.002;
oral-mus-concl/oral-mus-concl/NCI-mus-pos; Leafy veggies, fruits.
HERBICIDES
Chlorpropham=.016; oral-mus-sugg/IARC indef;
Potatos.
OTHER
PCB’s(r)=.001; CONCLUSIVE HUMAN CARCINOGEN;
meats, fish?
Note: {1 ug/kg = 1 ppb}.(r) Reproductive and
endocrine disrupters as of 1995. Note how many
carcinogens are also endocrine disrupters suggesting a
mechanism for carcinogenesis. Endocrine receptors
probably deliver the toxins to the genes.
The American Diet
For an accounting of chemical pollution of the
American diet the reader is encouraged to consult Marcia
J. Gartell, et. al. (1985).
The authors discuss daily dietary intake of
pesticides, industrial chemicals, and the elements.
They list the following pesticides and chemicals
And toxic heavy metals.
The total package Gartell and co-workers
uncovered in the American diet included the following
pesticides and other chemicals:
alpha,beta, gamma, delta BHC(r);
captan, carbaryl, chlordane(r)(Linked to breast cancer), octachlor epoxide,
chlorobenzilate, 2-chloroethyl caprate, 2-chlorethyl
laurate, 2-chloroethyllinoleate, 2-chloroethyl
myristate, 2-chloroethyl palmitate,chlorpropham,
chlorpyrifos, DCPA, DDT(r), DDE, TDE, DEF,
Demeton-s-sulfone, diazinon, dichloran, dicofol(r),
dieldrin(r), dimethoate, endosulfan I(r), endosulfan
II(r), endosulfan sulfate, endrin, ethion,
2-ethylhexyl diphenyl phosphate, fenitrothion, fenthion,
fonofos, heptachlor(r) epoxide,
hexachlorobenzene,(r) leptophos, linuron, malathion(r),
methidathion, methoxychlor(r), nitrofen(r), trans
-nonachlor(r), parathion, parathion methyl,,
pentachloroanisole, pentachlorobenzene,
pentachlorobenzonitrile, pentachlorophenol(r), perthane,
o-phenylphenol, phosalone, polychlorinated biphenyls,
quintozene, pentachloroaniline, pentachlorothioanisole,
ronnel, tecnazene, tetrachloroaniline,
tetrachloroanisidine, tetrachloroanisole,
tetrachlorobenzene, tetrachlorothioanisole, toxaphene(r),
tri-n-butyl phosphate, vinclozolin(r), arsenic,
cadmium(r), lead(r), mercury(r), zinc.
[Note:(r)Endocrine and reproductive disrupters, 1995;
vinclozolin is an anti-androgen linked experimentally with
hermaphrodism]
The reader is encouraged to assess the
carcinogenicity of the American diet.
The source and the route of the breast
contamination is thus clear.
It is from contamination of the environment,
entering our bodies by food, domestic products, air and water.
McLeod said that all residues detected were
within the United Nations Food and Agriculture
Organization (FAO) and World Health Organization (WHO)
proposed acceptable daily intakes but what does
that mean.
Safe Levels or Not?
Does this mean that it is safe and nobody will be
affected? There are many assumptions for this to
be true worthy of examination.
There is an argument circulating around amongst
The proponents that thresholds exist and effects are
Dose dependent and if there is a sufficient safety
factor in the amount of contamination, that it will not have
any significant effect.
There are others that believe that a safe level
cannot be established for a carcinogen (Becker and
Coye, 1984-cites NIOSH and OSHA; Surgeon General
of the USA).
A sample of one corporate Scientist’s viewpoint
follows.
George Paget, Director of the Biomedical program
for Monsanto (Tim Padmore, Vancouver Sun, Sat.
June 20, 1981) expressed a view more common to
proponents of pesticides.
He is reported to have told the Canadian
Federation of Biological Societies that some people may die
From environmental pollution is a price society should
be willing to pay, and that people should just be told the
risk, and make their own decisions.
However, human data hasn’t been and probably will
never be collected on sufficient numbers of
chemicals and pesticides to fully corroborate either
detailed dose dependency for carcinogenicity or
threshold hypotheses for humans specifically for
each residue.
Greim et. al. (1981) reports his findings on the
relevance of high doses used in animal studies to
the question of human carcinogenicity.
He concluded that between species extrapolation
and high to low dose extrapolation of chemicals undergoing
metabolic activation and inactivation is most complicated.
Greim’s comments about inactivation and
activation and species differences suggests that a great deal of
detailed biochemical study is required, in the subjects
who will be exposed, before we can state with assurance, that
deactivating mechanisms exist in humans for any
particular chemical.
Are there individual differences in carcinogen
metabolizing and excretion mechanisms? Cytochrome
p-450 enzyme systems which do precisely that do
vary significantly between individuals (Davis, L.
1986). Genetic polymorphisms exist in genes that
govern capacity to metabolize environmental
contaminants (MS Wolff et. al. 1997). Predicting a
safe level for all is imossible because of this.
How then do we get this complex data, is the
technical, moral and ethical question raised, except
by making guinea pigs of us all?
Safe or Not? Cancer Incidence Change
Have cancers changed in incidence since the
chemical era really began?
Cancer deaths have doubled in Canada since the
turn of the century (Statistics Canada Report, 1983) but
some unkown proportion of this may be due to
longevity and improvements in detection.
In males all neoplasms increased from 1923 to
1973 according to J. Cartwright (1984).
In the USA, amongst males, cancer of the
bronchus, pancreas and leukemia increased during this
period.
Cancers in females decreased slightly during the
First period but began a gentle increase again.
Leukemia and bronchial cancers increased significantly during
this period.
Melanoma’s which have been increasing (Swerdlaw.
A. J. 1979), can be caused by solar radiation,
x-rays, or pesticide pollution (see epidemiology
below).
Non-Hodgkin’s lymphomas (NHL) (Smith, P.G. 1978)
and multiple myelomas (Cuzick, J. Unpublished
Data, cited in Cartwright, 1984) are also
increasing and these have strong pesticide links (see
epidemiology below).
Childhood malignancies varying worldwide are
Brain tumor, Ewing’s sarcoma, lymphomas and leukemias
(Munoz, N. 1976) so that it is possible and
prudent to conclude that they have an environmental component and
certainly have strong associations with pesticide studies
(see epidemiology below).
Others may show a similar pattern if studied
closely or may vary on a smaller geographical scale leading
to a similar interpretation.
To complicate epidemiological findings is the
fact that people may change their life-styles and
occupations several times in a lifetime, so that
while they may be at one risk, say from being
exposed to a cancer initiator chemical at the one job
or chemical use area, that they will be at a
significantly increased risk at one or more of the
other arenas of exposure to cancer promoters or
carcinogens which start the cancers developing.
Safe or Not? Variability in Susceptibility
One needs to consider that some people are more
vulnerable to cancer than others (Rawis, 1983) and
they may not need much exposure to carcinogens so
that if their carcinogensis has a pesticide
causality, prevention in these types of people would
require complete banning of the pesticide.
This might be especially true of people with
Genetic predisposition to cancer and those with weakened
immune systems from disease, physical or
psychosocial factors or those possibly contaminated with
immune suppressors like TCDD (Raloff, J. 1986),
PCB or DDT contamination which is widespread and
affects the immune systems of all animals studied,
or those affected by poor nutrition and
especially those with HIV.
Safe or Not? The Epidemiology Story
Epidemiological studies are very slow to shed
light on the matter of human carcinogenicity.
Conclusive epidemiological findings are extremely
difficult to obtain, especially for cancers that
normally have a low frequency of occurrence.
For example, for n-nitroso-diethylamine, there is
An enormous body of evidence that it is a conclusive
Carcinogen in numerous animal species when administered
numerous ways, and it is almost certainly a human
carcinogen; yet IARC lists it as `a Suspected Human
Carcinogen’.
A large number of carcinogenic chemicals lack
epidemiological data (see Cartwright, 1984, pg 32.)
and their recommendations always come after the
fact of significant exposure and if positive,
significant human mortality.
It is useful to review some of the studies and
see what is consistent and what is not. A brief
survey of the literature follows.
There is evidence from California that pesticide
use in the home can lead to increased leukemias in
children (Science News, 1988).
In an epidemiological study in Sweden,
testicular, endocrine, CNS and Hodgkins cancers were
increased (Wiklund, K. 1989).
E. A. Barthel (1986) in a retrospective cohort
study of the cancer incidence in pesticide-exposed
male pest control workers found elevated
standardized mortality ratios (SMR’s)of 133 for all
malignant neoplasms and high SMR’s for stomach (180),
esophagus (430)! and melanoma (588)! which was
anomalously high, and we are being told its the
sun.
A study on OC’s pesticides exposure in the human
body (Wang X.Q. et.al. 1988) provides strong
evidence of a correlation between beta-HCH and cancer
mortality. The accumulation levels of beta-HCH in
the populations studied were highly significantly
correlatedwith the mortality rates from liver
cancer, colon/rectum cancer, and lung cancer in
males as well as colon/rectum cancer in females (P< 0.01), suggesting that the effect of HCH on the above cancers should be studied further. C. Wesseling et. al. (1996) found the following standardized incidence ratios for four cancers among pesticide exposed banana workers: SIR were observed for melanoma (SIR = 197, 95% CI: 94-362) and penile cancer (SIR = 149, 95% CI: 55-324); among women for cervix cancer (SIR = 182, 95% CI: 1.22-241)and leukaemia (SIR = 274, 95% CI: 86-639). P. Torchio (1994) working in Italy found increasing risks for melanoma, eye cancer, connective tissue and lymphomas. M. C. Allavanja et.al. (1987) studied pesticide exposed grain mill workers and found elevated cancers of the lymphatic systems and the blood forming systems. In particular they found elevated lymphosarcoma and reticulum cell sarcoma, other neoplasms of lymphoid tissue (i.e., giant follicular lymphoma and other primary malignant neoplasms of lymphoid tissue), and multiple myeloma. L.F. Burmeister (1990) found elevated multiple myeloma in Iowa farmers. It appears that melanoma, cancers of the lymphatics, lymphomas, and lymphosarcomas, and blood, leukaemia, multiple myeloma are clearly most consistent. Other cancers are also implicated but not so consistently but this may be due to a different mix of pesticides in the study cohort exposure history. The variability inherent in exposure history, genetic diversity, geographical location, migratory patterns, dietary preferences, synergism potentials and local natural carcinogen interactions, means that finding a consistent dose dependent relationship using epidemiology is very difficult and in many cases probably impossible even if it exists. Thus all of the above findings may be in fact real effects of pesticides. Waiting for epidemiological conclusiveness may subject many people to exposure before a safe or unsafe verdict is reached. But what if an unsafe verdict is reached as is emerging for the blood and lymphoid cancers above? A lot of people have now died from this large International experiment which could have been prevented and more are dying every day. Safe or Not? Multiple Chemical Exposure Thus, the public at large are part of a large and increasing experiment, to see if they and their children can survive multiple chemical pollution into the future, and the children are, due to the relatively recent findings of new pesticides in total diet in Canada, via their Mother’s milk, at the front line of the experiment. One cannot help wondering what the increased Lifetime risk is from all of these contaminants combined, plus that which might result from the enormous number of combinations of interactions that are also possible. These are called synergy’s, multiplicative effects, a well known phenomenon used in pesticide formulations and called `potentiation’ by toxicologists -where several chemicals exhibit greatly increased toxicity when used in a mixture together. An analogous example that we are more familiar with is smoking and alcohol exposure (Selikoff, I. et. al. 1968; Selikoff, I., et. al. 1980). Pharmacologists and the general public are familiar with this phenomena as drug interactions and these can be fatal (Sternon J., Gilles C. 1996). The concept of safe levels are based on the experimental presence in test animals of only one pesticide or pollutant. In the real world there are hundreds known, probably thousands that are not yet assayed for in each living organism. Pesticides are capable of interaction with various entities, which include formulating agents, solvents and carriers, impurities in formulation, and isomeric forms of active ingredients (Iyanimura, T.T. 1990) and of course the same things in all other pesticides. It is thus not even logical or ethical to speak of safe levels when extrapolating from experimental trials of single pesticides due to the existence of multiple chemical exposures and potentiation, and endocrine and synergistic effects in the real world. Estimates of `safe levels’ based on single chemical exposure trials with animals therefore doesn’t accurately describe the real world for humans, either in number and types of chemicals, chemical carcinogenic mechanisms, or potential interactions multiplying impacts. Safe or Not? Pesticide & Pathogens Multiply Mortality and Pesticides may also make viral infections more serious. A common familiar example of a virus drug interaction magnifying impacts are Reye’s Syndrome in humans, where aspirin and flu in children can kill. Another example is hepatitus and liver carcinogens. M. Friend and D. O. Trainer (1970) found that young ducks exposed to PCB’s were more vulnerable to hepatitus virus. Crocker et. al. (July 6, 1974) found that mice given mixtures of the pesticides DDT and fenitrothion and injected with a sublethal encephalomyocarditis virus that normally doesn’t lead to much mortality had a greatly increased incidence of mortality (33-60%) than those given pesticides DDT (6-17%) singly or fenitrothin (4-9%) singly compared to viral infected controls which had no mortality. Fatty livers and kidneys were found and these mice died in paralysis and convulsions (epilepsy?). Crocker et. al. (1976) also reports that Canadian children exposed to DDT and fenitrothin had CNS and liver pathology symptoms [the same as in the mice]. Clearly, the immune system is compromised in some way by this interaction and support for this hypothesis comes from the work of P.R. McConnachie and A. C. Zahalsky (1991) who report that 38 humans exposed to pentachlorophenol, a wood preservative, had activated T-cells in females, autoimmunity, functional immunosuppression, and B-cell dysregulation. Other accounts of immune effects can be found in the literature. A. Betta et. al. (1989) reviewed published data and found that pesticide exposure is often associated with depressed humoral and cellular responses in mammals. The immunomodulating effects are affected by the route of administration and can also occur without general toxic effects, with a clear dose-effect correlation and for different dose levels. These findings hint at the possibility that people who are more vulnerable to infectious vectors may also be afflicted by simultaneous pesticide immunosuppression. Note also that this viral interaction effect makes the concept of safe levels of pesticide meaningless. The only safe level was none in the experiment. Pesticides’ Secret Companions; the Inerts There is another enormous source of unassayed residues including toxic chemicals, and that is from the secret inert igredients most pesticides are mixed with for field use. The inerts can form a larger part of the spray than the pesticide so the potential contamination is very high. I have revisited this issue recently with Joe Cole (Jyrkkänen J. A. & J. Cole, 1997) and have made the following findings reported in a story to the Globe and Mail. See also J. Jyrkkänen & J. Cole, (June 10) A Nation At Risk; Bravo Veterans Outlook (June/July 1997 Issue, pages 14, 60). “Active Agents Classified as Non-Active by the Canadian Government- ExtensiveToxicological Ramifications. Covert Use; Ramifications Toxic chemicals labeled as `non-active’ (inerts) in a lengthy { >=75 pages) federal pesticide
ingredients list, pose a hazard to unsuspecting users
and the environment.
It has been discovered by the Researchers from
the tables examination that a long list of active
and toxic ingredients are in covert use in Canada
without user knowledge and have the potential to
harm persons and the environment.
The list includes chemicals with long and exotic
names like, 2,4,6-Trichlorophenoxyacetic acid
(2,4,6-T), 2,4-Dichlorophenoxyacetic acid (2,4-D),
Benzene Formaldehyde, Chlorofluorocarbon 11 &
12, Chromium oxide, Dioxane(r), Nickel acetate ,
Polyoxyethylene amine (POEA), Polyvinyl
chloride(r), Toluene. Also present in the Canadian Inert
List are chemicals found in the USA EPA 1989 list
of Inerts of toxicological Significance that they
were aware of: 2-ethylhexyl phthalate(r), acrylic
copolymer possibly, asbestos fiber, benzene,
dichlorebenzene, dimethyl formamide, hexane,
isophorone, lead compounds, malachite green, methyl
chloride, methyl ethyl ketone, nonylphenol(r),
perchloroethylene, ethyelene glycol monethyl ether,
rhodamine B compounds, trichloroethylene.
These health effects may include: gender bending
and reduced fertility effects, neurotoxicity,
fetotoxicity, mutagenesis, carcinogenicity,
teratogenicity, tumor promotion, immunotoxicity, or
synergicity between these classes.
These ingredients or numerous similar products
are in use widely without public awareness because
they have been classified as non-active
ingredients and are therefore also Trade Secrets which are
not subject to public disclosure. The precise
heading on these ingredients is `Non-Actives in
Registered Products; Non-Active Names (Chemical or
Trade)’.
Another level of cover-up is nested within this
group as well since within Trade named products,
there can be many non-listed ingredients and
contaminants.
A detailed look at what peer reviewed published
studies have found about just a few of these
non-actives regarding cancer causing potential
follows;
(2,4,6-T), (closely related to
2,4,5-Trichorophenoxyacetic acid used in production of Agent
Orange). 2,4-6 T carcinogenicity was conclusive in rats
and mice in 4 studies, positive in NCI bioassay
and questionable in only 1 study.
(2,4-D), a known carcinogen, linked to NH
Lymphoma, soft tissue sarcoma, also used in agent
orange; 2,4-D has been found to have the following
contaminants contained within; octachlorobisfirone,
xanthen-9-ones, mono, di, tri, and tetradioxins
and probably furans, n-nitrosomethylamines and
n-nitrosodiethylamines, ortho and para
monochlorophenol isomers, (2,6-Di, 2,4,6 tri-) chloromethoxy
phenol isomers, n-nitrosodiethanolamine, 3
chlorophenoxymethanes. These contaminants are thus part
of the Non-Active package delivered and most are
toxic.
Benzene-a well studied cause of human leukemia.
Formaldehyde-human cancer initiator and probable
promoter. (CFC’s ) 11 & 12, now banned for use because of
their harmful effects on ozone but included in the
list.
Chromium oxide-closely related chromium dioxide
was found to be a conclusive carcinogen in rats in
two studies and suspected in another.
Dioxane-six conclusive carcinogenicity studies in
rats and mice, 2 positive findings and one
suggestive; discovered by J. Jyrkkänen and Dr. D.
Monroe in 1989 in Vision herbicide.
Nickel acetate-three conclusive cancer studies in
rats and mice.
(POEA)-a suspected human carcinogen. POE sorbitan
monooleate and sorbitan monolaureate have been
linked to human cancers of lung, skin, alimentary
tract and bladder.
(PVC’s)-human carcinogen which oxidizes in low
heat to dioxins.
Toluene-cancer promoter.
One can see readily from perusal of the
toxicology sample above that these substances are far
from non-active, and may in fact be highly
dangerous.
Inert ingredients are defined as: Non-Active
against the Targeted Pest, in Canada and the United
States. They are also called formulants and are part
of the other ingredients including contaminants.
Because of the potentially serious
harmful effects of these toxic chemicals, the consumer
has to wonder what the Canadian government has
been up to in the Health Protection Branch to allow
these dangerous chemicals to go unreported in
commercial and domestic products.
The ramifications for Canadian Federal liability
are enormous if these toxins are exported in
pesticide products or consumer goods and can be
linked to diseases in the end users.
There is also a serious jeopardy to Trade
relations with Green countries or States who presently
import Canadian goods.
The reason given to the lead investigator by one
official for classifying substances as Trade
Secrets was that proprietary information in
development would be disclosed to competitors. It now
appears that there was a more insidious purpose to
the Secrecy.”
Contaminants Add to Residue Burden
A good example is 2,4-D which has been found to
have the following contaminants contained within;
octachlorobisfirone, xanthen-9-ones, mono, di,
tri, and tetradioxins and probably furans,
n-nitrosomethylamines and n-nitrosodiethylamines, ortho
and para monochlorophenol isomers ,(2,6-Di, 2,4,6
tri-) chloromethoxy phenol isomers,
n-nitrosodiethanolamine, 3 chlorophenoxymethanes.
Pesticide contaminants are thus part of the
Non-Active (active in reality in the human body)
package delivered to the environment and most are
toxic.
Conclusion
This review has demonstrated the existence of
chemical carcinogens in Mother’s milk and that the
problem is widespread and that we are waging
chemical warfare against our own children.
* Epidemiology has been largely ineffective at
providing answers fast enough to keep pace with the
growing use and distribution of pesticides as
evidenced by the contamination with numerous
carcinogens and it exposed people to danger before
finding out if it is safe, and in many cases, unsafe.
* Evidence was brought forward that other
potentially carcinogenic substances might be present
that have not been disclosed or assayed for ie.
amongst the inerts, and contaminants.
* Unknown isomers and formulants may also be
present. There is the long list of anthropogenic
chemicals which N. Irving Sax (1981) and others like
The Merck Index, an Encyclopedia of Chemicals,
Drugs and Biologicals, list as potential human
exposure hazards.
* It appears that the concept of safe levels is
meaningless in the multichemical milieu that we
find ourselves due to interactions.
* There was evidence to suggest that the infant
and fetus are at greatest risk from exposure.
* Most of the contamination is through food,
though not all.
* Chlorinated organic pesticides have been found
in all diet samples and all food classes within
samples.
* What appears to be a distinct possibility from
the above world-wide data, is that there is
world-wide a large number of cancers induced by
these chemicals because of their known experimental
carcinogenicity and because of the enormous
numbers of infants being exposed in milk, and the many
years that they continue to be exposed through
the dietary intake throughout life. Supporting this
proposition are Erving J. Selikoff, MD. and E.
Cuyler Hammond, SC.D. (1979) who estimated that
from 75-85 % of cancers have an environmental
origin. These percentages are however hotly debated by
scientists working on risk models. However, most
of these ignore synergy, potentiation,
immunosuppression, individual susceptibility and the total
load.
* Regarding breast cancer; accepted risk factors
ie; unsaturated fat intake, socio-economic
status, obesity, etc., are implicated in less than half
of all cases…. halogenated hydrocarbons [to
which group many pesticides belong]–acting as
either co-carcinogens or promoting agents…. may play
a role in breast cancer risk; elevated levels of
polychlorinated biphenyls, bis
(4-chlorophenyl)-1,1 dichloroethene, and bis(4-chlorophenyl)-1,1,1
trichloroethane were found in fat samples from
women with cancer, suggesting a role for
environmentally derived suspect carcinogens in the genesis
of mammary carcinoma (Falck F. Jr et. Al. 1992).
Also, MS Wolff et. al. 1997, found studies
linking OC’s and DDT to breast cancer in four
different countries.
* Ramamoorthy K. et. al. (1997) found that
10(-4)M endosulfan caused a 2000 fold increase in
activity in the Beta Galactosidase reporter gene in
yeast which had estrogen receptor inserts,
suggesting that it is a steroid analogue. Estrogen
substitution therapy hs been linked to increased risk
of breast cancer. Endosulfan is part of the
Canadian and American diet, and is used on fruits and
vegetables. However, 10(-4)M is a very high
concentration.
* This review has focused primarily on
carcinogenicity.
* My review of epidemiology studies and cancer
trends has concluded that modern childhood cancers
are linked to pesticides and also the following
cancers in all age groups: melanoma, cancers of
the lymphatics, lymphomas, and lymphosarcomas, and
blood, leukaemia, are clearly most consistent and
multiple myeloma.
* Five percent of papers given this summer at a
Reproductive Symposium in Portland Oregon were
dedicated to chemical and pesticide toxicology
suggesting real concern by high level scientists for
the effects of these substances.
* This review has shown that the suspicion that
cancer causing pesticides found in the breast and
in its milk and probably also in utero, mostly
derived from food contaminated with residues,
probably causes significant increases in childhood
cancers, and later in adults as well due to time
lags before onset and continued ingestion of
residues from food. Other avenues of contamination are
probably minor except for those occupationally
exposed. Melanoma, blood cancers, sarcomas, and
lymphomas and multiple myeloma are clear contenders
for breast milk linked cancers.
* It saddens me to reach the conclusion, based on
this review of scientific evidence, that many
people have already died and many more are doomed
world-wide from these preventable cancers.
* The strong pesticide association of melanoma
and the widespread nature of its occurrence amongst
north temperate caucasians suggests an
interaction of solar radiation and chemical pollution as
causal, and it would be interesting to find out
what proportion is due to which venue in a
restrosective synergism study.
* The problem is of course an International one
because of
the export and import of food items, and varying
regulations and pesticide usage patterns between
countries (Table III) .
Table. III
Average (avg) Total Pesticide Residues in
Mother’s Milk From Around the World & Canada; (DATA in
ppb’s)
PESTICIDE COUNTRY/AVG RESIDUE
( avg(range)) (avg/(range) ( Yr))
ALDRIN; FRG=50 PPB.
1+/(1978/79)
DDT; Guatemala= 3100(410-12,200).
154+/(1967/68)
DIELDRIN; Lisbon Portugal= 18-31.
5+/(<1-60)(1967/68)
HCB; Melbourne=2-330.
2/1(<1-21)(1975)
HCH; Punjab=14-820.
1(1975)
BETA-HCH; Griefswald DDR=0-900.
<21(1975)
GAMMA-HCH; Spain=73.
<(1-35)(1967/8)
HEPTACHLOR AND HEPT. EPOXIDE; Spain=39.
OXYCHLORDANE AND CHLORD; USA<=20.
1
PCB; USA=50-4091.
MEDIAN=4(1979)
TRANS-NONACHLOR; USA=<10.
1(1975)
What Should We Do?
* This review supports the proposition that there
is enough evidence to conclude that action to
prevent chemical carcinogenesis is warranted and
prudent and could save many lives from disease,
keeping in mind the social costs of potentially
reduced quantity of foods.
* In North Termperate regions quanity of food is
not a problem so much as distribution and access
to food varying according to income level and
education. In the tropics, and in poor countries in
general, exposure through dermal and inhalation
routes due to ignorance and poverty are probably
higher.
* It concurs with and supports fully the alarm
sounded by WHO in 1987.
* If it is chosen to eliminate these carcinogens
from mother’s milk, this will require a
coordinated effort on the part of citizens and governments
amongst all trading partners.
* Organic gardening, biological pest control
offer solutions. Soils may actually increase in
quality through application of these procedures. IPM
however still uses suspected pesticides and
undisclosed inerts.
* Regulatory measures offer a means to reduce
exposure. Italy has already registered lower levels,
in Mother’s’ milk, of conclusive animal
carcinogens HCB, alpha-HCH, beta-HCH, lindane, DDE and DDT
due to tougher Italian and European restrictions
of 1982 (Dommarco, et al. 1987). So has Norway
(Brundtland, Gro, 1989). However, governments
cannot as we have seen all be trusted.
* Banning them at the source, along with toxic
inerts would be the only way to get rid of all
residues completely, but this would have to be by
international agreement. Governments will have to
come under scrutiny by independent auditors to
ensure they do not use toxic inerts.
There are those who will oppose tougher
legislation. They may argue that the exponential growth
of resistance to pesticides by pest species
(Georgia, G. 1981) argues for an increase in the number
of pesticides to deal with them, if that route of
control is not effectively replaced by
alternative methods.
* They may argue that agricultural production
requires pesticides.
* One cannot but wonder at what kind of milk
future generations of infants will be consuming if the
demonstrated trend continues.
* I believe strongly that strides to improve the
quality of our chemical environment will be made
by those that become aware of what is in our
environment, in Mother’s’ milk, because protection of
our children and the future of life itself is,
after all, a motherhood issue.
* What I have identified above hints strongly
that chemical exposure is the probable main cause of
breast cancer in most women. It seems highly
unlikely that such a collection of carcinogens
passing into and through the breast, cannot at some
point turn on that breast tissue itself and cause
cancerous transformation. One needs only a brief
look at how fats are turned into milk to realize
how intimately these lipophilic pesticides are
associated with crucial cellular metabolic pathways.
* In Israel, studies suggest that the dramatic
drop in breast cancer mortality rates is associated
with a ban on alpha-BHC and lindane (Westin J. B.
1993)(Linked to breast cancer). DDT was also present but had already been
banned, implying a causal connection at most or a
correlation at least for any or all of these
pesticides for breast cancer. They are a
different set of pesticides than those identified as
linked to breast cancer by Falck F. Jr. et. al. 1992,
who report an association of polychlorinated
biphenyls, bis (4-chlorophenyl)-1,1 dichloroethene,
and bis(4-chlorophenyl)-1,1,1 trichloroethane in
cancerous breast tissue. Clearly these seven
pesticides/contaminants need immediate attention.
* We must keep in mind that other effects may be
present as well; teratogenicity, fetotoxicity,
gender bending, fertility effects, neurotoxicity,
and immunotoxicity and a chemical role in cancer
promotion. There may also be behavioural effects.
* Some epilepsy may turn out to be linked to DDT
and or fenitrothion and viral infections since we
saw the mice die in siezures and children
similarly exposed had similar gross pathological
symptoms.
* Of these other effects, the greatest risk to
life and natural selection processes are those
affecting reproduction and the immune system. The
immune system is of course under assault from loss
of ozone as well, and so should have a great
amount of funding for research. Chemically
diminishing the effectiveness of the immune system will
make organisms more vulnerable to all manner of
diseases including cancer.
* Other species are often at greater risk than we
humans because they are more often exposed to the
direct toxicity as well as these side effects of
our pesticide use and many species are assaulted
from combined habitat loss, alienation, physical
and chemical alteration of their environment.
Footnote
When discussing this issue, I am often
confronted by anxious women who worry about continuing
breast feeding.
Everything in this article and my analysis cries
out; “Stop Breast Feeding!” However, we are in a
Catch .22. We are damned if we do and more damned
if we don’t, but for the infant, the chance to
get a normal immune system depends upon being
exposed to human milk.
This leaves us no choice except to conclude that
for practical purposes, benefits of limited
breast feeding might outweigh the harmful potential.
A poisoned immune system is better than no immune
system at all. The duration or length of time
spent breast feeding is the issue which does need
detailed examination until such time as we clean
up the pollution of Mother’s milk.
The infant needs human milk to prime the immune
system and to transfer antibodies when its own
are as yet undeveloped. Mother’s milk has human
specific fats and proteins vital to the infants
development. The child needs its Mother’s touch to
ensure normal physiological and psychological
development and the mother needs it too to bond
properly.
If one is still concerned about a potential
risk, then get tested although this is a worrisome
and expensive procedure, which would probably only
return what we already know.
Reducing life-time burden or exposure by eating
organic foods and washing foods thoroughly and by
peeling fruits, can help. Most importantly, lobby
for change in pesticide and inert management to
eliminate those that are capable of affecting the
health of humans and the environment.
Demand labels with full disclosure of active,
inert and contaminant ingredients on all products
used. Boycott serious polluters.
Do not stop early breast feeding unless you
have reason to believe that you are seriously
polluted. If seriously concerned still, reduce the time
spent breast feeding or find an unpolluted Wet
Nurse.
My personal bias is to go the above route while
eliminating carcinogens and those chemicals
affecting the endocrine systems and reproduction and
the immune system at their point of origin.
Health and Welfare Canada should also answer an
important question. Do Material Safety Data
Sheets (MSDS) have allowance for the toxicities of
the inert ingredients and contaminants and where
are these toxicity databases kept? I want a copy.
Also, whose idea was it to create the secret inert
database?
Literature Cited
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Dommarco, Roberto, Alphonso De Muccio, Ivano
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Falck F Jr, Ricci A Jr, Wolff MS, Godbold J,
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Fleming L, Mann JB, Bean J, Briggle T,
Sanchez-Ramos JR 1994 . Parkinson’s disease and brain
levels of organochlorine pesticides. Department of
Epidemiology and Public Health, University of Miami
School of Medicine, FL 33136. Ann
Neurol;36(1):100-103. July . [Epidemiological studies have
suggested an etiologic relationship between pesticide
exposure and Parkinson's disease (PD).
Organochlorine pesticides were assayed in postmortem brain
samples from 20 PD, 7 Alzheimer's disease (AD),
and 14 nonneurological control cases. The three
groups were similar in age at death, sex, and
demographic variables. Only two of 16 pesticide
residues screened were detected. A long-lasting residue
of DDT(pp-DDE) was found in the majority of cases
of PD and AD, as well as in all the control
cases; pp-DDT was significantly more likely to be
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(c) 1998 Jorma Jyrkkanen, All rights Reserved Return of the Fenni; [Original in Jyrkkänen Autobiography]
Since this study was updated, there has been a
major development in reporting of inerts. Many
companies are divulging the so called inert contents
probably to head off litigation down the road.
However, importantly, many are not. Contaminants remain
mostly undisclosed.
What it all means: Press Summary
1. We are being exposed globally to a
carcinogenic endocrine disrupting
chemical/pesticide soup which is not disclosed to
us and it is ending up in mothers milk and our
infants. It is composed of pesticides, other chemicals,
inerts which often are not inert, and contaminants all of which
which may have a variety of toxic effects, or not.
2. I have found an association between
carcinogenicity and endocrine dispruption. If a
pesticide or chemical is one, it is likely the
other, suggesting the mechanism for
carcinogenesis. Carcinogenicity may come about by
the same types of mechanisms as synthetic
estrogens is the suggestion.
3. This exposure has occurred for the most part without our
knowledge or permission but with the knowledge
and permission of the chemical companies and our
Governments top regulatory scientists who dismiss
it as too low to have an effect but who also go
along with covering up the more insidious
effects. I call it chemical rape.
4. They ignore multiple
chemical/pesticide-pathogen interaction multiplying
toxicity of pathogens and the fact that some of
these chemicals can harm the immune system and
the role this may have in cancer promotion
leading to frank carcinogenesis as well as the
different susceptibility of different people
depending on the state of their immune system,
as with AIDS patients. They ignore their own
experience that mixing multiple chemicals, i.e. our soup,
makes them more toxic, a process called potentiation.
5. They also ignore that cancer can be caused by
multiple mutations of a succession of genes as
has been demonstrated for colon cancer and that
all a pesticide or chemical needs to be is a
mutagen to lead inevitably to cancer with
successive incremental mutagenic exposures.
6. I demonstrate that there is no safe threshold
for carcinogens, only imposed assumed risks, and other
end points like effects on secondary sexual
expression are not even part of the Federal
regulatory considerations. There is a distinct
and high probability, based on my findings, that
gender alteration is occurring by this
pesticide/disruptor exposure and that the
variations in peoples genders in our contemporary
society are pathological chemical inductions.
7. Work with the master hormone
prostaglandin-f2-alpha shows that parts per
trillion of some hormones can have profound
influences on things like pregnancy, suggesting
that the potential exists for endocrine
disrupting chemicals to exert influences at
levels far below present consideration or even
comprehension and consistent with the exposure
levels I have found.
8. There is the profound question of the chemical
warfare agent found by Pellizzerri,
Crotonaldehyde and need for its explanation in
American samples of mothers milk.
9. My review raises huge questions about the
safety of breast feeding and the trade-offs
around priming the immune system versus harming
it, and the need for nurturing and bonding versus
the safety of the child. For example, should all
mothers get tested and limit breast feeding
depending on the results? It also raises huge
questions around pest management and the
trade-offs in saving lives by reducing
insect/plant pathogens and by increased food
production versus lives lost to chemical induced
mortalities and the difficulty of knowing where
to draw the line.
10. Our trust in the regulatory agencies and
their processes based on my findings is shattered
and we should demand an immediate explanation of
how this global contamination by carcinogenic
pesticides and chemicals was allowed to happen.
11. Finding a clean control group to estimate the
impacts is virtually impossible because of the
pervasiveness of the problem globally (Amazon?). The soup
acts differently in different people because each
one of us has a different sensitivity and a
different exposure history, so it is hard to
prove a particular carcinogensis by classical
scientific methods so that the regulatory
agencies and companies who approve and those who
manufacture these toxins have the almost perfect
crime, that is until I exposed their dirty secrets.
12. We have been poisoning our environment and it
has come home to roost, endangering our own and
our childrens lives and generations as yet unborn. It
proves that we are an intimate part of the ecosystem
of this fragile planet, and that we have to respect and
care for it like we do our own children.
13. These findings speak to us that the other species high
in the food chain are in great peril, but then we already
know that. From my study, we have another possible
explanation of why so many may be disappearing
from this Planet.
14. A great many mystery illnesses may have their explanation
in these findings.
Jorma Jyrkkanen
Researcher
Tags: carcingens, diet, gender benders, Jyrkkanen, mothers milk, pesticide
