• Due to length,
we are presenting this effect as a
separate section for PFOS and PFOA.
The study of the adverse effects of PFOS-PFOA chemicals is in
its infancy and we anticipate that more effects will be presented
and published over the next several years. Most of the animal
studies (as of early 2004) have been performed by the major producers
of PFOS-PFOA (3M and DuPont).
•
Click here to return to the same
section for fluorine & organofluorine pesticides.
•
This is not an exhaustive list. The
review of data was performed in 2003 to early 2004.
When time allows more information will be added,
"So far, five different pathways have been identified that
might explain how PFOA causes cancer and other types of toxicity.
These include mitochondrial toxicity; cell membrane disruption
that results in decreased cell communication; peroxisome proliferation;
increased levels of estrogen and decreased levels of testosterone;
and decreased thyroid hormone levels."
Ref: Environmental Working Group. 2003
report: PFCs:
a family of chemicals that contaminate the planet. Part 4: PFC
Health Concerns
... PFOS
is persistent, bioaccumulative and toxic to mammalian species.
There are species differences in the elimination
half-life of PFOS; the half-life is 100 days in rats, 200 days
in monkeys, and years in humans. The toxicity profile of
PFOS is similar among rats and monkeys. Repeated exposure results
in hepatotoxicity and mortality; the dose-response curve is very
steep for mortality. This occurs in animals of all ages, although
the neonate may be more sensitive. In addition, a 2-year bioassay
in rats has shown that exposure to PFOS results in hepatocellular
adenomas and thyroid follicular cell adenomas;
the hepatocellular adenomas do not appear to be related to peroxisome
proliferation. Further work to elucidate the species differences
in toxicokinetics and in the mode of action of PFOS will increase
our ability to predict risk to humans.
... The potential carcinogenicity of PFOS has been examined in
a dietary 2-year bioassay in Sprague-Dawley rats. There was a
significant increase in the incidence of hepatocellular adenomas
in males and females at the highest dose of 20 ppm; the females
at 20 ppm also had a significant increase in combined hepatocellular
adenomas and carcinomas. In addition, there was
a significant increase in thyroid follicular cell adenomas and
combined thyroid follicular cell adenomas and carcinomas in the
male recovery group at 20 ppm. There was no evidence of
peroxisome proliferation in the livers of the treated animals.
Ref:
November 21, 2002 report:
Hazard Assessment of Perfluorooctane sulfonate
(PFOS) and its salts.
Organisation
for Economic Co-operation and Development. ENV/JM/RD(2002)17/FINAL.
http://www.fluorideaction.org/pesticides/pfos.final.report.nov.2002.pdf
Abstract: The maternal
and developmental toxicities of perfluorooctane sulfonate (PFOS)
were evaluated in the rat and mouse. PFOS is an environmentally
persistent compound used as a surfactant and occurs as a degradation
product of both perfluorooctane sulfonyl fluoride and substituted
perfluorooctane sulfonamido components found in many commercial
and consumer applications. Pregnant Sprague-Dawley rats were given
1, 2, 3, 5, or 10 mg/kg PFOS daily by gavage from gestational
day (GD) 2 to GD 20; CD-1 mice were similarly treated with 1,
5, 10, 15 and 20 mg/kg PFOS from GD 1 to GD 17. Controls received
0.5% Tween-20 vehicle (1 ml/kg for rats and 10 ml/kg for mice).
Maternal weight gain, food and water consumption, and serum chemistry
were monitored. Rats were killed on GD 21, and mice on GD 18.
PFOS levels in maternal serum, maternal and fetal livers were
determined. Maternal weight gains in both species were suppressed
by PFOS in a dose-dependent manner, likely attributed to reduced
food and water intake. Serum PFOS levels increased with dosage,
and liver levels were approximately 4-fold
higher than serum. Serum thyroxine (T4)
and triiodothyronine (T3) in the PFOS-treated rat dams were significantly
reduced as early as one week after chemical exposure, although
no feedback response of thyroid-stimulating hormone (TSH) was
observed. A similar pattern of reduction
in T4 was also seen in the pregnant mice. Maternal serum
triglycerides were significantly reduced, particularly in the
high dose groups, although cholesterol levels were not affected.
In the mouse dams, PFOS produced a marked enlargement of the liver
at 10 mg/kg and higher dosages. In the rat fetuses, PFOS was detected
in the liver, but at levels nearly half of those in the maternal
counterparts, regardless of administered doses. In both
rodent species, PFOS did not alter the numbers of implantations
or live fetuses at term, although small deficits in fetal weight
were noted in the rat. A host of birth defects
including cleft palate, anasarca, ventricular septal defect, and
enlargement of the right atrium were seen in both rats and mice,
primarily in the 10 and 20 mg/kg dosage groups, respectively.
Our results demonstrate both maternal and developmental toxicity
of PFOS in the rat and mouse.
Ref: Toxicol Sci 2003 May 28; Exposure
to Perfluorooctane Sulfonate During Pregnancy in Rat and Mouse.
I. Maternal and Prenatal Evaluations; by Thibodeaux JR, Hanson
RG, Rogers JM, Grey BE, Barbee BD, Richards JH, Butenhoff JL,
Stevenson LA, Lau C. Reproductive Toxicology
Division, National Health and Environmental Effects Research Laboratory,
Office of Research and Development, U.S. Environmental Protection
Agency, Research Triangle Park, North Carolina 27711, USA.
*
Note from FAN:
Triiodothyronine
- thyroid hormone similar to thyroxine but with one less iodine
atom per molecule and produced in smaller quantity; exerts the
same biological effects as thyroxine but is more potent and
briefer.
Ref: http://www.thefreedictionary.com/triiodothyronine
Abstract: The postnatal
effects of in utero exposure to perfluorooctane sulfonate (PFOS)
were evaluated in the rat and mouse. Pregnant Sprague-Dawley rats
were given 1, 2, 3, 5, or 10 mg/kg PFOS daily by gavage from gestation
day (GD) 2 to GD 21; pregnant CD-1 mice were treated with 1, 5,
10, 15 and 20 mg/kg PFOS from GD 1 to GD 18. Controls received
0.5% Tween-20 vehicle (1 ml/kg for rats and 10 ml/kg for mice).
At parturition, newborns were observed for clinical signs and
survival. All animals were born alive and initially appeared to
be active. In the highest dosage groups (10 mg/kg for rat and
20 mg/kg for mouse), the neonates became pale, inactive and moribund
within 30-60 min, and all died soon afterward. In the 5 mg/kg
(rat) and 15 mg/kg (mouse) dose groups, the neonates also became
moribund but survived for a longer period of time (8-12 h). Over
95% of these animals died within 24 hr. Approximately 50% of offspring
died at 3 mg/kg for rat and 10 mg/kg for mouse. Cross-fostering
the PFOS-exposed rat neonates (5 mg/kg) to control nursing dams
failed to improve survival. Serum concentrations of PFOS in newborn
rats mirrored the maternal administered dosage and were similar
to those in the maternal circulation at GD 21; PFOS levels in
the surviving neonates declined in the ensuing days. Small but
significant and persistent growth lags were detected in surviving
rat and mouse pups exposed to PFOS prenatally, and slight delays
in eye-opening were noted. Significant increases in liver weight
were observed in the PFOS-exposed mouse pups. Serum
thyroxine levels were suppressed in the PFOS-treated rat pups,
although triiodothyronine and TSH levels were not altered. Choline
acetyltransferase activity (an enzyme that is sensitive to thyroid
status) in the prefrontal cortex of rat pups exposed to PFOS prenatally
was slightly reduced, but activity in the hippocampus was
not affected. Development of learning, determined by T-maze delayed
alternation in weanling rats, was not affected by PFOS exposure.
These results indicate that in utero exposure to PFOS severely
compromised postnatal survival of neonatal rats and mice, and
caused delays in growth and development
that were accompanied by hypothyroxinemia in the surviving rat
pups.
Ref:
Toxicol Sci 2003 May 28. Exposure
to Perfluorooctane Sulfonate During Pregnancy in Rat and Mouse.
II. Postnatal Evaluation; by Lau C, Thibodeaux JR, Hanson
RG, Rogers JM, Grey BE, Stanton ME, Butenhoff JL, Stevenson LA.