• 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.
Abstract excerpt: "... We conclude that exposure to PFOS
late in gestation is sufficient to induce 100% pup mortality and
that inhibition of lung maturation may be
involved."
Ref: 2003. Birth Defects Res Part B Dev
Reprod Toxicol. Dec;68(6):465-71. Prenatal
window of susceptibility to perfluorooctane sulfonate-induced
neonatal mortality in the Sprague-Dawley rat; by Grasty RC,
Grey BE, Lau CS, Rogers JM.
Abstract: The critical
period for increased neonatal mortality induced by perfluorooctane
sulfonate (PFOS) exposure was evaluated in the rat. Timed-pregnant
Sprague-Dawley rats were treated by oral gavage with 25 mg/kg/d
PFOS/K(+) on four consecutive days (gestation days (GD) 2-5, 6-9,
10-13, 14-17, or 17-20) or with 0, 25, or 50 mg/kg/d PFOS/K(+)
on GD 19-20. Controls received vehicle (10 ml/kg 0.5% Tween-20)
on these days. Maternal weight gain was reduced in treated animals
during dosing, as were food and water consumption. Following a
4-day treatment, litter size at birth was unaffected while pup
weight was similarly reduced in the three earliest PFOS groups.
All PFOS groups experienced decreases in survival while controls
remained near 100%. Neonatal survival decreased in groups dosed
later during gestation, approaching 100% with dosing on GD 17-20.
Most deaths occurred before postnatal day (PND) 4, with the majority
in the first 24 hours. Maternal serum PFOS levels on GD 21 were
higher in groups exhibiting higher mortality. Following a 2-day
treatment, PFOS groups experienced significant pup mortality by
PND 1. Neonatal mortality continued through PND 5, when survival
was 98, 66, and 3% for the 0, 25, and 50 mg/kg groups, respectively.
Pup weight was reduced in treated groups with surviving litters.
Gross dissection and histological examination
of lungs revealed differences in maturation between control and
treated animals on PND 0. We conclude
that exposure to PFOS late in gestation is sufficient to induce
100% pup mortality and that inhibition of lung maturation may
be involved.
Ref: Birth Defects Res Part B Dev Reprod
Toxicol. 2003 Dec;68(6):465-71. Prenatal
window of susceptibility to perfluorooctane sulfonate-induced
neonatal mortality in the Sprague-Dawley rat; by Grasty RC,
Grey BE, Lau CS, Rogers JM.
In
the second study, Goldenthal et al. (1978a) administered rhesus
monkeys, 2/sex/group,
doses of 0, 0.5, 1.5 or 4.5 rng/kg/day PFOS (FC-95) in distilled
water by gavage for 90 days... All monkeys in the 4.5 mg/kg/day
group died or were sacrificed in extremis between week 5 and 7
of the study. Beginning on the first or second day of the study,
these monkeys exhibited signs of gastrointestinal tract toxicity
including anorexia, emesis, black stool and dehydration. All of
the monkeys had decreased activity and just prior to death showed
marked to severe rigidity, convulsions, generalized body trembling
and prostration... Two males and one female had moderate diffuse
atrophy of the serous alveolar cells characterized by decreased
cell size and loss of cytoplasmic granules.
Ref:
Sulfornated Perfluorochemicals
in the Environment: Sources, Dispersion, Fate and Effects.
Prepared by 3M. March 1,2000.
Ylinen et al.(1990) studied the difference between male and female
Wistar rats in the
distribution and accumulation of PFOA after single and subchronic
administration. For the single
dose study, 50 mg/kg of PFOA was administered by ip injection
to groups of 20 male and 20
female 10 week old rats. For the subchronic study, PFOA was administered
by gavage at doses
of 3, 10, and 30 mg/kg/day to groups of 18 male and 18 female
newly weaned rats. For both studies, samples were collected for
determination of PFOA levels 12 hr after treatment, at 24-168
hr at 24 hr intervals, at 244 hr and at 336 hrs after treatment.
For the subchronic study,
samples were also taken on Day 28. ... In the single-dose study,
concentrations of PFOA in the serum and tissues were higher in
males than females at all time periods.Twelve hours after the
administration of PFOA about 10% of the administered dose was
found in the serum of females, whereas about 40%of the administered
dose was in the serum of males. ...
Samples taken on the 28th day indicated significantly higher PFOA
concentrations in the serum and tissues of males versus females
at all three dose levels. After subchronic, as well as single-
dose administration, PFOA was mainly distributed in the serum
of rats. High concentrations of PFOA were also found in the liver,
kidney, and lung of males and females.
...
A significant positive correlation existed between the administered
dose and the concentration of PFOA in the liver, kidney, spleen,
and lung of females. On the contrary,
no significant correlation between the administered dose and the
concentration of PFOA was observed in the males, as 10 mg/kg/day
produced higher PFOA concentrations in the serum and organs than
30 mg/kg/day. However, in males ,the concentration in the spleen,
testis, and brain correlated positively with the concentration
in the serum.
Ref:
April
10, 2003: Preliminary
Risk Assessment of the Developmental Toxicity associated with
Exposure to Perfluorooctanoic Acid and its Salts. US
EPA Office of Pollution Prevention and Toxics. 63 pages.