By: Christy Fischer
Erin Mascarenas
Sadie Yurista
Introduction
Plastics
• have been around since the mid 1800s
•
are in everything from cosmetics to medical equipment
•
are known to have toxic components such as bisphenol A
(BPA) and di(2-ethylhexyl) phthalate (DEHP) that are
capable of leaching out
Because plastics are so prevalent in our lives, the
environmental and health implications should be further
investigated
Take a moment and think…
How many times a day do you, your food,
or drink come in contact with plastics?
Here’s just a few ways!
History- Timeline
1839
1863 1872
Beginning of
Plastic Era
1891 1908
PVC first
created
Celluloid
developed to
replace ivory
for billiard
balls
1926
Cellophane
developed
BPA first
synthesized
Plasticized
PVC (Vinyl)
1953
1970
Saran Wrap
introduced
Thermoplastic
Polyester
(Mylar)
Commonly-Used Plastic
Components
 BPA and DEHP are found in polyvinyl chloride
(PVC) and polycarbonate plastics
 BPA is an organic building block of several
plastics including type 3 and 7 plastics.
 DEHP is a common organic additive used to
impart plasticity (fluidity) to materials such as
plastic.
BPA and DEHP
Production
• BPA is prepared by the condensation of acetone with
phenol, catalyzed by an acid, such as hydrochloric
acid.
• DEHP is created by the reaction of phthalic
anhydride with 2-ethylhexanol
Other Plasticizers
• Though BPA and DEHP have been well-studied,
other plasticizers are now being used
BPA and DEHP Uses
BPA has been used in:
• Coating of food cans, baby bottles, food containers,
water bottles, dental sealants, toys, makeup, lotion,
shampoo
DEHP has been used in:
• IV tubing and bags, blood-storage bags, medical
devices, PVC gloves, garden hoses, food packaging,
toys, paints, adhesives, floor and wall coverings
BPA ADAME
Absorption
•
Ingestion, inhalation, dermal contact
Distribution
• Depends on point of origin, circulated
throughout body by circulatory system
Action
• BPA mimics estradiol – endocrine disruptor
• Disrupts differentiation of androgen-dependant tissues
• Causes failures in cleavage plane determination and cytokinesis due
to disruption of microtubule formation (SEE LINK to sea urchin
development, Control (without BPA):
http://www.youtube.com/watch?v=nrJcQCTvuh4
with BPA: http://www.youtube.com/watch?v=RJ0uGeMxgX0
•
BPA has an oral LD50 of 3250 mg/kg in rats
BPA ADAME (continued)
Metabolism
 BPA has an oral LD50 of 3250 mg/kg in rats
 BPA conjugated with glucuronic acid to form
glucuronide
 Nearly entire oral dose metabolized during first pass
Excretion
 Glucuronide completely excreted via urine within 24
hours
DEHP ADAME
Absorption
 Ingestion, inhalation, dermal contact
Distribution
 Depends on point of origin, circulated throughout
body by circulatory system
Action
 Peroxisome proliferation
 Inhibits fetal testicular testosterone production
DEHP ADAME (continued)
Metabolism
 DEHP hydrolyzes to mono-ethylhexyl phthalate and
then to phthalate salts. The released alcohol is
susceptible to oxidation to aldehyde and carboxylic
acid.
Excretion
 90% of metabolites excreted in urine
 10% of metabolites excreted in feces
 One-time dose no longer in plasma after 24 hours,
70% excreted from body by that time
Studies on BPA
 Induces fibroblast differentiation into adipocytes in vitro
 Developmental toxicity, carcinogenic effects, and possible
neurotoxicity at low doses in animal models
 Linked to obesity by triggering fat-cell activity and
produces precursors of breast cancer
 Interferes with chemotherapeutic agents in breast cancer
cells
 Studies by the Centers for Disease Control and
Prevention found BPA in the urine of 93% of children
and adults tested in 2003–04.
Studies on BPA (continued)
 Infants fed with liquid formula are among the most
exposed and those fed from polycarbonate bottles can
consume up to 13 μg/kg/day of BPA. Some animal studies
show effects at much lower doses.
 The U.S. Environmental Protection Agency considers
exposures up to 50 µg/kg/day to be safe.
 Some research methods and funding sources have been
criticized: some involved injecting BPA directly into
animals and some were funded by plastic manufacturers.
BPA Health Implications
 Low doses of BPA can mimic the body's hormones, possibly
causing negative health effects. Long term low dose
exposure to BPA may induce chronic toxicity in humans.
 High BPA levels were significantly associated with heart
disease, diabetes, and abnormally high levels of certain
liver enzymes.
 Can promote breast-cancer cell growth
 High exposure may be associated with recurrent
miscarriage
Control
2.2 µM BPA
Studies on DEHP
 Hepatotoxic at 300 mg/kg in rodents
 Metabolites produced by soil microbes are more toxic
than the original substance
 Brief oral exposure to high levels caused sperm
damage in mice
 Reduces testicular testosterone levels in fetal and
neonatal male rats
 Humans may be affected by lower levels than study
animals
DEHP Health Implications
 Decreased motility of sperm was noted in men
exposed to phthalates
 Exposure to phthalates resulted in increased birth
weights and longer gestation periods
 May be carcinogenic
 May be linked to kidney damage
Environmental Impacts
The abundance of plasticizers has lead to their and the
presence of their metabolites in the environment,
sometimes in high concentrations
•Many plastics end up in landfills
•Degradation/chemical release
-soil micro-organisms degrade plasticizers
-these metabolites can be more toxic than
original and resist further biodegradation
•Chemicals can seep into water supplies, which effects all
biological life to some degree
Conclusion
 More studies should be conducted as to the long-term
effects of BPA, DEHP, and other plastic compounds on
health and the environment
 Avoid microwaving food in plastic containers, putting
plastics in the dishwasher, using harsh detergents, and
avoid storing containers above room temperature to
minimize leaching
 Recycling reduces the amount of plastic that the
environment is exposed to and protects our water
Refrences







Barnabe, S., Beauchesne, I., Cooper, D.G., Nicell, J.A. 2008. Plasticizers and their degradation
products in the process streams of a large urban physicochemical sewage treatment plant. Water
Research. 42: 153-162.
Bellis, M. The history of plastics: time line of plastics. [Internet]. 2009 April [cited 2009 April 25].
Available from http://inventors.about.com/od/pstartinventions/a/plastics.htm
Biello, D. 2008. Plastic (not) fantastic: Food containers leach a potentially harmful chemical.
Scientific American. Available from http://www.sciam.com/article.cfm?id=plastic-not-fantastic-withbisphenol-a
Cao, X., Corriveau, J. 2008. Survey of bisphenol A in bottled water products in Canada. Food Additives
and Contaminants: Part B. 1: 161-164.
George, O., Bryant, B.K., Chinnasamy, R., Corona, C., Arterburn, J.B., Shuster, C.B. 2007. Bisphenol A
Directly Targets Tubulin to Disrupt Spindle Organization in Embryotic and Somatic Cells [Internet].
ACS Chemical Biology [cited 2009 April 25]. Available from http://www.acschemicalbiology.org.
Ghisari, M., Bonefeld-Jorgensen, E.C. 2008. Effects of Plasticizers and phenols on estrogen and
thyroid hormone function. Toxicology Letters. 1805: S104.
Gray, L.E., Ostby, J., Furr, J., Price, M., Veeramachaneni, D.N.R., Parks, L. 2000. Perinatal Exposure to
the Phthalates DEHP, BBP, and DINP, but Not DEP, DMP, or DOTP, Alters Sexual Differentiation of
the Male Rat. Toxicological Sciences. 58: 350-365.
References (continued)






Huber, W.W., Grasl-kraupp, B., Schulte-hermann, R. 1996. Hepatocarcinogenic potential of di(2Ethylhexyl)phthalate in rodents and its implications on human risk. Critical Reviews in Toxicology.
26(4):365-481.
Integrated Risk Information Stystem. Bisphenol A. (CASRN 80-05-7). [Internet]. Washington (DC):
United States Environmental Protection Agency; 2008 Jan [cited 2009 April 25]. Available from
http://www.epa.gov/iris/subst/0356.htm
LaPensee, E.W., Tuttle, T.R., Fox, S.R., Ben-Jonathan, N. 2009. Bisphenol A at low Nanomolar Doses
Confers Chemoresistance in Estrogen Receptor-α-Positive and –Negative Breast Cancer Cells.
Environmental Health Perspectives. 117: 175-180.
Masuno H, Kidani T, Sekiya K, Sakayama K, Shiosaka T, Yamamoto H, et al. 2002. Bisphenol A in
combination with insulin can accelerate the conversion of 3T3-L1 fibroblasts to adipocytes. J. Lipid.
Res. 43(5): 676–684.
National report on human exposure to environmental chemicals - Spotlight on bisphenol A.
[Internet]. Atlanta (GA): Centers for Disease Control and Prevention; 2008 May [cited 2009 April 25].
2 p. Available from http://www.cdc.gov/exposurereport/pdf/factsheet_bisphenol.pdf
National Toxicology Program. Bisphenol A (BPA). [Internet]. Research Triangle Park (NC): United
States Department of Health and Human Servies– National Institutes of Health; 2008 September
[cited 2009 April 25]. 2 p. Available from http://www.niehs.nih.gov/health/docs/bpa-factsheet.pdf
References (continued)
 Peck, C.C., Albrot, P.W. 1982. Toxic potential of the plasticizer di(2-ethylhexyl) phthalate in
the context of its disposition and metabolism in primates and man. Environmental Health
Perspectives. 45:11-17.
 Polydorou, O., Konig, A., Hellwig, E., Kummerer, K. 2009. Long-term release of monomers
from modern dental-composite materials. European Journal of Oral Sciences. 117: 68-75.
 Satoh, K., Nonaka, R., Ohyama, K., Nagai, F., Ogata, A., Iida, M. 2008. Endocrine Disruptive
Effects of Chemicals Eluted from Nitrile-Butadiene Rubber Gloves Using Reporter Gene Assay
Systems. Biol. Pharm. Bulletin. 31: 375-379.
 Steinmetz, R., Brown, N.G, Allen, D.L., Bigsby, R.M., Ben-Jonathan, N. 1997. The
Environmental Estrogen Bisphenol A Stimulates Prolactin Release in Vitro and in Vivo.
Endocrinology. 138, 5;1780-1786.




Sugiura-Ogasawara, M., Ozaki, Y., Sonta, S., Makino, T., Suzumori, K. 2005. Exposure to bisphenol A
is associated with recurrent miscarriage. Hum. Reprod. 20(8): 2325-2329.
Trasande, L., Cronk, C., Durkin, M., Weiss, M., Schoeller, D. A., Gall, E. A., Hewitt, J.B., Carrel, A. L.,
Landrigan, J., Gillman, M. W. 2009. Environment and Obesity in the National Children’s Study.
Environmental Health Perspectives. 117: 159-166.
Völkel, W., Colnot, T., Csanády, G.A., Filser, J.G., Dekant, W. 2002. Metabolism and kinetics of
bisphenol A in humans at low doses following oral administration. Chem. Res. Toxicol. 15(10): 12811287.
Wolff, M.S., Engel, S.M., Berkowitz, G.S., Ye, X., Silva, M.J., Zhu, C., et al. 2008. Prenatal phenol and
phthalate exposures and birth outcomes. Environmental Health Perspectives. 116: 1092–1097.