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General chemical structure of phthalates. R and R' = CnH2n+1; n = 4-15

Phthalates, or phthalate esters, are esters of phthalic acid and are mainly used as plasticizers (substances added to plastics to increase their flexibility, transparency, durability, and longevity). They are primarily used to soften polyvinyl chloride. Phthalates are being phased out of many products in the United States and European Union over health concerns.



Phthalates are used in a large variety of products, from enteric coatings of pharmaceutical pills and nutritional supplements to viscosity control agents, gelling agents, film formers, stabilizers, dispersants, lubricants, binders, emulsifying agents, and suspending agents. End applications include adhesives and glues, agricultural adjuvants, building materials, personal care products, medical devices, detergents and surfactants, packaging, children's toys, modelling clay, waxes, paints, printing inks and coatings, pharmaceuticals, food products, and textiles. Phthalates are also frequently used in soft plastic fishing lures, caulk, paint pigments, and sex toys made of so-called "jelly rubber." Phthalates are used in a variety of household applications such as shower curtains, vinyl upholstery, adhesives, floor tiles, food containers and wrappers, and cleaning materials. Personal care items containing phthalates include perfume, eye shadow, moisturizer, nail polish, liquid soap, and hair spray.[1] They are also found in modern electronics and medical applications such as catheters and blood transfusion devices. The most widely-used phthalates are the di-2-ethyl hexyl phthalate (DEHP), the diisodecyl phthalate (DIDP) and the diisononyl phthalate (DINP). DEHP is the dominant plasticizer used in PVC due to its low cost. Benzylbutylphthalate (BBP) is used in the manufacture of foamed PVC, which is mostly used as a flooring material. Phthalates with small R and R' groups are used as solvents in perfumes and pesticides.

As of 2004 manufacturers produced about 363 thousand metric tonnes (800 million pounds or 400 000 short tons) of phthalates each year. They contribute 10-60% of plastic products by weight.[1]


The development of cellulose nitrate in 1846 led to castor oil being patented in 1856 for use as the first plasticizer. In 1870 camphor became the more favored plasticizer for cellulose nitrate. Phthalates were first introduced in the 1920s and quickly replaced the volatile and odorous camphor. In 1931 the commercial availability of polyvinyl chloride and the development of di-2-ethylhexyl phthalate began the boom of the plasticizer PVC industry.


Phthalate esters are the dialkyl or alkyl aryl esters of phthalic acid (also called 1,2-benzenedicarboxylic acid, not be confused with the isomeric terephthalic or isophthalic acids ); the name phthalate derives from phthalic acid, which itself is derived from word "naphthalene". When added to plastics, phthalates allow the long polyvinyl molecules to slide against one another. The phthalates have a clear syrupy liquid consistency and show low water solubility, high oil solubility, and low volatility. The polar carboxyl group contributes little to the physical properties of the phthalates, except when R and R' are very small (such as ethyl or methyl groups).[citation needed] They are colorless, odorless liquids produced by reacting phthalic anhydride with an appropriate alcohol (usually 6 to 13 carbon).

Table of the most common phthalates

Name Acronym Structural formula CAS No.
Dimethyl phthalate DMP C6H4(COOCH3)2 131-11-3
Diethyl phthalate DEP C6H4(COOC2H5)2 84-66-2
Diallyl phthalate DAP C6H4(COOCH2CH=CH2)2 131-17-9
Di-n-propyl phthalate DPP C6H4[COO(CH2)2CH3]2 131-16-8
Di-n-butyl phthalate DBP C6H4[COO(CH2)3CH3]2 84-74-2
Diisobutyl phthalate DIBP C6H4[COOCH2CH(CH3)2]2 84-69-5
Butyl cyclohexyl phthalate BCP CH3(CH2)3OOCC6H4COOC6H11 84-64-0
Di-n-pentyl phthalate DNPP C6H4[COO(CH2)4CH3]2 131-18-0
Dicyclohexyl phthalate DCP C6H4[COOC6H11]2 84-61-7
Butyl benzyl phthalate BBP CH3(CH2)3OOCC6H4COOCH2C6H5 85-68-7
Di-n-hexyl phthalate DNHP C6H4[COO(CH2)5CH3]2 84-75-3
Diisohexyl phthalate DIHxP C6H4[COO(CH2)3CH(CH3)2]2 146-50-9
Diisoheptyl phthalate DIHpP C6H4[COO(CH2)4CH(CH3)2]2 41451-28-9
Butyl decyl phthalate BDP CH3(CH2)3OOCC6H4COO(CH2)9CH3 89-19-0
Di(2-ethylhexyl) phthalate DEHP, DOP C6H4[COOCH2CH(C2H5)(CH2)3CH3]2 117-81-7
Di(n-octyl) phthalate DNOP C6H4[COO(CH2)7CH3]2 117-84-0
Diisooctyl phthalate DIOP C6H4[COO(CH2)5CH(CH3)2]2 27554-26-3
n-Octyl n-decyl phthalate ODP CH3(CH2)7OOCC6H4COO(CH2)9CH3 119-07-3
Diisononyl phthalate DINP C6H4[COO(CH2)6CH(CH3)2]2 28553-12-0
Diisodecyl phthalate DIDP C6H4[COO(CH2)7CH(CH3)2]2 26761-40-0
Diundecyl phthalate DUP C6H4[COO(CH2)10CH3]2 3648-20-2
Diisoundecyl phthalate DIUP C6H4[COO(CH2)8CH(CH3)2]2 85507-79-5
Ditridecyl phthalate DTDP C6H4[COO(CH2)12CH3]2 119-06-2
Diisotridecyl phthalate DIUP C6H4[COO(CH2)10CH(CH3)2]2 68515-47-9

Health effects


Phthalates are easily released into the environment because there is no covalent bond between the phthalates and plastics in which they are mixed. As plastics age and break down the release of phthalates accelerates. Phthalates in the environment are subject to biodegradation, photodegradation, and anaerobic degradation and, therefore, they do not generally persist in the outdoor environment. Outdoor air concentrations are higher in urban and suburban areas than in rural and remote areas.[1]

Indoor air concentrations are generally higher than outdoor air concentrations due to the nature of the sources. Because of their volatility, DEP and DMP are present in higher concentrations in air in comparison with the heavier and less volatile DEHP. Higher air temperatures result in higher concentrations of phthalates in the air. PVC flooring leads to higher concentrations of BBP and DEHP which are more prevalent in dust.[1]

People are commonly exposed to phthalates, and most Americans tested by the Centers for Disease Control and Prevention have metabolites of multiple phthalates in their urine. Because phthalate plasticizers are not chemically bound to PVC they can easily leach and evaporate into food or the atmosphere. Phthalate exposure can be through direct use or indirectly through leaching and general environmental contamination. Diet is believed to be the main source of DEHP and other phthalates in the general population. Fatty foods such as milk, butter, and meats are a major source. Low molecular weight phthalates such as DEP, DBP, BBzP may be dermally absorbed. Inhalational exposure is also significant with the more volatile phthalates.[2]

In a 2008 Bulgarian study higher dust concentrations of DEHP were found in homes of children with asthma and allergies, compared with healthy children's homes.[3] The author of the study stated, "The concentration of DEHP was found to be significantly associated with wheezing in the last 12 months as reported by the parents."[3] Phthalates were found in almost every sampled home in Bulgaria. The same study found that DEHP, BBzP, and DnOP were in significantly higher concentrations in dust samples collected in homes where polishing agents were used. Data on flooring materials was collected but there was not a significant difference in concentrations between homes where no polish was used that have balatum (PVC or linoleum) flooring verses homes with wood. High frequency of dusting did decrease the concentration.[3]

Children's exposure to phthalates generally is greater than adults. In a 1990's Canadian study that modelled ambient exposures it was estimated that daily exposure to DEHP was "9mcg/kg bodyweight/day in infants, 19 mcg/kg bodyweight/day in toddlers, 14 mcg/kg bodyweight/day in children, and 6 mcg/kg bodyweight/day in adults.[2] Infants and toddlers are at the greatest risk of exposure due to their mouthing behavior. Body care products containing phthalates are a source of exposure for infants. The authors of a 2008 study "observed that reported use of infant lotion, infant powder, and infant shampoo were associated with increased infant urine concentrations of [phthalate metabolites], and this association is strongest in younger infants. These findings suggest that dermal exposures may contribute significantly to phthalate body burden in this population." Though they did not examine health outcomes, they noted that "Young infants are more vulnerable to the potential adverse effects of phthalates given their increased dosage per unit body surface area, metabolic capabilities, and developing endocrine and reproductive systems."[4]

In 2008 the Danish Environmental Protection Agency (EPA) found a variety of phthalates in erasers and warned of health risks when children regularly suck and chew on them. The European Commission Scientific Committee on Health and Environmental Risks (SCHER), however, considers that, even in the case when children bite off pieces from erasers and swallow them, it is unlikely that this exposure leads to health consequences.[5]

Phthalates are also found in medications, where they are used as inactive ingredients in producing enteric coatings. It's not known how many medications are made using phthalates, but some include omeprazole, didanosine, mesalamine, and theophylline. A recent study found that urinary concentrations of monobutyl phthalate, the DBP metabolite, of mesalamine users was 50 times higher than the mean of nonusers (some formulations of mesalamine do not contain phthalates).[6] The study showed that exposures from phthalate containing medications can far exceed population levels from other sources.[6] DBP in medications raises concern about health risks due to the high level of exposures associated with taking these medications especially in vulnerable segments of the population, including pregnant women and children.[6]

In 2008 the United States National Research Council recommended that the cumulative effects of phthalates and other antiandrogens be investigated. It criticized US EPA guidances, which stipulate that when examining cumulative effects the chemicals examined should have similar mechanisms of action or similar structures, as too restrictive. It recommended instead that the effects of chemicals which cause similar adverse outcomes should be examined cumulatively.[7]:9 Thus the effect of phthalates should be examined together with other antiandrogens, which otherwise may have been excluded because their mechanisms or structure were different.

In a recent study of girls with precocious puberty, there was no difference in phthalate levels in girls with or without the condition, leading to the conclusion that phthalates were not a cause of precocious puberty in humans.[8]

Endocrine disruption

In studies of rodents exposed to certain phthalates high doses have been shown to change hormone levels and cause birth defects.[9] A recent British study showed that the phthalate di(n-butyl) phthalate (DBP) or its metabolite monobutyl phthalate (MBP) suppresses steroidogenesis by fetal-type Leydig cells in primates as in rodents.[10]

A study published in 2005, lead investigator Dr. Shanna Swan (hence a.k.a. the "Swan Study") reported that human phthalate exposure during pregnancy resulted in decreased anogenital distance among baby boys. In this study phthalate metabolites were measured in urine samples collected from the pregnant women who gave birth to the infants. After birth the genital features and anogenital distance of these women's babies were measured and correlated with the residue levels in the mother's urine. Boys born to mothers with the highest levels of phthalates were 7 times more likely to have a shortened anogenital distance.[11] An editorial concerning this paper in the same volume stated that the study population was small, and "needs to be investigated more thoroughly in a larger, more diverse population".[12] While anogenital distance is routinely used as a measure of fetal exposure to endocrine disruptors in animals,[13] this parameter is rarely assessed in humans and its significance is unknown.[14] One paper states that "Whether anogenital distance measurements in humans relate to clinically important outcomes … remains to be determined,"[15] and a National Toxicology Program expert panel concluded that anogenital distance is a "'novel index' whose relevance in humans 'has not been established,'" and that there is "insufficient evidence in humans" that DEHP causes harm.[16] The Swan study is thought by some to "suggest that male reproductive development in humans could be affected by prenatal exposure to environmentally relevant levels of phthalates."[17] Authors of a more recent study of boys with undescended testis hypothesized that exposure to a combination of phthalates and anti-androgenic pesticides may have contributed to that condition.[18]

In contrast to the Swan study an earlier study found that "adolescents exposed to significant quantities of DEHP as neonates showed no significant adverse effects on their physical growth and pubertal maturity."[19] This study, however, examined children exposed intravenously to phthalate diesters, and intravenous exposure results in little metabolic conversion of the relatively nontoxic phthalate diester to its more toxic monoester metabolite.[20]

In November 2009, Swan et al., in the International Journal of Andrology, in a paper titled "Prenatal phthalate exposure and reduced masculine play in boys",

"... suggest that prenatal exposure to antiandrogenic phthalates may be associated with less male-typical play behaviour in boys. ... [and] ... suggest that these ubiquitous environmental chemicals have the potential to alter androgen-responsive brain development in humans." [21]

Other effects

There may be link between the obesity epidemic and endocrine disruption and metabolic interference. Studies conducted on mice exposed to phthalates in utero did not result in metabolic disorder in adults.[22] Although, "in a national cross-section of U.S. men, concentrations of several prevalent phthalate metabolites showed statistically significant correlations with abnormal obesity and insulin resistance."[22] Mono-ethyl-hexyl-phthalate, a metabolite of DEHP, has been found to interact with all three peroxisome proliferator-activated receptors (PPARs).[22] PPARs are members of the nuclear receptor superfamily. The author of the study stated "The roles of PPARs in lipid and carbohydrate metabolism raise the question of their activation by a sub-class of pollutants, tentatively named metabolic disrupters."[22] Phthalates belong to this class of metabolic disruptors. It is a possibility that over many years of exposure to these metabolic disruptors, they are able to deregulate complex metabolic pathways in a subtle manner.[22]

Large amounts of specific phthalates fed to rodents have been shown to damage their liver and testes,[9] and initial rodent studies also indicated hepatocarcinogenicity. Following this result diethyl hexyl phthalate was listed as a possible carcinogen by IARC, EC, and WHO. Later studies on primates showed that the mechanism was specific to rodents - humans are resistant to the effect.[23] The carcinogen classification was subsequently withdrawn.

In 2004 a joint Swedish-Danish epidemiologic team found a link between allergies in children and the phthalates DEHP and BBzP. Their review article and meta-analysis of published data relating to phthalates and asthma found an association between phthalates in the home and asthma, especially in children, but this evidence was limited by imprecise data on levels of exposure.[24]

In 2007 a cross-sectional study of U.S. males concluded that urine concentrations of four phthalate metabolites correlate with waist size and three phthalate metabolites correlate with the cellular resistance to insulin, a precursor to Type II diabetes. The authors note the need for follow-up longitudinal studies, as waist size is known to correlate with insulin resistance.[25]

On November 15, 2009, South Korean scientists reported findings of a statistically-significant correlation between urine phthalate concentrations in children and symptoms of ADHD. Although more research is needed in order to conclusively determine the relationship between phthalate and ADHD, the article suggests that consumers should be aware of its potential effects on behavior and neurological disorders.[26] The findings were replicated in The Mount Sinai Children's Environmental Health Study, which enrolled a multiethnic prenatal population in New York City between 1998 and 2002 (n= 404), published in Jan 2010. There was an association of prenatal phthalate exposure with offspring behavior and executive functioning at ages 4 to 9 years. [27]

Legal status

European Union

The use of some phthalates has been restricted in the European Union for use in children's toys since 1999.[28] DEHP, BBP, and DBP are restricted for all toys; DINP, DIDP, and DNOP are restricted only in toys that can be taken into the mouth. The restriction states that the amount of phthalates may not be greater than 0.1% mass percent of the plasticized part of the toy. These phthalates are allowed at any concentration in other products and other phthalates are not restricted.

There are no other specific restrictions in the European Union although draft proposals have been tabled for the inclusion of BBP, DEHP and DBP on the Candidate list of Substances for Authorisation under REACH.[29] The Dutch office of Greenpeace UK sought to encourage the European Union to ban sex toys that contained phthalates.[30]

United States

In August 2008, the United States Congress passed and President George W. Bush signed the Consumer Product Safety Improvement Act (CPSIA) which became public law 110-314[31]. Section 108 of that law specified that as of 10 February 2009, "it shall be unlawful for any person to manufacture for sale, offer for sale, distribute in commerce, or import into the United States any children’s toy or child care article that contains concentrations of more than 0.1 percent of" DEHP, DBP, or BBP and "it shall be unlawful for any person to manufacture for sale, offer for sale, distribute in commerce, or import into the United States any children’s toy that can be placed in a child’s mouth or child care article that contains concentrations of more than 0.1 percent of" DINP, DIDP, DnOP. Furthermore, the law requires the establishment of a permanent review board to determine the safety of other phthalates. Prior to this legislation, the Consumer Product Safety Commission had determined that voluntary withdrawals of DEHP and DINP from teethers, pacifiers, and rattles had eliminated the risk to children, and advised against enacting a phthalate ban.[32]

Some phthalates were restricted in children's toys sold in California starting in 2009.[33]


In January 2010 the Australian Consumer Affairs Minister Craig Emerson announced a ban on items containing more than one per cent Diethylhexyl phthalate (DEHP) because of international research linking it to reproductive difficulties.[34]

Identification in plastics

Some type 3 plastics may leach phthalates.[citation needed]

Phthalates are used in some but not all PVC formulations, and there are no labeling requirements for phthalates specifically. PVC plastics are typically used for various containers and hard packaging, medical tubing and bags, and are labelled "Type 3" for recycling reasons. However, the presence of phthalates rather than other plasticizers is not marked on PVC items. Plasticizers such as phthalates are only used for making flexible PVC, so it stands to reason that they should only be present in soft forms of PVC. If a more accurate test is needed, chemical analysis, for example by gas chromatography, can establish the presence of phthalates.

Polyethylene terephthalate ethylene (PETE) is the main substance used to package bottled water and many sodas. Products containing PETE are labeled "Type 1" (with a "1" in the recycle triangle) for recycling purposes. Although the word "phthalate" appears in the name, however, PETE is not a phthalate. They are chemically different substances. [1]

Detection in food products

In February 2009, the Joint Research Centre (JRC) of the European Commission published a review of methods to measure phthalates in food.[35]

See also


  1. ^ a b c d Rudel R, Perovich L (January 2008). "Endocrine disrupting chemicals in indoor and outdoor air". Atmospheric Environment 43 (1): 170–81. doi:10.1016/j.atmosenv.2008.09.025. 
  2. ^ a b Heudorf U, Mersch-Sundermann V, Angerer J (October 2007). "Phthalates: toxicology and exposure". Int J Hyg Environ Health 210 (5): 623–34. doi:10.1016/j.ijheh.2007.07.011. PMID 17889607. 
  3. ^ a b c Kolarik B, Bornehag C, Naydenov K, Sundell J, Stavova P, Nielsen O (December 2008). "The concentration of phthalates in settled dust in Bulgarian homes in relation to building characteristic and cleaning habits in the family". Atmospheric Environment 42 (37): 8553–9. doi:10.1016/j.atmosenv.2008.08.028. 
  4. ^ Sathyanarayana S, Karr CJ, Lozano P, et al. (February 2008). "Baby care products: possible sources of infant phthalate exposure". Pediatrics 121 (2): e260–8. doi:10.1542/peds.2006-3766. PMID 18245401. 
  5. ^ "Phthalates in school supplies". GreenFacts Website. Retrieved 2009-06-10. 
  6. ^ a b c Hernández-Díaz S, Mitchell AA, Kelley KE, Calafat AM, Hauser R (February 2009). "Medications as a potential source of exposure to phthalates in the U.S. population". Environ. Health Perspect. 117 (2): 185–9. doi:10.1289/ehp.11766. PMID 19270786. 
  7. ^ Committee on the Health Risks of Phthalates, National Research Council. (2008). Phthalates and Cumulative Risk Assessment: The Task Ahead. National Academies Press. Free full-text available.
  8. ^ Lomenick JP, Calafat AM, Melguizo Castro MS, Mier R, Stenger P, Foster MB, Wintergerst KA (November 2009). "Phthalate Exposure and Precocious Puberty in Females". The Journal of Pediatrics. doi:10.1016/j.jpeds.2009.09.047. PMID 19892364. "exposure is not associated with precocious puberty in female children.". 
  9. ^ a b Third National Report on Human Exposure to Environmental Chemicals, U.S. CDC, July 2005.
  10. ^ Hallmark N, Walker M, McKinnell C, et al. (March 2007). "Effects of monobutyl and di(n-butyl) phthalate in vitro on steroidogenesis and Leydig cell aggregation in fetal testis explants from the rat: comparison with effects in vivo in the fetal rat and neonatal marmoset and in vitro in the human". Environ. Health Perspect. 115 (3): 390–6. doi:10.1289/ehp.9490. PMID 17431488. 
  11. ^ Swan SH, Main KM, Liu F, Stewart SL, Kruse RL, Calafat AM, Mao CS, Redmon JB, Ternand CL, Sullivan S, Teague JL (August 2005). "Decrease in anogenital distance among male infants with prenatal phthalate exposure". Environ. Health Perspect. 113 (8): 1056–61. PMID 16079079.& PMC 1280349. 
  12. ^ Barrett, Julia R. (2005). "Phthalates and Baby Boys: Potential Disruption of Human Genital Development". Environ Health Perspect 113(8): A542.. 
  13. ^ Salazar-Martinez E, Romano-Riquer P, Yanez-Marquez E, Longnecker MP, Hernandez-Avila M (2004). "Anogenital distance in human male and female newborns: a descriptive, cross-sectional study". Environ Health 3 (1): 8. doi:10.1186/1476-069X-3-8. PMID 15363098.& PMC 521084. Retrieved 2008-06-20. 
  14. ^ Postellon, Daniel C. (June 2008). "Baby Care Products" (letter). Pediatrics 121 (6): 1292. doi:10.1542/peds.2008-0401. PMID 18519505. Retrieved 2008-06-03. 
  15. ^ Romano-Riquer SP, Hernández-Avila M, Gladen BC, Cupul-Uicab LA, Longnecker MP (2007). "Reliability and determinants of anogenital distance and penis dimensions in male newborns from Chiapas, Mexico". Paediatr Perinat Epidemiol 21 (3): 219–28. doi:10.1111/j.1365-3016.2007.00810.x. PMID 17439530. 
  16. ^ Kaiser J (October 2005). "Toxicology. Panel finds no proof that phthalates harm infant reproductive systems". Science 310 (5747): 422. doi:10.1126/science.310.5747.422a. PMID 16239449. 
  17. ^ Tilson HA (June 2008). "EHP Papers of the Year, 2008". Environ. Health Perspect. 116 (6): A234. doi:10.1289/ehp.11684. PMID 18560492. 
  18. ^ Toppari J, Virtanen H, Skakkebaek NE, Main KM (2006). "Environmental effects on hormonal regulation of testicular descent". J Steroid Biochem Mol Biol 102 (1-5): 184–6. doi:10.1016/j.jsbmb.2006.09.020. PMID 17049842. 
  19. ^ Rais-Bahrami K, Nunez S, Revenis ME, Luban NL, Short BL (September 2004). "Follow-up study of adolescents exposed to di(2-ethylhexyl) phthalate (DEHP) as neonates on extracorporeal membrane oxygenation (ECMO) support". Environ. Health Perspect. 112 (13): 1339–40. PMID 15345350.& PMC 1247527. 
  20. ^ Huber WW, Grasl-Kraupp B, Schulte-Hermann R. (1996). "Hepatocarcinogenic potential of di(2-ethylhexyl)phthalate in rodents and its implications on human risk". Crit Rev Toxicol 26 (4): 365–481. doi:10.3109/10408449609048302. PMID 8817083. 
  21. ^ AU: S. H. Swan AU: F. Liu AU: M. Hines AU: R. L. Kruse AU: C. Wang AU: J. B. Redmon AU: A. Sparks AU: B. Weiss TI: Prenatal phthalate exposure and reduced masculine play in boys SO: International Journal of Andrology VL: 9999 NO: 9999 YR: 2009 CP: © 2009 The Authors. Journal compilation © 2009 European Academy of Andrology ON: 1365-2605 PN: 0105-6263 AD: Department of Obstetrics and Gynecology, University of Rochester, Rochester, NY, USA; Department of Social and Developmental Psychology, University of Cambridge, Cambridge, UK; Department of Family and Community Medicine, University of Missouri, Columbia, MO, USA; Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Los Angeles, CA, USA; Department of Medicine, University of Minnesota Medical School, Minneapolis, MN, USA; Department of Pediatrics, University of Iowa, Iowa City, IA, USA; Department of Environmental Medicine, University of Rochester, Rochester, NY, USA DOI: 10.1111/j.1365-2605.2009.01019.x US:
  22. ^ a b c d e Desvergne B, Feige J, Casals-Casas C (2009). "PPAR-mediated activity of phthalates: A link to the obesity epidemic?". Mol Cell Endocrinol. 304: 43. doi:10.1016/j.mce.2009.02.017. 
  23. ^ p. 87. "Chronic Hazard Advisory on Diisononyl Phthalate". 2001. p. 87.. Retrieved 2009-01-31. "Human risk is therefore seen as negligible" 
  24. ^ Bornehag CG, Sundell J, Weschler CJ, Sigsgaard T, Lundgren B, Hasselgren M, Hägerhed-Engman L (October 2004). "The association between asthma and allergic symptoms in children and phthalates in house dust: a nested case-control study". Environ. Health Perspect. 112 (14): 1393–7. doi:10.1289/ehp.10846. PMID 15471731.& PMC 1247566. "The lack of objective exposure information limits the epidemiologic data". 
  25. ^ Stahlhut RW, van Wijngaarden E, Dye TD, Cook S, Swan SH (June 2007). "Concentrations of urinary phthalate metabolites are associated with increased waist circumference and insulin resistance in adult U.S. males". Environ. Health Perspect. 115 (6): 876–82. doi:10.1289/ehp.9882. PMID 17589594. 
  26. ^ Bung-Nyun Kim, Soo-Churl Cho, Yeni Kim, Min-Sup Shin, Hee-Jeong Yoo, Jae-Won Kim, Young Hee Yang, Hyo-Won Kim, Soo-Young Bhang, Yun-Chul Hong Biological Psychiatry - 15 November 2009 (Vol. 66, Issue 10, pp. 958-963, DOI: 10.1016/j.biopsych.2009.07.034)
  27. ^ Engel SM, Miodovnik A, Canfield RL, Zhu C, Silva MJ, Calafat AM, Wolff MS. "Prenatal Phthalate Exposure is Associated with Childhood Behavior and Executive Functioning". Environ. Health Perspect. 2010 Jan 8. [Epub ahead of print]. doi:10.1289/ehp.0901470. PMID 20106747. 
  28. ^ Ban of phthalates in childcare articles and toys, press release IP/99/829, 10 November 1999
  29. ^ ECHA Website - Proposal for identification of Substances of Very High Concern
  30. ^ News24
  31. ^ "H.R. 4040--110th Congress (2007): Consumer Product Safety Improvement Act of 2008, (database of federal legislation) (accessed 14 August 2009)
  32. ^ Public Concern, Not Science, Prompts Plastics Ban by Jon Hamilton, NPR.
  33. ^ California Bans Phthalates In Toys For Children, Bette Hileman, Chemical and Engineering News, OCT. 22, 2007, P. 12.
  34. ^ Australia Bans Phthalates in Toys, Dr C. Emerson, ALP.
  35. ^ Methods for the determination of pthalates in food, European Commission, Joint Research Centre

Further reading

External links


Sources suggesting low/no health risks


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