U.S. Environmental Protection Agency 12/30/2009

1 Phthalates

Action Plan

I. Overview

U.S. Environmental Protection Agency’s (EPA ’s) current management plan includes the following eight phthalates: dibutyl phthalate (DBP ), diisobutyl phthalate (DIBP), butyl benzyl phthalate (BBP), di- n -pentyl phthalate (DnPP), di(2-eth ylhexyl) phthalate (DEHP), di- n -octyl phthalate (DnOP), diisononyl phtha late (DINP), and d iisodecyl phthalate (D IDP). In developing this plan, EPA considered the toxicity of phtha lates, their prevalence in the environment and their widespread use and human exposure.

Phthalates are produced in high volume, over 470 million pounds per year (EPA 2006).

Manufacturers use them in numerous industrial an d consumer products, primarily as plasticizers in poly(vinyl chloride) (PVC) products. Many phthal ates can potentially lead to high exposure, both individually and together with other phthalat es. They can often substitute for each other in products. They are used in medical applications and have been detected in food. A number of phthalates appear in biomonitoring surveys of human tissues, evidencing widespread human exposure (CDC 2009). Although exposure to phthal ates can produce a variety of effects in laboratory animals, for certain phthalates the ad verse health effects on the development of the male reproductive system are the most serious. Se veral studies have shown associations between phthalate exposures and human health (although no causal link has been established). Recent scientific attention is focusing on evaluating the cumulative effects of mixtures of phthalates in an exposed organism.

EPA is concerned about phthalates because of their toxicity and the evidence of pervasive human and environmental exposure to them. Thus, EPA intends to initiate action to address the manufacturing, processing, distribu tion in commerce, and/or use of these eight phthalates. EPA intends to take action as part of a coordina ted approach with the Consumer Product Safety Commission (CPSC) and the Food and Drug Administration (FDA).

II. Introduction

As part of EPA’s efforts to enhance th e existing chemicals program under the Toxic Substances Control Act (TSCA) 1 , the Agency identified an ini tial list of widely recognized chemicals, including phthalates (e.g., see Sect ion VIII of this document), for action plan development based on one or more of the following factors their presence in humans; persistent, bioaccumulative, and toxic (PBT) 2 characteristics; use in cons umer products; production volume.

This Action Plan is based on EPA’ s initial review of readily avai lable use, exposure, and hazard

information on eight phthalate esters. EPA considered which of the various authorities provided under TSCA and other statutes might be appropr iate to address poten tial concerns with phthalates in developing the Action Plan. The Action Plan is intende d to describe the courses of action the Agency plans to pursue in the near te rm to address its concerns. The Action Plan does not constitute a final Agency determination or other final Agency action. Regulatory proceedings

1 15 U.S.C. §2601 et seq.

2 Information on PBT chemicals can be found on the EPA website at http://www.epa.gov/pbt/

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2 indicated by the Action Plan will include approp riate opportunities for public and stakeholder input, including through notice a nd comment rulemaking processes.

III. Scope of Review

Dialkyl ortho -phthalates (or phthalate esters) have the general chemical structure shown

below:

O O O O

R

R' (R, R' groups can be linear, branched, or linear/branched

or cyclic ring)

For purposes of this Action Plan, EPA identif ied eight individual phthalate esters as appropriate subjects for developing an assessmen t and management strategy. This group of eight phthalates includes the phthalates identified by CPSIA and those being evaluated by EPA for the Integrated Risk Information System (IRIS), based on advice from the National Academy of Sciences (NAS, 2008). Four phthalates are comm on to CPSIA and the IRIS assessment. This Action Plan includes the following eight chemi cal substances, identified by 10 separate Chemical Abstracts Service Registry Numbers (CASRNs):

No CASRN CA Index Name Acronym Common Name
1 84-74-2 1,2-Benzenedicarboxylic acid, 1,2-dibutyl ester DBP Dibutyl phthalate 2 84-69-5 1,2-Benzenedicarboxylic acid, 1,2-bis-(2- methylpropyl) ester DIBP Diisobutyl phthalate

3 85-68-7 1,2-Benzenedicarboxylic acid, 1-butyl 2- (phenylmethyl) ester BBP Butyl benzyl phthalate 4 131-18-0 1,2-Benzenedicarboxylid acid, 1,2-dipentyl ester DnPP Di- n -pentyl phthalate 5 117-81-7 1,2-Benzenedicarboxylic acid, 1,2-bis(2- ethylhexyl) ester DEHP Di(2-ethylhexyl) phthalate 6 117-84-0 1,2-Benzenedicarboxylic acid, 1,2-dioctyl ester DnOP Di- n -octyl phthalate 7 28553-12-0 1,2-Benzenedicarboxylic acid, 1,2-diisononyl ester DINP * Diisononyl phthalate 68515-48-0 1,2-benzenedicarboxylic acid, di-C 8 -C 10 -branched alkyl esters, C 9 -rich (Part of DINP)* Di-(C 9 -rich

branched C 8 -C 10 - alkyl) phthalate 8 26761-40-0 1,2-Benzenedicarboxylic acid, 1,2-diisodecyl ester DIDP * Diisodecyl phthalate 68515-49-1 1,2-Benzenedicarboxylic acid, di-C 9 -C 11 -branched alkyl esters, C 10 -rich (Part of DIDP)* Di-(C 10 -rich

branched C 9 -C 11 - alkyl) phthalate

* Note that each of the commercial products DINP and DIDP is a mixture of two phthalates.

IV. Uses and Substitutes Summary

According to the 2006 TSCA Inventory Upda te Reporting (IUR) database (EPA, 2006), reported volume of production (inc luding imports) for the 10 indivi dual phthalates ranged from none up to 500 million pounds. DINP had the highe st production volume, followed by DIDP andU.S. Environmental Protection Agency 12/30/2009

3 DEHP, then BBP, DBP, DnOP and DIBP. Ther e was no production volume data reported for

DnPP in the 2006 IUR database.

The major use of phthalates is as plasticizers (Australian Government, 2008a-h; HSDB, 2009). A major application of plas ticizers is in PVC, [poly(vinyl chloride)], where they are added to impart flexibility a nd other desirable properties. Ph thalate-containing PVC products included a variety of industrial and commercial produc ts, as well as specialized medical and dental applications. The particul ar phthalate or combin ation of phthalates used in a particular product’s formulation depends on the properties the phthalates impart, as well as their cost. BBP is the most widely used stain-resistant plasticiz er in PVC (Wickson, 1993); vinyl tile represents its largest use (NTP, 2003e). A number of uses of DBP have been id entified including the manufacture of plastics, paints, wood varnishes and lac quers, use in cosmetics, medical supplies, textiles, propellants, food packaging, dent al materials, and paper (OSHA, 2009). More specifically, it is used as a plastic izer in uses such as nail polis hes, explosives, and solid rocket propellants. Nearly half of DEHP consumption in the United States occurs in medical devices, such as intravenous (IV) tubing and blood bags. Th e rest is split between consumer products and construction-related products (TURI, 2006). DIBP is considered a specialty plasticizer, too volatile to be used in PVC, and is often combined with other phthalates. As such, it is used in nitrocellulose, cellulose ether, and polyacrylat e and polyacetate dispersions (ECPI, 2009). The major use of DIDP is in PVC as a plasticizer (9 5%) (EC2003b). DIDP is ex tensively used in wire and cable applications, a nd is, the main plasticizer used in this application (TURI, 2006). NonPVC uses of DIDP include polymer-related uses and nonpolymer uses such as anti-corrosion and anti-fouling paints, sealing compounds, and te xtile inks (EC2003b). DINP is a mixture of phthalates and is a commonly used plasticizer (TURI, 2006). PVC applications account for 95 percent of the volume. There are no known comm ercial uses for pure DnOP. However, DnOP constitutes approximately 20 percent of the C 6–10 phthalate mixtures used in PVC products (NTP, 2003a).

There are various possible alternatives fo r phthalates in plasticized PVC (Biron, 2009; SCENIHR, 2007). Four chemicals have been cited as already being used in various children’s products; they are acetyl tri- n -butyl citrate (ATBC); di(2-e thylhexyl) adipate (DEHA); 1,2- cyclohexanedicarboxylic acid, diis ononyl ester (DINCH), and di (2-ethylhexyl) terephthalate (DEHT or DOTP). Citrate-based plasticizers, lik e ATBC, are drop-in substitutes for DEHP made from citric acid and have been available for y ears as plasticizers in medical devices (Tickner, 2001). DINCH is an alternative for applicatio ns such as medical devices (SCENIHR, 2007). Another chemical, trioctyltrimellitate (TOTM) performs as a plasticizer in PVC and it has potential to be used commercially. Promisi ng non-phthalate substitutes for DEHP in vinyl flooring material include DGD (d ipropylene glycol dibenzoate ) and DEHA (di(2-ethylhexyl) adipate). Other possible phthalate substitute s include: phosphate esters (e.g., tris(2- ethylhexyl)phosphate); sebacate and azelate esters (e.g., diisodecyl sebacate (DIDS), di-butyl sebacate, and di(2-ethylhexyl) azelate (DOZ)); isosorbide es ters (made from renewable resources), and other organic esters such as isobutyrate trimethylpent anediol, and diethyl succinate. In addition, low-molecular-weight poly meric ester plasticizers that are derived from polymeric multifunctional alcohols and adipic, seb acic or glutaric acid; polymeric rubbers and plastics; and reactive plasticizers may also be potential substitutes fo r phthalates (Biron, 2009;U.S. Environmental Protection Agency 12/30/2009

4 SCENIHR, 2007). As part of its inquiry, EPA w ill explore the potential risks as well as costs presented by phthalate substitutes.

In response to a European ban on the use of some phthalates in toys and personal care products for children, plasticizers based on isos orbide esters were developed (Roquett, 2009). These plasticizers can cover a br oad range of phthalate applicati ons, such as adhesive, sealants, inks, floor coverings, wall paper, and medical disposables. It is worth noting that isosorbide esters could be prepared under solvent-fr ee conditions (Chalecki, 1997), providing an environmentally friendly a pproach to manufacturing.

V. Hazard Identification Summary

Human Health Effects

A comparison of toxicity information from la boratory animal studies for phthalates as a chemical group allows generalizations to be draw n with respect to certain health endpoints. For example, acute toxicity, skin and eye irritati on and sensitization potential are low for all phthalates tested, and the majority of the pht halates were not genotoxic. The most sensitive health outcomes following exposures of some ph thalates in animal studies are the phthalate syndrome effects, which consist of changes in the fetal development of the reproductive system (NAS, 2008; NTP-CERHR, 2003a-e, 2006; EC, 2003a-b, 2003-4, 2008a-b; Australian Government, 2008a-h). The phthalates that are the most potent at causing the phthalate syndrome effects are generally those with linear ester si de chains having 4-6 carbons. Phthalates with shorter or longer linear chain lengths typically exhibit less se vere or no effects; however, branching of the ester side chain is important. It appears that the age of the animal at the time of exposure is critical with respect to the severity of the effects; pubertal animals show effects at

doses lower than those in the corresponding studies in adult an imals. The fetus is the most sensitive life stage (NAS 2008).

Several human studies have reported associa tions of exposure of some phthalates with adverse reproductive outcomes and developmental e ffects similar to those in the rat, although no causal link has been established (Swan et al , 2005; Huang et al., 2009). The reproductive developmental effects observed in humans in clude shortened anogenita l distance observed in newborn boys; and shortened pregnancy, lower se x and thyroid hormones, and reduced sperm quality observed in adults. Since the pathway fo r sexual differentiation in the fetus is highly conserved in all mammals, the reproductive develo pmental effects observed in the rat studies are potentially relevant to humans. Data from the National Health and Nutrition Examination survey (NHANES) indicates widespread exposure of the gene ral population to phthalates (CDC, 2009). Biomonitoring data from amniotic fluid and urine have demonstrated that humans are exposed to phthalates in utero , as infants, during puberty, and in adul t life, and that people are exposed to several phthalates at once. In addition, recent stud ies in animals evaluating the cumulative effects of mixtures of several active ph thalates on testosterone producti on, fetal mortality, and male and female reproductive development later in life showed all mixtures were cumulative for all endpoints (Rider et al., 2008, 2009; Howdeshell, et al., 2007, 2008a, 2008b; Gray et al., 2006; Hotchkiss et al., 2004). In conclusion, taken to gether, the reproductive effects observed in animal studies and in humans, the human biomon itoring data, and the data on cumulative effectsU.S. Environmental Protection Agency 12/30/2009

5 of mixtures support EPA’s concern for potential human health hazard following exposure to phthalates.

A major cumulative hazard assessment of pht halates is scheduled to be conducted by the CPSC’s Chronic Hazard Advisory Panel (CHAP) as directed by the Consumer Product Safety Improvement Act of 2008 (CPSIA). The anticipated date of completion for the CPSC/CHAP activity is 2012 3 . EPA is conducting its own cumu lative hazard assessment of six of the phthalates in this Action Pl an as part of the updating of th e IRIS database. In a separate effort EPA is screening certain phthalates to assess their endocrine disrupting properties.

Environmental Effects

Of the 8 phthlates, BBP, DEHP, and DBP e licit the most toxicity to terrestrial organisms, fish, and aquatic inve rtebrates (EC, 2008a,; Staples et al. 1997). Ecotoxicity studies with these phthalates showed adverse effects to aquatic organisms with a broad range of endpoints and at concentrations that coincide with measured environmental concentrations. Toxic effects were observed at environmentally re levant exposures in the low ng/L to μg/L range (Oehlmann et al. 2008). The ot her three phthalates which had data: DIBP, DINP, and DIDP, exhibited much lower toxicity to aquatic organism s (Staples et al. 1997). There are no available ecotoxicity data for DnPP or DnOP.

Some phthalates studied have been shown to affect reproduction and impair development in all studied animal groups. Most phthalates app ear to act by interfering with the functioning of various hormone systems, but so me phthalates have wider pathwa ys of effects (Jobling et al. 1995). Effect concentrations of phthalates in laboratory experiments are consistent with

measured environmental concentr ations (Oehlmann, et al., 2008).

VI. Physical/Chemical Properties andFate Characterization Summary

The chemicals in this category are oily liquids at room temperature. They have low to moderate vapor pressures and negligible to mode rate water solubility. The water solubility and vapor pressure decrease a nd the octanol-water part ition coefficient (log K

ow ) increases with increasing molecular weight (i.e., as the side chain length increas es). The vapor pressure ranges

from 8  10 -5 to 1.38  10 -8 mm Hg at 20 o C; the water solubility range from 10 mg/L to 3.81

 10 -5 mg/L at 20 o C; and the log K

ow ranges from 4.11 (for DIBP) to 9.46 (for DIDP) (Australian Government, 2008a-h; HSDB, 2009; Crossfir e Beilstein, 2009; ExxonMobil Biomedical Sciences, Inc., 2001).

The chemicals in this category have moderate volatility from moist soil surfaces and water. They have low to moderate mobility in soil and water syst ems. They are expected to be readily biodegradable and the rate of abiotic hydr olysis is considered negligible to slow under environmental conditions. Based on available data, the phthalates are ranked low for persistence

3 CPSIA gives the CHAP 18 months to complete its evaluation, and 6 months to complete its final report, for a total of 24 months. Previous CHAPs have requested additional time. The CPSC staff estimates that the CHAP will begin work in early calendar year 2010. Thus, for planning purp oses, the staff estimates that the report will be completed

in 2012U.S. Environmental Protection Agency 12/30/2009

6 and low for bioaccumulation although bioconcentra tion factors for DEHP in freshwater shrimp were moderate (HSDB, 2009; NITE, 2002).

VII. Exposure Characterization Summary

Releases

Phthalates are released to the environmen t from multiple sources including industrial releases, the disposal of manuf acturing, processing and industrial wastes, municipal solid waste, land application of sewage sludge, and release fro m products containing phtha lates. Only two (DBP and DEHP) of the 8 phthalate s are listed on EPA’s Toxics Release Inventory (TRI).list of

toxic chemicals. The available release data fo r these two phthalates indi cate that releases of phthalates can be expected to all primary environmental media. 2007 TRI data (EPA, 2009) for

DBP and DEHP show total on-site and off-site releases of more than 336,000 pounds from 134 sites and 1,229,000 pounds from 251 sites, respecti vely; however, under TRI, some volume of releases are not reported by some facilities. These data also indicate that the volume of releases to particular media generally ranks in the fo llowing order (from highest to lowest release volume): land, air, water. Some facilities re port relatively high releases and may create potentially high localized environmental concentr ations of phthalates. Based on a comparison of TRI releases to IUR data, production and import vol umes indicate that the vast majority (likely between 95% and 99.9%) of phthalates can be expected to be incorpor ated into plastics and other products.

Human Exposure

People may be exposed to phthalates from mu ltiple sources, (including air, water, food, soil, sediments, and biota) and in multiple environments (including home, work, and when undergoing medical procedures) (Babich, 2004; Clausen 2004; EC, 2003 a-b; 2003-04; 2008 a-b; CPSC, 2001; 2002). The most studi ed population and route of exposure for this class of chemicals has been direct exposure via inge stion by small children and infants from the mouthing of toys, teethers, or other children’s products made of flexible PVC (Babich, 2004; EU 2003 a,b; 2003-04; 2008 a,b; CPSC 2001, 2002). Exposures have also been shown to occur via prenatal exposures. (Adibi et al., 2004)

Medical device assessments for DEHP have been developed by FDA, Health Canada Medical Devices Bureau and the European Un ion Scientific Committ ee on Medicinal Products and Medical Devices (FDA, 2002a; Health Canada , 2002; EC 2002). The overarching conclusion is that premature infants are th e population most highly exposed to phthalates via these uses. In 2002, the FDA recommended the use of alternatives to DEHP-containing medical devices for a specific list of procedures that were to be performed on high-risk individuals. Depending on the procedure, these individuals include male ne onates, pregnant women who are carrying male fetuses, and peripubert al males (FDA, 2002b).

Exposure routes of concern will depend on th e product and its use patterns. For example, inhalation exposure for adults and children could be of concern in vehicle interiors, particularly in summer due to elevated temperatures in ve hicles given the vapor pressure range of theseU.S. Environmental Protection Agency 12/30/2009

7 chemicals. Exposure to phthalates can occur from releases that result from the manufacturing, processing or industrial use of phthalates as well as contamination of air, water, food, and dust from the use or disposal of pr oducts containing phthalates. The pub lished literature indicates that the exposure sources listed fr om highest to lowest are : food, cosmetics, consumer products (other than toys), and toys (NTP-CERHR, 2003 a-e, 2006; HSDB , 2009). There are limited data on the migration of phthalate from plasticized PV C into environmental media. However, due the total volume of plasticized PVC produced, it is possible that PV C or other polymer/polymericlike materials containing phthalates may be long- term and dispersive sources of human and environmental exposures to phthalates.

Data from the NHANES (CDC, 2009) indicates widespread exposur e of the general population to phthalates. Biomonitoring data from amniotic fluid and urine have demonstrated that humans are exposed to phthalates in utero , as infants, during pubert y, and in adult life, and that people are exposed to several phthalates at once. For example, NHANES detected a DEHP urinary metabolite in 78% of the 2541 samples te sted with women having a higher exposure than men (CDC, 2009). Children have been reported as ha ving the highest exposure s; specifically to DEHP, DBP, BBP and DnOP.

Available information indicates that workers may be exposed to phthalates by inhalation and dermal routes, with the dermal route seeming to be more prevalent. The Occupational Safety and Health Administration (OS HA) has established Permissibl e Exposure Limits (PELs) of 5 mg/m 3 time-weighted average (TWA) for both DBP and DEHP (OSHA, 2006). According to the IUR data, industrial workers exposed to th ese phthalates number in the thousands.

Environmental Exposure

Due to their pervasive use and release, as well as its propensity for global transport, phthalates are found in most environmental media, for example ambient air, surface water, soil, sediment, etc (EC, 2003a-b; 2008a-b; NTP-CERHR, 2003 a-e; 2006). Aquatic organisms, fish and terrestrial animals have evident exposur e to DEHP (EC 2008a; Staples et al. 1997).

VIII. Risk Management Considerations

Phthalate exposures can produce a variety of adverse effects in laboratory animals; especially on the development of the male reproductive system, a nd therefore there are implications for human health. Animal data on th e cumulative effect of mixtures of several phthalates showed an increase in the reproductive effects in the organism exposed. Phthalates are produced in high volume and they are used in numerous industrial and consumer products. Phthalates appear in biomonitoring surveys, such as NHANES, that provide evidence of widespread human exposure. Phth alates are also found in the e nvironment and wildlife species. EPA is concerned with phthalates based on toxicit y, particularly to the development of the male reproductive system, prevalence in the environm ent, widespread use and human exposure and recent work focusing on the potential cumulativ e effect of mixtures of phthalates.U.S. Environmental Protection Agency 12/30/2009

8 Potential Impacts on Children

Phthalate exposures are a potential concern for children’s health. In animal studies, exposure to phthalates during fetal developmen t results in adverse effects on the male reproductive system. The timing of exposure is critical to the severity of eff ects. The fetus is the most sensitive life stage for male reproductive e ffects, and pubertal animals show effects at lower doses than those showing effects in adu lt animals. Children are exposed to phthalates through environmental sources (e.g., air, water, f ood) as well as consumer products (e.g., toys).. Children’s estimated exposures are often greater than those in adults which may be due to increased intakes of food, water, and air on a bodyweight basis, as well children’s unique exposure pathways such as mouthing of object s and ingestion of non-food items. The 1999-2000 and 2001-2002 biomonitoring data in the Third National Report on Human Exposure to

Environmental Chemicals demonstrate that children have the highest exposures to phthalates of all groups monitored, and other biomonitoring data indicate in utero exposures to phthalates (CDC, 2005). Given the well-charac terized health effects of phtha late exposure in animals in conjunction with the demonstrated widespread phthalate exposure in children, EPA believes that the cumulative health risks of phthalates should be assessed to determine what actions are warranted to insure protection of children’ s health from this group of chemicals.

Existing Risk Management Activities

Federal Government

The federal government both regulates and con tinues to study phthala tes. Federal entities involved in phthalate manage ment and research include:

Consumer Products Safety Commission (CPSC)

– Among other provisions, the Consumer Product Safety Improvement Act of 2008 (CPSIA) banned the use of six phthalates in toys and child care articles at concentrations greate r than 0.1 percent: DEHP, DBP, BBP, DINP,

DIDP and DnOP. The use of three of these bann ed phthalates, DINP, DIDP, and DnOP may be reinstituted by CPSC pending revi ew by the Chronic Hazard Adviso ry Panel. The CPSIA tasks the CPSC with appointing a Chronic Hazard A dvisory Panel and examining the cumulative health risks of phthalates and phthalate s ubstitutes. The CHAP will recommend to the

Commission whether to continue the ban of DINP, DIDP, and DnOP and whether any other phthalates or phthalate substitutes should be banned.

Food and Drug Administration (FDA) – The FDA regulates pht halates in food contact substances (such as plastic wrap), cosme tics, pharmaceuticals and medical devices. FDA announced in June 2008 that it is conducting a co mprehensive inventory of regulated products that contain phthalate and is re viewing available use and toxicol ogy information associated with phthalate exposure from FDA regulated products to better characterize an y potential risk from

these uses.U.S. Environmental Protection Agency 12/30/2009

9 Environmental Protection Agency (EPA)

– Existing EPA Actions affecting phthalates

include:

 DEHP is regulated under the Safe Drinki ng Water Act. The highest concentration allowed, the maximum contaminant level (MCL), is 0.006 mg/L.

 DEHP and DBP are listed as hazardous ai r pollutants under the Clean Air Act.

 Under the Resource Conservation and Recovery Act (RCRA), phthalate s are regulated as

a hazardous waste if discarded as a commercial chemical product.

 DBP and DEHP are reportable to the Toxic Re lease Inventory (TRI) under section 313 of the Emergency Planning and Commun ity Right-to-know Act (EPCRA).

 BBP, DBP and DEHP are included in the firs t group of 67 chemicals to be screened as part of the Endocrine Disrupt or Screening Program (EDSP).

 Phthalates that are listed on the TSCA I nventory are subject to TSCA section 8(e) Inventory Update Reporting (IUR) requi rements, including production and use information for sites having production volum es of at least 2 5,000lbs/yr. All eight Phthalates (10 CASRNs) included in this Ac tion Plan are listed on the TSCA Chemical Substance Inventory.

 In 1989, EPA entered an Enforceable Consent Agreement under TSCA section 4 with six companies to perform certain chemical fate and environmental effects on certain Alkyl Phthalates (54 FR 618).

 In 2001, under the voluntary HPV Challenge Prog ram, the Phthalate Esters Panel Testing Group of the American Chemical Council s ponsored a phthalates ester category. The panel has submitted to EPA robust study summaries or other information for 26 phthalates, including several of those being considered in this Action Plan (BBP, DEHP, DINP, DIDP and DnOP)

State Governments

California, Vermont and Washingt on have established standard s for the content of certain phthalates in children’ s articles. California prohibits the manufacture, sale, or distribution in commerce of any toy or child-care article that co ntains DEHP, DBP, or BBP at greater than 0.1% and of any toy or child-care arti cle, intended for use by children under three years of age that can be mouthed, that contains DINP , DIDP or DnOP at greater th an 0.1%. Vermont prohibits the manufacture, sale, or distributi on in commerce of any toy or child -care article intended for use by a child younger than three years old that cont ains DEHP, DBP, or BBP in concentrations greater than 0.1% and of any toy or child-care article intended for us e by a child under three years of age that can be placed in the mouth and that contains DINP, DIDP, or DnOP in concentrations greater than 0.1% ( CRS, 2008)

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10 As part of a statute concerning chemicals in children’s products ge nerally, Washington prohibits a manufacturer, wholes aler, or retailer from manufacturing, know ingly selling, offering for sale, or distributing for sale or for use in the state a children’s pr oduct or product component containing phthalates (DEHP, DBP, BBP, DINP, DIDP, DnOP) individually or in combination, at a concentration exceeding 0.1% by weight ( CRS, 2008) . Other States such as Hawaii have introduced legislati on to prohibit the manufacture, sale, or distribution of certain toys and child care articles containing certain types of phthalates (Hawaii House of Representatives, 2009; CRS, 2008)

Foreign Governments

A number of nations have taken steps to manage risk associated with phthalates or further assess those risks. For example, in 2005, the European Commission banned DEHP, DBP and BBP in all toys and childcare articles (Dir ective 2005/84/EC). DINP, DIDP and DnOP were banned from use in toys and childcare articles, if they can be put in the mouth by children. Canada proposed in June, 2009 to harmonize their phthalate requirements with those already in effect in the EU and U.S., ensuri ng the same level of protection as children in the U.S. and the

EU ( Canada Consumer Product Safety Act). In 20 06, the Australian Government declared the phthalates DEHP, DIDP, DMP, DINP, DBP, BBP, DnOP, DEP and bis(2-methylethyl) phthalate as Priority Existing Chemicals and initiated public risk assessments for these phthalates. Phase 1 the development of the public health hazard assessments was concluded in 2008 (Australian Government, 2008a-h). Phase 2 the development of the risk assessments is currently in progress (Australian Government, 2009).

Risk Management Approach

Phthalates are used in products that are s ubject to EPA, FDA, and the CPSC. People may be exposed to phthalates from a variety of produc t uses, as well as from industrial releases and environmental exposures; these e xposure pathways should be asse ssed together to appropriately characterize exposures and avoid underestimating risk. The assessment of combined exposure is important to determine the potential impacts of these chemicals. Focusing individually on these phthalates would likely underestimat e their impact since they appear to produce similar adverse effects. Also, many phthalates are interchangeable in their uses as plasticizers for flexible PVC products, so restrictions on one c ould simply shift use to another of similar toxicity. Given this cumulative impact, the management of the risk from combined exposure requires a coordinated approach by all three agencies, and, as appropriate, additional fe deral agencies. Therefore, EPA intends to work closely with CPSC and FDA to address the range of exposures.

In assessing potential restric tions on certain phthalates, EPA plans to weigh the relative toxicity and feasibility of othe r phthalate substitutes. Identifi cation of safer and affordable nonphthalate substitutes will be an important consider ation in any action that would restrict the use

of these chemicals.

IX. Next Steps

On the basis of existing information, the Ag ency believes that the following regulatory actions would be warranted to manage the risk that may be presented by the eight phthalates identified in the plan.U.S. Environmental Protection Agency 12/30/2009

11 EPA intends to initiate rulemaking to add the 8 phthalates to the list under TSCA section 5(b)(4). Section 5(b)(4) authori zes the EPA to compile and keep current a list of chemicals it finds present or may present an unreasonable risk of injury to health or the environment. EPA intends to publish a notice of proposed rulemaking in autumn, 2010.

EPA intends to initiate rulemaking in late 2010 to add the six phthalates not listed on the Toxics Release Inventory to that list. Only two of the eight phthalates in this Action Plan are currently on this Emergency Planning and Comm unity Right-to-Know Act (EPCRA) section 313

list of toxic chemicals.

EPA intends to lay the groundwork to cons ider initiating in 2012 rulemaking under TSCA section 6(a) to regulate th e eight phthalates In prepar ation for rulemaking, EPA intends, in cooperation with CPSC and FDA, to continue its work to more fully assess the use, exposure

and substitutes for these chemicals. In its further review, EPA plans to consider the future results of the cumulative assessment that will be developed by the CPSC. The cumulative assessment approach under development by CPSC, which may be completed in 2012, as well as the ongoing review of phthalates at the FDA and the a ssessment for EPA’s IRIS program, due to be completed in 2011, will inform EPA’s determination of the extent of any future TSCA section 6 action addressing these chemicals. Depending on th e nature of its final determination about the eight phthalates, EPA’s potential control measures may include a ban of all or several of these chemicals. EPA expects to exercise its risk ma nagement authorities in coordination with CPSC, FDA and, as appropriate, other agencies. EPA will develop more detailed assessments to support the TSCA section 6(a) “presents or will present an unreasonable risk” find ings. If these more detailed assessments indicate that a different appr oach to risk management is appropriate, EPA will consider additional approaches.

Before taking TSCA section 6(a) action on DnPP, EPA may consider pursuing additional rulemaking under TSCA section 5(a)(2) in late 2010 or early 2011 to re quire manufacturers and processors of DnPP to notify EPA before manu facturing or processing DnPP for a significant new use. The most recent Inventory Update Reporti ng data contains no reports of this phthalate being produced or imported into the United States, and thus it is possible that any use of DnPP may be a significant new use.

EPA intends to conduct a Design for the Envi ronment and Green Chemistry alternatives assessment by 2012. The information developed coul d be used to encourage industry to move away from phthalates in a non -regulatory setting to expand risk management effects beyond whatever regulatory action might be taken under TSCA or could be used as input to a regulatory

action. The alternatives assessment would build upon existing knowledge and would consider exposures for all human subpopulations, as well as environmental exposure.

As part of the Agency's efforts to address phthalates, EPA also intends to evaluate the potential for disproportionate impact on children and other sub-populations.U.S. Environmental Protection Agency 12/30/2009

12 X. References

Adibi, J.; Perera, F.; Jedrychowski, W.; Camann, D.; Jacek, R.; Whyatt, R. 2003. Prenatal Exposures to Phthalates among Women in New York City and Krakow, Poland. Environ. Health Perspect

. 2003, 111 (14) , 1719–1722.

Australian Government. 2008a. Existing Chemical Hazard Assessment Report for Butylbenzyl Phthalate

. Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008b. Existing Chemical Hazard Assessment Report for Dibutyl Phthalate . Department of Health and Ageing, National Industrial Chemicals No tification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008c. Existing Chemical Hazard Assessmen t Report for Diethylhexyl Phthalate

. Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008 http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008d. Existing Chemical Hazard Assessmen t Report for Diisobutyl Phthalate . Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008e. Existing Chemical Hazard Assessmen t Report for Diisodecyl Phthalate . Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008f. Existing Chemical Hazard Assessmen t Report for Diisonoyl Phthalate . Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS):Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008g. Existing Chemical Hazard Assessment Report for Di-n-octyl Phthalate . Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. http://www.nicnas.gov.au/Publica tions/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2008h. Phthalates Hazard Compendium. A Summary of Physicochemical and Human Health Hazard Data for 24 Ortho-Phthalate Chemicals . Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2008. www.nicnas.gov.au/Publications/CAR/Other/Phthalates.asp (accessed Aug 13, 2009).

Australian Government. 2009. NICNAS Existing Chemicals Information Sheet: Phthalates December 2009. Department of Health and Ageing, National Industrial Chemicals Notification and Assessment Scheme (NICNAS): Sydney, Australia, 2009. http://www.nicnas.go v.au/Publications/Information_S heets/Existing_Chemical_Infor mation_Sheets/ECIS_Phthalate _PDF.pdf (accessed Dec 28, 2009).

Babich, M.; Chen, S.; Greene, M.; Kiss, C.; et al. 2004. Risk Assessment of Or al Exposure to Diisononyl Phthalate

from Children’s Products. Regul. Toxicol. Pharmacol. 2004, 40 (2) , 151–167.U.S. Environmental Protection Agency 12/30/2009

13 Biron, M. Phthalate Ousting: Not So Easy But Some Alternatives are Viable. SpecialChem. http://www.specialchem4polymers.co m/resources/print.aspx?id=3980 (accessed Oct 14, 2009).

CDC. 2005. Centers for Dise ase Control and Prevention. Third National Report on Human Exposure to

Environmental Chemicals

. http://www.cdc.gov/exposurereport/ . July 2005.

Chalecki, Z.; Guibe-Jampel, E. 1997. Lipozyme-Mediated Regioselective Esterification of Isosorbide under SolventFree Conditions. Synth. Commun

. 1997, 27(22) , 3847–3852.

Clausen, P. A.; Hansen, V.; Gunnarsen, L.; Afshari, A. 2004. Emission of Di-2-ethylhexyl Phthalate from PVC Flooring into Air and Uptake in Dust: Emission and Sorption Experiments in FLEC and CLIMPQA. Environ. Sci.

Technol

. 2004, 38 , 2531–2537.

CPSC. 2001. U.S. Consumer Product Safety Commission. Ch ronic Hazard Advisory Panel on Diisononyl Phthalate (DINP). Directorate of Health Sciences: Bethesda, MD 20814.

CPSC. 2002. U.S. Consumer Product Safety Commission. Memorandum to Marilyn L. Wind from S.B. Chen. Screening of Toys for PVC and Phthalates Migration.

Crossfire Beistein Database. 2009 . Elsevier Information Systems GmbH. Frankfurt, Germany. http://www.info.crossf irebeilstein.com/

CRS. 2008 Congressional Research Service. CRS Report to Congress Phthalates in Plastics and Possible Human Health Effects , Updated July 29, 2008. http://www. policyarchive.org/bitstream/handle/ 10207/19121/RL34 572_20080729.pdf?sequence=2 (accessed Dec 28, 2009).

EC. 2002. European Commission. Opinion on Medical Devices Containing DEHP Plasticised PVC; Neonates and Other Groups Possibly at Risk from DEHP Toxicity. 26 September 2002. Scientific Committee on Medicinal

Products and Medical Devices. http://ec.europa.eu/health/ph_risk/committees/scmp/documents/out43_en.pdf

.

EC. 2003a. European Commission. European Union Risk Assessment Report: 1,2-Benzenedicarboxylic Acid, Di-C8- 10-Branched Alkyl Esters, C9-Rich And Di-“Isononyl” Phthalate (DINP), CAS-Nos. 68515-48-0, 28553-12-0. Vol. 35; EUR 20784EN; Office for Official Publications of the European Communities: Luxembourg, 2003.

EC. 2003b. European Commission. European Union Risk Assessment Report: 1,2-Benzenedicarboxylic Acid, Di-C9- 11-Branched Alkyl Esters, C10-Rich And Di-“Isodecyl” Phthalate (DIDP) , CAS-Nos 68515-49-1 and 26761-40-0

. Vol. 36; EUR 20785EN; Office for O fficial Publications of the Europ ean Communities: Luxembourg, 2003.

EC. 2003-04. European Commission. European Union Risk Assessment Report: Dibutyl Phthalate, CAS-No. 84-74-

2 . Vol. 29; EUR 19840EN; Office for Of ficial Publications of the European Communitie s: Luxembourg, 2003-04.

EC. 2008a. European Commission. European Union Risk Assessment Report Bis(2-Ethylhexyl) Phthalate (DEHP),

CAS-No. 117-81-7 . Vol. 80; EUR 23384EN; Office for Official Publications of the European Communities: Luxembourg, 2008.

EC. 2008b. European Commission. European Union Risk Assessment Report Benzyl Butyl Phthalate (BBP), CASNo. 85-68-7. Vol. 76; EUR 22773EN; Luxembourg: Office for Offi cial Publications of the European Communities,

2008.

ECPI. 2009. European Council for Plasticisers and Intermediates. DIBP—A Specialty Plasticiser. http://www.dibpfacts.com/ (accessed Dec 9, 2009).

EPA. 2006. U.S. Environmental Protection Agency. Inventory Update Reporting (IUR): Non-Confidential 2006 TSCA Inventory Update Rule (IUR) Records. http://cfpub.epa.gov/iurse arch/index.cfm?s=chem . (accessed Dec
9, 2009).U.S. Environmental Protection Agency 12/30/2009

14 EPA. 2009. U.S. Environmental Protection Agency. Toxics Release Inventory (TRI) Program: Get TRI Data and

Tools. 2007 Public Data Rele ase, Released March 14, 2009. http://www.epa.gov/tri/tr idata/index.htm#pdr . (accessed Dec 9, 2009).

ExxonMobil Biomedical Sciences, Inc. 2001. Robust Summary and Test Plan for the Phthalate Esters Category

. Dec 10, 2001. http://www.epa.gov/chemrtk/pubs/summaries/benzene/c13467tc.htm (accessed Aug 13, 2009).

FDA. 2002a. U.S. Food and Drug Administration. Sa fety Assessment of Di(2-ethylhexyl)phthalate (DEHP)

Released from PVC Medical Devices. 2002. Ce nter for Devices and Radiological Health. http://www.fda.gov/downloads/Medical Devices/DeviceRegulationandGuidance/GuidanceDocuments/UCM080457. pdf (accessed Dec 9, 2009).

FDA 2002b. U.S. Food and Drug Administration. FDA Public Health Notification: PVC Devices Containing the Plasicizer DEHP. July 12, 2002. Med Watch, HF-2 Fishers Lane, Rockville, MD 20857. 2002. http://www.fda.gov/MedicalDevices/S afety/AlertsandNotices/PublicH ealthNotifications/ucm062182.htm

Gray L.E. Jr, Wilson V.S., Stoker T., Lambright C., Furr J., Noriega N., Howdeshell K. , Ankley GT, Guillette L. 2006. Adverse effects of environmental antiandrogens and androgens on reproductive development in mammals. Int J Androl. Feb;29(1):96-104; discussion 105-8. Review.

Hawaii House of Representatives. 2009. Twen ty-fifth Legislature, House Bill No. 796. http://www.capitol.hawaii.go v/session2009/bills/HB796_.pdf (accessed Dec 28, 2009).

Health Canada. 2002. DEHP in Medical Devices: An Expo sure and Toxicity Assessmen t. Medical Devices Bureau Therapeutic Products Directorate, Health Products & Foods Branch, Health Canada, July 2001; Revised: February

2002. http://www.hc-sc.gc.ca/dhp-mps/alt_formats/hpfb-d gpsa/pdf/md-im/sapdehp_rep_gcsdehp_rap_2001-04-26- eng.pdf (accessed Dec 22, 2009).

Hotchkiss A..K, Parks-Saldutti L..G, Ostby .J.S, Lambright C ., Furr .J, Vandenbergh J.G., Gray L.E. Jr. 2004. A mixture of the "antiandrogens" linuron and butyl benzyl phthalate alters sexual differentiation of the male rat in a cumulative fashion. Biol Reprod. 71(6):1852-61.

Howdeshell KL, Furr J, Lambright CR, Rider CV, Wilson VS, Gray LE Jr. 2007. Cumulative effects of dibutyl phthalate and diethylhexyl phthalate on male rat reproductive tract development: altered fetal steroid hormones and genes. Toxicol Sci. Sep;99(1):190-202.

Howdeshell K.L., Rider C.V., Wilson V.S., Gray L.E. Jr . 2008a. Mechanisms of action of phthalate esters, individually and in combination, to induce abnormal reproduc tive development in male laboratory rats. Environ Res. Oct;108(2):168-76. Review.

Howdeshell K.L., Wilson V.S., Furr J., Lambright C.R., Ri der C.V., Blystone C.R., Hotchkiss A.K., Gray L.E. Jr. 2008b. A mixture of five phthalate esters inhibits fetal testicular testosterone production in the sprague-dawley rat in a cumulative, dose-additive manner. Toxicol Sci. Sep;105(1):153-65.

HSDB. 2009. Hazardous Substance Data Bank. U.S. National Library of Medicine TOXNET System. http://toxnet.nlm.nih.gov/cgi-bin/sis/htmlgen?HSDB (accessed Aug 13, 2009).

Huang, P. C.; Kuo, P. L.; Chou, Y. Y.; Lin, S. J.; Lee, C. C. 2009. Association between prenatal exposure to phthalates and the health outcome of newborns. Environ. Int. 2009, 35(1) , 14–20.

Jobling, S.; Reynolds, T.; White, R.; Parker, M. G.; Sumpte r, J. P. 1995. A Variety of Environmentally Persistent Chemicals, including Some Phthalate Plasticizers, Are Weakly Estrogenic. Environ. Health Perspect. 1995, 103

, 582–587.

NAS. 2008. National Academy of Scie nces. Phthalates and Cumulative Ri sk Assessment; The Tasks Ahead. Dec

2008. http://dels.nas.edu/dels/rpt_briefs/phthalates_final.pdf (accessed Dec 9, 2009).U.S. Environmental Protection Agency 12/30/2009

15 NITE. 2002. National Institute of Technology and Evaluatio n (Japan). Biodegradation and Bioaccumulation of the Existing Chemical Substances under th e Chemical Substances Control Law. http://www.safe.nite.go.jp/english/ kizon/KIZON_start_hazkizon.html (accessed Aug 13, 2009).

NTP-CERHR. 2003a. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Octyl Phthalate (DnOP); NIH Pub. No. 03-4488; U.S. Department of Health and Human Services, May 2003.

NTP-CERHR. 2003b. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Re productive and Developmen tal Effects of Di-n-H exyl Phthalate (DnHP); NIH Pub. No. 03-4489; U.S. Department of Health and Human Services, May 2003.

NTP-CERHR. 2003c. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Re productive and Developmen tal Effects of Di-Isodecyl Phthalate (DIDP); NIH Pub. No. 03-4485; U.S. Department of Health and Human Services, April 2003.

NTP-CERHR. 2003d. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Re productive and Developmen tal Effects of Di-Isodecyl Phthalate (DIDP); NIH Pub. No. 03-4485; U.S. Department of Health and Human Services, April 2003.

NTP-CERHR. 2003e. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Repr oductive and Develo pmental Effects of Butyl Benzyl Phthalate (BBP); NIH Pub. No. 03-4487; U.S. Department of Health and Human Services, March 2003.

NTP-CERHR. 2006. National Toxicology Program - Center for the Evaluation of Risks to Human Reproduction. Monograph on the Potential Human Re productive and Developm ental Effects of Di-( 2-ethylhexyl) Phthalate (DEHP); NIH Pub. No. 06-4476; U.S. Department of Health and Human Services, March 2006.

Oehlmann, J.; Schulte-Oehlmann, U.; Wern er, K.; Jagnytsch, O.; Lutz, I.; Kres ten, K.; Wollenberger, L.; Santos, E. M.; Paull, G. C.; Van Look

, K. J. W.; Tyler, C. R. 2008. A Critical Analysis of the Biological Impacts of

Plasticizers on Wildlife. Philos. Trans. R. Soc

., B: Biol. Sci. 2008, 364(1526) , 2047–2062.

OSHA. 2006. Occupational Safety and Health Admini stration. Permissible Exposure Limits (PELs)Establishing PELs. Regulations (Standards - 29 CFR) Table Z-1 Limits for Air Contaminants. - 1910.1000 Table Z1. http://www.osha.gov/SLTC/pel/recognition.html (accessed Dec 9, 2009).

OSHA 2009. Occupational Safety and Health Guideline for Dibutyl Phthalate. http://www.osha.gov/SLTC/healthguide lines/dibutylphthalate/recognition.html (accessed Dec 22, 2009).

Rider C.V., Furr J., Wilson V.S., Gray L.E. Jr. 2008. A mixture of seven antiandrogens induces reproductive

malformations in rats. Int J Androl . Apr;31(2):249-62.

Rider CV, Wilson VS, Howdeshell KL, Hotchkiss AK, Fu rr JR, Lambright CR, Gray LE Jr. 2009. Cumulative effects of in utero administration of mixtures of "antiandrogens" on male rat reproductive development. Toxicol

Pathol . 37(1):100-13.

Roquette. 2009. Roquette receives the 2009 Pierre Potier prize for its POLYSORB ® ID 37. http://www.roquette.com /delia-CMS/t1/article_id-5614 /topic_id-1691/roquette-recei ves-the-2009-pierre-potierprize-for-its-polysorb-r-id-37.html (accessed Oct 14, 2009).

SCENIHR. 2007. Scientific Committee on Emerging and Newly-Identified Health Risks. European Commission. Preliminary Report on The Safety of Medical Devices Containing DEHP-Plasticized PVC or Other Plasticizers on Neonates and Other Groups Possibly at Risk . Approved for public consultation during the 19 th Plenary of June 21- 22, 2007. http://ec.europa.eu/health/ph_risk/commi ttees/04_scenihr/docs/scenihr_o_008.pdf (accessed Oct 27, 2009).U.S. Environmental Protection Agency 12/30/2009

16 Staples, C. A.; Adams, W. J.; Parkerton, T. F.; Gorsuch, J. W.; Biggingers, G. R.; Reiner, K. H. 1997. Aquatic Toxicity of Eighteen Phthalate Esters. Environ. Toxicol. Chem . 1997, 16 (5) , 875–891.

Swan, S. H.; Main, K. M.; Stew art, S. L.; Kruse, R. L.; Ca lafat, A. M.; Mao, C. S.; Redmon, J. B.; Ternand, C. L.; Sullivan, S.; Teague. J. L. 2005. Study for Future Familie s Research Team. Decrease in Anogenital Distance among

Male Infants with Prenat al Phthalate Exposure. Environ. Health Perspect

. Aug 2005, 113(8) , 1056–61.

Tickner, J. A.; Schettle, T. R.; Guidotti, T.; McCally, M. ; Rossi, M. 2001. Health Risks Posed by Use of Di-2- Ethylhexyl Phthalate (DEH P) in PVC Medical Devices: A Critical Review. Am. J. Ind. Med

. 2001, 39(1) , 100–111. http://www3.interscience.wiley.com/cgi-bin/fulltext/76505754/PDFSTART (accessed Dec 9, 2009).

TURI. 2006. Massachusetts Toxics Use Reduction Institute. Five Chemicals Alternatives Assessment Study

. University of Massachusetts Lowell: Lowell, Massachusetts, June 2006. http://www.turi.org/library/turi_publications/five_chemicals_study (accessed Dec 9, 2009).

Wickson, E. J. 1993. Handbook of Polyvinyl Chloride Formulating; John Wiley & Sons: Baton Rouge, Louisiana,

1993.