NP 30 (NONYLPHENOL 30 EO)

NP 30 (NONYLPHENOL 30 EO)

CAS No. : 25154-52-3
EC No. : 284-325-5

Synonyms:
4-(2,4-dimethylheptan-3-yl)phenol; Phenol, nonyl-; (2,6-Dimethylheptan-4-yl)phenol; Monononylphenol; n-Nonylphenol; nonilfenol; Nonylphenol; NONYLPHENOL; (ISOMERENGEMISCH); Nonylphenol (mixed isomers); Nonylphenol and its ethoxylates; Phenol, nonyl; Phenol, nonyl-; UN 2810; 25154-52-3; nonylphenol; (2,6-Dimethylheptan-4-yl)phenol; Monononylphenol; n-Nonylphenol; nonilfenol; Nonylphenol; NONYLPHENOL; (ISOMERENGEMISCH); Nonylphenol (mixed isomers); Nonylphenol and its ethoxylates; Phenol, nonyl; Phenol, nonyl-; UN 2810; 25154-52-3; nonylphenol; NONYLPHENOL; (ISOMERENGEMISCH); Nonylphenol (mixed isomers); Nonylphenol and its ethoxylates; NONYLPHENOL 30 EO; Phenol; Nonylphenol, ethoxylated; 30 EO; 4-nonylphenol; 4-n-Nonylphenol; p-Nonylphenol; 104-40-5; Phenol, 4-nonyl-; para-Nonylphenol; p-n-Nonylphenol; 4-nonyl phenol; Phenol, p-nonyl-; Phenol, nonyl derivs.; NP 30; Nonylphenol (mixed); p-nonyl phenol; para Nonyl phenol; p -n -Nonylphenol; 4-Nonyl-Phenol; 4-n-Nonyl phenol; CCRIS 1251; HSDB 5359; EINECS 203-199-4; 68081-86-7; DTXSID5033836; CHEBI:34440; P-NONYLPHENOL (ENDOCRINE DISRUPTER); Nonylphenol 30 EO; 4-NP; CAS-104-40-5; C9-Alkylated phenol; (C9)Alkylated phenol; 1-(4-Hydroxyphenyl)nonane; nonyl-phenol; p-nonyl-phenol; Para-nonyl phenol; EINECS 268-359-8; 1-Nonyl-4-phenol; 211947-56-7; 4-Nonyl Phenol-13C6; 4-n-Nonylphenol, 85%; 4-n-Nonylphenol, 98%; 4-Nonylphenol, analytical standard; ZINC1850497; 4-n-Nonylphenol 10 microg/mL in Acetonitrile; 4-n-Nonylphenol 10 microg/mL in Cyclohexane; 4-n-Nonylphenol 100 microg/mL in Cyclohexane; C14550; 4-Nonylphenol, PESTANAL(R), analytical standard; NP 30 (NONYLPHENOL 30 EO); 4-Nonylphenol, certified reference material, TraceCERT(R); 4-Nonylphenol (mixture of compounds with branched sidechain)

Nonylphenol 30 EO

Nonylphenol 30 EO (NP 30)s are a family of closely related organic compounds composed of phenol bearing a 9 carbon-tail. Nonylphenol 30 EO (NP 30)s can come in numerous structures, all of which may be considered alkylphenols. They are used in manufacturing antioxidants, lubricating oil additives, laundry and dish detergents, emulsifiers, and solubilizers.[2] These compounds are also precursors to the commercially important non-ionic surfactants alkylphenol ethoxylates and Nonylphenol 30 EO (NP 30) ethoxylates, which are used in detergents, paints, pesticides, personal care products, and plastics. Nonylphenol 30 EO (NP 30) has attracted attention due to its prevalence in the environment and its potential role as an endocrine disruptor and xenoestrogen, due to its ability to act with estrogen-like activity.[3] The estrogenicity and biodegradation heavily depends on the branching of the nonyl sidechain.[4][5][6] Nonylphenol 30 EO (NP 30) has been found to act as an agonist of the GPER (GPR30).

Properties
Chemical formula C15H24O
Molar mass 220.35 g/mol
Appearance Light yellow viscous liquid with phenolic smell [1]
Density 0.953
Melting point −8 to 2 °C (18 to 36 °F; 265 to 275 K)
Boiling point 293 to 297 °C (559 to 567 °F; 566 to 570 K)
Solubility in water 6 mg/L (pH 7)

Structure and basic properties
Nonylphenol 30 EO (NP 30)s fall into the general chemical category of alkylphenols.[8] The structure of NPs may vary. The nonyl group can be attached to the phenol ring at various locations, usually the 4- and, to lesser extent, the 2-positions, and can be either branched or linear. A branched Nonylphenol 30 EO (NP 30), 4-Nonylphenol 30 EO (NP 30), is the most widely produced and marketed Nonylphenol 30 EO (NP 30).[9] The mixture of Nonylphenol 30 EO (NP 30) isomers is a pale yellow liquid, although the pure compounds are colorless. The Nonylphenol 30 EO (NP 30)s are moderately soluble in water [9] but soluble in alcohol.

Nonylphenol 30 EO (NP 30) arises from the environmental degradation of Nonylphenol 30 EO (NP 30) ethoxylates, which are the metabolites of commercial detergents called alkylphenol ethoxylates. NPEs are a clear to light orange color liquid. Nonylphenol 30 EO (NP 30) ethoxylates are nonionic in water, which means that they have no charge. Because of this property they are used as detergents, cleaners, emulsifiers, and a variety of other applications. They are amphipathic, meaning they have both hydrophilic and hydrophobic properties, which allows them to surround non-polar substances like oil and grease, isolating them from water.[2]

Production
Nonylphenol 30 EO (NP 30) can be produced industrially, naturally, and by the environmental degradation of alkylphenol ethoxylates. Industrially, Nonylphenol 30 EO (NP 30)s are produced by the acid-catalyzed alkylation of phenol with a mixture of nonenes. This synthesis leads to a very complex mixture with diverse Nonylphenol 30 EO (NP 30)s.[10][11][12] Theoretically there are 211 constitutional isomers and this number rise to 550 isomers if we take the enantiomers into account.[4] To make NPEs, manufacturers treat NP with ethylene oxide under basic conditions.[9] Since its discovery in 1940, Nonylphenol 30 EO (NP 30) production has increased exponentially, and between 100 and 500 million pounds of Nonylphenol 30 EO (NP 30) are produced globally every year,[9][13] meeting the definition of High Production Volume Chemicals.

Nonylphenol 30 EO (NP 30)s are also produced naturally in the environment. One organism, the velvet worm, produces Nonylphenol 30 EO (NP 30) as a component of its defensive slime. The Nonylphenol 30 EO (NP 30) coats the ejection channel of the slime, stopping it from sticking to the organism when it is secreted. It also prolongs the drying process long enough for the slime to reach its target.[14]

Another surfactant called nonoxynol, which was once used as intravaginal spermicide and condom lubricant, was found to metabolize into free Nonylphenol 30 EO (NP 30) when administered to lab animals.[8]

Applications
Nonylphenol 30 EO (NP 30) is used in manufacturing antioxidants, lubricating oil additives, laundry and dish detergents, emulsifiers, and solubilizers.[2] It can also be used to produce tris(4-nonyl-phenyl) phosphite (TNPP), which is an antioxidant used to protect polymers, such as rubber, Vinyl polymers, polyolefins, and polystyrenics in addition to being a stabilizer in plastic food packaging. Barium and calcium salts of Nonylphenol 30 EO (NP 30) are also used as heat stabilizers for polyvinyl chloride (PVC).[15] Nonylphenol 30 EO (NP 30) is also often used an intermediate in the manufacture of the non-ionic surfactants Nonylphenol 30 EO (NP 30) ethoxylates, which are used in detergents, paints, pesticides, personal care products, and plastics. Nonylphenol 30 EO (NP 30) and Nonylphenol 30 EO (NP 30) ethoxylates are only used as components of household detergents outside of Europe.[2] Nonyl Phenol, is used in many epoxy formulations mainly in North America.

Prevalence in the environment
Nonylphenol 30 EO (NP 30) persists in aquatic environments and is moderately bioaccumulative. It is not readily biodegradable, and it can take months or longer to degrade in surface waters, soils, and sediments. Nonbiological degradation is negligible.[3] Nonylphenol 30 EO (NP 30) is partially removed during municipal wastewater treatment due to sorption to suspended solids and biotransformation.[16][17] Many products that contain Nonylphenol 30 EO (NP 30) have "down-the-drain" applications, such as laundry and dish soap, so the contaminants are frequently introduced into the water supply. In sewage treatment plants, Nonylphenol 30 EO (NP 30) ethoxylate degrades into Nonylphenol 30 EO (NP 30), which is found in river water and sediments as well as soil and groundwater.[18] Nonylphenol 30 EO (NP 30) photodegrades in sunlight, but its half-life in sediment is estimated to be more than 60 years. Although the concentration of Nonylphenol 30 EO (NP 30) in the environment is decreasing, it is still found at concentrations of 4.1 μg/L in river waters and 1 mg/kg in sediments.[2]

A major concern is that contaminated sewage sludge is frequently recycled onto agricultural land. The degradation of Nonylphenol 30 EO (NP 30) in soil depends on oxygen availability and other components in the soil. Mobility of Nonylphenol 30 EO (NP 30) in soil is low.[2]

Bioaccumulation is significant in water-dwelling organisms and birds, and Nonylphenol 30 EO (NP 30) has been found in internal organs of certain animals at concentrations of 10 to 1,000 times greater than the surrounding environment.[3] Due to this bioaccumulation and persistence of Nonylphenol 30 EO (NP 30), it has been suggested that Nonylphenol 30 EO (NP 30) could be transported over long distances and have a global reach that stretches far from the site of contamination.[19]

Nonylphenol 30 EO (NP 30) is not persistent in air, as it is rapidly degraded by hydroxyl radicals.[3]

Environmental hazards
Nonylphenol 30 EO (NP 30) is considered to be an endocrine disruptor due to its ability to mimic estrogen and in turn disrupt the natural balance of hormones in affected organisms.[4][5][6][20][21] The effect is weak because Nonylphenol 30 EO (NP 30)s are not very close structural mimics of estradiol, but the levels of Nonylphenol 30 EO (NP 30) can be sufficiently high to compensate.

Structure of the hormone estradiol and one of the Nonylphenol 30 EO (NP 30)s.
The effects of Nonylphenol 30 EO (NP 30) in the environment are most applicable to aquatic species. Nonylphenol 30 EO (NP 30) can cause endocrine disruption in fish by interacting with estrogen receptors and androgen receptors. Studies report that Nonylphenol 30 EO (NP 30) competitively displaces estrogen from its receptor site in rainbow trout.[22] It has much less affinity for the estrogen receptor than estrogen in trout (5 x 10−5 relative binding affinity compared to estradiol) making it 100,000 times less potent than estradiol.[22][23] Nonylphenol 30 EO (NP 30) causes the feminization of aquatic organisms, decreases male fertility, and decreases survival in young fish.[2] Studies show that male fish exposed to Nonylphenol 30 EO (NP 30) have lower testicular weight.[22] Nonylphenol 30 EO (NP 30) can disrupt steroidogenesis in the liver. One function of endogenous estrogen in fish is to stimulate the liver to make vitellogenin, which is a phospholipoprotein.[22] Vitellogenin is released by the maturing female and sequestered by developing oocytes to produce the egg yolk.[22] Males do not normally produce vitellogenin, but when exposed to Nonylphenol 30 EO (NP 30) they produce similar levels of vitellogenin to females.[22] The concentration needed to induce vitellogenin production in fish is 10 ug/L for NP in water.[22] Nonylphenol 30 EO (NP 30) can also interfere with the level of FSH (follicle-stimulating hormone) being released from the pituitary gland. Concentrations of NP that inhibit reproductive development and function in fish also damages kidneys, decreases body weight, and induces stressed behavior.[24]

Human health hazards
Alkylphenols like Nonylphenol 30 EO (NP 30) and bisphenol A have estrogenic effects in the body. They are known as xenoestrogens.[25] Estrogenic substances and other endocrine disruptors are compounds that have hormone-like effects in both wildlife and humans. Xenoestrogens usually function by binding to estrogen receptors and acting competitively against natural estrogens. Nonylphenol 30 EO (NP 30) has been shown to mimic the natural hormone 17β-estradiol, and it competes with the endogeous hormone for binding with the estrogen receptors ERα and ERβ.[2] Nonylphenol 30 EO (NP 30) was discovered to have hormone-like effects by accident because it contaminated other experiments in laboratories that were studying natural estrogens that were using polystyrene tubes.[8]

Effects in pregnant women
Subcutaneous injections of Nonylphenol 30 EO (NP 30) in late pregnancy causes the expression of certain placental and uterine proteins, namely CaBP-9k, which suggest it can be transferred through the placenta to the fetus. It has also been shown to have a higher potency on the first trimester placenta than the endogenous estrogen 17β-estradiol. In addition, early prenatal exposure to low doses of Nonylphenol 30 EO (NP 30) cause an increase in apoptosis (programmed cell death) in placental cells. These “low doses” ranged from 10−13-10−9 M, which is lower than what is generally found in the environment.[26]

Nonylphenol 30 EO (NP 30) has also been shown to affect cytokine signaling molecule secretions in the human placenta. In vitro cell cultures of human placenta during the first trimester were treated with Nonylphenol 30 EO (NP 30), which increase the secretion of cytokines including interferon gamma, interleukin 4, and interleukin 10, and reduced the secretion of tumor necrosis factor alpha. This unbalanced cytokine profile at this part of pregnancy has been documented to result in implantation failure, pregnancy loss, and other complications.[26]

Effects on metabolism
Nonylphenol 30 EO (NP 30) has been shown to act as an obesity enhancing chemical or obesogen, though it has paradoxically been shown to have anti-obesity properties.[27] Growing embryos and newborns are particularly vulnerable when exposed to Nonylphenol 30 EO (NP 30) because low-doses can disrupt sensitive processes that occur during these important developmental periods.[28] Prenatal and perinatal exposure to Nonylphenol 30 EO (NP 30) has been linked with developmental abnormalities in adipose tissue and therefore in metabolic hormone synthesis and release (Merrill 2011). Specifically, by acting as an estrogen mimic, Nonylphenol 30 EO (NP 30) has generally been shown to interfere with hypothalamic appetite control.[27] The hypothalamus responds to the hormone leptin, which signals the feeling of fullness after eating, and Nonylphenol 30 EO (NP 30) has been shown to both increase and decrease eating behavior by interfering with leptin signaling in the midbrain.[27] Nonylphenol 30 EO (NP 30) has been shown mimic the action of leptin on neuropeptide Y and anorectic POMC neurons, which has an anti-obesity effect by decreasing eating behavior. This was seen when estrogen or estrogen mimics were injected into the ventromedial hypothalamus.[29] On the other hand, Nonylphenol 30 EO (NP 30) has been shown to increase food intake and have obesity enhancing properties by lowering the expression of these anorexigenic neurons in the brain.[30] Additionally, Nonylphenol 30 EO (NP 30) affects the expression of ghrelin: an enzyme produced by the stomach that stimulates appetite.[31] Ghrelin expression is positively regulated by estrogen signaling in the stomach, and it is also important in guiding the differentiation of stem cells into adipocytes (fat cells). Thus, acting as an estrogen mimic, prenatal and perinatal exposure to Nonylphenol 30 EO (NP 30) has been shown to increase appetite and encourage the body to store fat later in life.[32] Finally, long-term exposure to Nonylphenol 30 EO (NP 30) has been shown to affect insulin signaling in the liver of adult male rats.[33]

Cancer
Nonylphenol 30 EO (NP 30) exposure has also been associated with breast cancer.[2] It has been shown to promote the proliferation of breast cancer cells, due to its agonistic activity on ERα (estrogen receptor α) in estrogen-dependent and estrogen-independent breast cancer cells. Some argue that Nonylphenol 30 EO (NP 30)'s suggested estrogenic effect coupled with its widespread human exposure could potentially influence hormone-dependent breast cancer disease.[34]

Human exposure and breakdown
Exposure
Diet seems the most significant source of exposure of Nonylphenol 30 EO (NP 30) to humans. For example, food samples were found with concentrations ranging from 0.1 to 19.4 µg/kg in a diet survey in Germany and a daily intake for an adult were calculated to be 7.5 µg/day.[35] Another study calculated a daily intake for the more exposed group of infants in the range of 0.23-0.65 µg/ kg bodyweight/ day.[36] In Taiwan, Nonylphenol 30 EO (NP 30) concentrations in food ranged from 5.8 to 235.8 µg/kg. Seafood in particular was found to have a high concentration of Nonylphenol 30 EO (NP 30).[37]

One study conducted in Italian women showed that Nonylphenol 30 EO (NP 30) was one of the highest contaminants at a concentration of 32 ng/mL in breast milk when compared to other alkyl phenols, such as octylphenol, Nonylphenol 30 EO (NP 30) monoethoxylate, and two octylphenol ethoxylates. The study also found a positive correlation between fish consumption and the concentration of Nonylphenol 30 EO (NP 30) in breast milk.[37] This is a large problem because breast milk is the main source of nourishment for newborns, who are in early stages of development where hormones are very influential. Elevated levels of endocrine disruptors in breast milk have been associated with negative effects on neurological development, growth, and memory function.

Drinking water does not represent a significant source of exposure in comparison to other sources such as food packing materials, cleaning products, and various skin care products. Concentrations of Nonylphenol 30 EO (NP 30) in treated drinking water varied from 85 ng/L in Spain to 15 ng/L in Germany.[2]

Microgram amounts of Nonylphenol 30 EO (NP 30) have also been found in the saliva of patients with dental sealants.[34]

Breakdown
When humans orally ingest Nonylphenol 30 EO (NP 30), it is rapidly absorbed in the gastrointestinal tract. The metabolic pathways involved in its degradation are thought to involve glucuronide and sulfate conjugation, and the metabolites are then concentrated in fat. There is inconsistent data on bioaccumulation in humans, but Nonylphenol 30 EO (NP 30) has been shown to bioaccumulate in water-dwelling animals and birds. Nonylphenol 30 EO (NP 30) is excreted in feces and in urine.[3]

Analytics
Since Nonylphenol 30 EO (NP 30)s are ubiquitous in different environmentally relevant matrices like food, drinking water and human tissue samples there are many possible analytical methods for their detection. Most common methods are the analysis with GC-MS. Also as special two-dimensional application with a GCxGC-ToF-MS.[38] Nevertheless, Nonylphenol 30 EO (NP 30)s are also separated via HPLC technics.[39]

As the branching of the nonyl sidechain plays an important role because of their varying estrogen potential different Nonylphenol 30 EO (NP 30)s where synthesized and analyzed on GC-MS or GC-FID systems.[40][41][42][43] In these studies the scope was also on the enantioselective separation of different Nonylphenol 30 EO (NP 30)s since biological systems are usually enantioselective.

Regulation
The production and use of Nonylphenol 30 EO (NP 30) and Nonylphenol 30 EO (NP 30) ethoxylates is prohibited in the European Union due to its effects on health and the environment.[2][44] In Europe, due to environmental concerns, they also have been replaced by more expensive alcohol ethoxylates, which are less problematic for the environment due to their ability to degrade more quickly than Nonylphenol 30 EO (NP 30)s. The European Union has also included NP on the list of priority hazardous substances for surface water in the Water Framework Directive. They are now implementing a drastic reduction policy of NP's in surface waterways. The Environmental quality standard for NP was proposed to be 0.3 ug/l.[2] In 2013 Nonylphenol 30 EO (NP 30)s were registered on the REACH candidate list.

In the US, the EPA set criteria which recommends that Nonylphenol 30 EO (NP 30) concentration should not exceed 6.6 ug/l in fresh water and 1.7 ug/l in saltwater.[45] In order to do so, the EPA is supporting and encouraging a voluntary phase-out of Nonylphenol 30 EO (NP 30) in industrial laundry detergents. Similarly, the EPA is documenting proposals for a "significant new use" rule, which would require companies to contact the EPA if they decided to add Nonylphenol 30 EO (NP 30) to any new cleaning and detergent products. They also plan to do more risk assessments to ascertain the effects of Nonylphenol 30 EO (NP 30) on human health and the environment. It was suggested that Nonylphenol 30 EO (NP 30) could be added to the list of chemicals on the Toxic Substances Control Act of 1976, but this has yet to occur as of 2014.[3]

In other Asian and South American countries Nonylphenol 30 EO (NP 30) is still widely available in commercial detergents, and there is little regulation.

Uses
Nonylphenol 30 EO (NP 30) is an alkylphenol and together with its derivatives, such as trisnonylphenol phosphite (TNP) and nonylphenol polyethoxylates (NPnEO), they are used as additives in the plastic industry, e.g., in polypropylene where nonylphenol ethoxylates are used as hydrophilic surface modifiers or as stabilizer during crystallization of polypropylene to enhance their mechanical properties. They are also used as antioxidant, antistatic agents, and plasticizer in polymers, and as stabilizer in plastic food packaging materials.

Uses
In the preparation of lubricating oil additives, resins, plasticizers, surface active agents.

Uses
Principal use as an intermediate in the production of nonionic ethoxylated surfactants; as an intermediate in the manufacture of phosphite antioxidants used for the plastics and rubber industries

Definition
A mixture of isomeric monoalkyl phenols, predominantly p-substituted.

General Description
A thick, yellowish liquid with a slight phenolic odor. Insoluble in water. Flash point 285°F. Burns although difficult to ignite. May irritate the skin. Used in the manufacture of oil additives, surfactants, fungicide preparations and plastics and rubber.

Air & Water Reactions
Insoluble in water.

Reactivity Profile
Nonylphenol 30 EO behaves as a very weak organic acid. Incompatible with strong reducing substances such as hydrides, nitrides, alkali metals, and sulfides. Flammable gas (H2) is often generated, and the heat of the reaction may ignite the gas. Likely to react exothermically with concentrated sulfuric acid and nitric acid.

Health Hazard
Moderately toxic if swallowed. Severely irritating to skin and eyes.

Fire Hazard
Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Some are oxidizers and may ignite combustibles (wood, paper, oil, clothing, etc.). Contact with metals may evolve flammable hydrogen gas. Containers may explode when heated.

Chemical Reactivity
Reactivity with Water: No reaction; Reactivity with Common Materials: No reaction; Stability During Transport: Stable; Neutralizing Agents for Acids and Caustics: Not pertinent; Polymerization: Not pertinent; Inhibitor of Polymerization: Not pertinent.

Nonylphenol is a toxic xenobiotic compound classified as an endocrine disrupter capable of interfering with the hormonal system of numerous organisms. It originates principally from the degradation of nonylphenol ethoxylates which are widely used as industrial surfactants. Nonylphenol ethoxylates reach sewage treatment works in substantial quantities where they biodegrade into several by-products including nonylphenol. Due to its physical–chemical characteristics, such as low solubility and high hydrophobicity, nonylphenol accumulates in environmental compartments that are characterised by high organic content, typically sewage sludge and river sediments, where it persists. The occurrence of nonylphenol in the environment is clearly correlated with anthropogenic activities such as wastewater treatment, landfilling and sewage sludge recycling. Nonylphenol is found often in matrices such as sewage sludge, effluents from sewage treatment works, river water and sediments, soil and groundwater. The impacts of nonylphenol in the environment include feminization of aquatic organisms, decrease in male fertility and the survival of juveniles at concentrations as low as 8.2 μg/l. Due to the harmful effects of the degradation products of nonylphenol ethoxylates in the environment, the use and production of such compounds have been banned in EU countries and strictly monitored in many other countries such as Canada and Japan. Although it has been shown that the concentration of nonylphenol in the environment is decreasing, it is still found at concentrations of 4.1 μg/l in river waters and 1 mg/kg in sediments. Nonylphenol has been referred to in the list of priority substances in the Water Frame Directive and in the 3rd draft Working Document on Sludge of the EU. Consequently there is currently a concern within some industries about the possibility of future regulations that may impose the removal of trace contaminants from contaminated effluents. The significance of upgrading sewage treatment works with advanced treatment technologies for removal of trace contaminants is discussed.

Alkylphenols are weak estrogenic environmental contaminants and have been implicated in the disruption of endocrine function in wildlife. The influence of biotransformation, tissue distribution, and elimination on biological activity was investigated in juvenile rainbow trout following a single iv dose of [(3)H]Nonylphenol 30 EO (NP 30). Distribution and elimination of [(3)H]Nonylphenol 30 EO (NP 30) residues in tissues sampled 1, 2, 4, 24, 48, 72, and 144 hr after dosing was determined by sample combustion and liquid scintillation counting (LSC). Total 3H-labeled residue concentrations in trout 144 hr after dosing were in order: bile >> feces >> liver > pyloric caeca > kidney > brain, gill, gonad, heart, plasma, skeletal muscle, and skin. The depletion kinetics of [(3)H]residues from tissues and plasma was biphasic with prolonged beta-phase half-lives in muscle and liver of 99 hr. Radio-HPLC analysis of metabolites in bile, liver, pyloric caeca, and feces samples demonstrated similar profiles and contrasted with muscle where only parent compound was found. The predominant metabolite in bile was a glucuronide conjugate of Nonylphenol 30 EO (NP 30). Other metabolites included glucuronide conjugates of ring or side chain hydroxylated Nonylphenol 30 EO (NP 30). Liver contained a low level (1.7%) of covalently bound residues. Metabolism studies using isolated trout hepatocytes produced a similar range of metabolites and a sulfate conjugate of hydroxylated Nonylphenol 30 EO (NP 30). Despite rapid metabolism and excretion, a substantial depot of parent compound remained in muscle which will have implications for the maintenance of Nonylphenol 30 EO (NP 30) residues and associated biological activity.

IDENTIFICATION: Nonylphenol 30 EO (NP 30) is a thick, yellow liquid. It is very slightly to insoluble in water. USE: Nonylphenol 30 EO (NP 30) is used to make lubricating oil additives, resins, plasticizers, fungicides, rubbers and plastics. These products are used in industry, agriculture and in the home. Household products containing Nonylphenol 30 EO (NP 30) include food packaging and rubber items intended for repeated use in contact with food . Nonylphenol 30 EO (NP 30) is a mixture component of nonylphenol which is present in many household maintenance products such as epoxy. Nonylphenols are being phased out of use in consumer products. EXPOSURE: Workers that use Nonylphenol 30 EO (NP 30) may breathe in vapors or have direct skin contact. The general population may be exposed by ingestion of or dermal contact with contaminated water and dermal contact with products containing this compound. Nonylphenol 30 EO (NP 30) has been detected in human breast milk, blood and urine. If Nonylphenol 30 EO (NP 30) is released to the environment, it will be very persistent. It will be broken down in air but is not expected to be broken down by sunlight. It will move slowly into air from moist soil and water surfaces. It is not expected to move through soil. It will be broken down by microorganisms and is expected to build up in fish, animals and humans. RISK: Altered function has been observed in human immune cells exposed to Nonylphenol 30 EO (NP 30) in a laboratory setting. These studies suggest that exposure to Nonylphenol 30 EO (NP 30) may increase the risk of autoimmune diseases, where the body's immune system attacks healthy cells, such as inflammatory bowel disease. However, there are no studies evaluating potential associations between Nonylphenol 30 EO (NP 30) exposure levels in humans and immune function. No additional data on the potential toxic effects of Nonylphenol 30 EO (NP 30) in humans were available. Severe eye damage was observed in laboratory animals following direct exposure. Increased immune responses to known allergens were observed in laboratory animals exposed to Nonylphenol 30 EO (NP 30) via injection, indicating that Nonylphenol 30 EO (NP 30) may aggravate allergic diseases. Data on the potential for Nonylphenol 30 EO (NP 30) to cause infertility, abortion, or birth defects were not available. However, risk factors for obesity (increases in body weight, fat mass and serum cholesterol) were observed in both first and second generation offspring of laboratory animals exposed to oral doses of Nonylphenol 30 EO (NP 30) during pregnancy only. Obesity risk factors were also observed in young laboratory animals directly exposed to Nonylphenol 30 EO (NP 30) via injection. Data on the potential for Nonylphenol 30 EO (NP 30) to cause cancer in laboratory animals were not available. The potential for Nonylphenol 30 EO (NP 30) to cause cancer in humans has not been assessed by the U.S. EPA IRIS program, the International Agency for Research on Cancer, or the U.S. National Toxicology Program 14th Report on Carcinogens.

The two commercial purity grades of Nonylphenol 30 EO (NP 30) are a technical grade which is composed of 10-12% 2-nonylphenol, 85-90% Nonylphenol 30 EO (NP 30), and up to 5% 2,4-dinonylphenol, and a high purity grade which contains 5% maximum 2-nonylphenol, 95% minimum Nonylphenol 30 EO (NP 30), and only a trace of 2,4-dinonylphenol.

A method for the determination of alkylphenols in food using cold solvent extraction with methanol, followed by a two-stage chromatographic purification and GC-MS analysis, was developed. The method was validated and used to measure concentrations of 4-octylphenol and Nonylphenol 30 EO (NP 30) congener totals in UK duplicate diet samples. Individual 4-n-octylphenol and 4-n-nonylphenol congeners were also measured, although these were not detected in any sample. Only one sample showed 4-tert-octylphenol at 8.7 ug/kg, but levels of Nonylphenol 30 EO (NP 30) ranged from not detectable (<3.8 ug/kg) to 25 ug/kg. This concentration range is lower than that reported by others. Tests carried out on the stability of the octyl- and nonylphenol congeners in a duplicate diet matrix over 6 months suggest that some analyte depletion might have occurred during extended frozen storage, which in part may account for the relatively lower concentrations detected, although the extent of usage of these compounds also needs to be taken into consideration.

A novel hyphenated method based on ultrasound-assisted dispersive liquid-liquid microextraction coupled to precolumn derivatization has been established for the simultaneous determination of bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) by high-performance liquid chromatography with fluorescence detection. Different parameters that influence microextraction and derivatization have been optimized. The quantitative linear range of analytes is 5.0-400.0 ng/L, and the correlation coefficients are more than 0.9998. Limits of detection for soft drinks and dairy products have been obtained in the range of 0.5-1.2 ng/kg and 0.01-0.04 ug/kg, respectively. Relative standard deviations of intra- and inter-day precision for retention time and peak area are in the range of 0.47-2.31 and 2.76-8.79%, respectively. Accuracy is satisfactory in the range of 81.5-118.7%. Relative standard deviations of repeatability are in the range of 0.35-1.43 and 2.36-4.75% for retention time and peak area, respectively. Enrichment factors for bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) are 170.5, 240.3, and 283.2, respectively. The results of recovery and matrix effect are in the range of 82.7-114.9 and 92.0-109.0%, respectively. The proposed method has been applied to the determination of bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) in soft drinks and dairy products with much higher sensitivity than many other methods.

The pressurized liquid extraction (PLE) of Nonylphenol 30 EO (NP 30) (4-NP) with methanol (100 degrees C and 100 atm) from river sediments was compared with methanolic Soxhlet extraction, the standard method for the sediment analysis. The PLE method showed a precision (average RSD ranged from 6 to 33%) and an accuracy (average recovery 85 and 87% for 4-NP and 4-NPE, respectively) comparable to those of Soxhlet. The extraction was performed on river sediments and no organic carbon content influence was found. The comparative study presented in this paper demonstrates that PLE is an alternative suitable extraction method for Nonylphenol 30 EO (NP 30) and Nonylphenol 30 EO (NP 30) ethoxylate determination in sediments.

By the combination of solid-phase extraction as well as isotope dilution gas chromatography with mass spectrometry, a sensitive and reliable method for the determination of endocrine-disrupting chemicals including bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) in vegetable oils was established. The application of a silica/N-(n-propyl)ethylenediamine mixed solid-phase extraction cartridge achieved relatively low matrix effects for bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) in vegetable oils. Experiments were designed to evaluate the effects of derivatization, and the extraction parameters were optimized. The estimated limits of detection and quantification for bisphenol A, 4-octylphenol, and Nonylphenol 30 EO (NP 30) were 0.83 and 2.5 ug/kg, respectively. In a spiked experiment in vegetable oils, the recovery of the added bisphenol A was 97.5-110.3%, recovery of the added 4-octylphenol was 64.4-87.4%, and that of Nonylphenol 30 EO (NP 30) was 68.2-89.3%. This sensitive method was then applied to real vegetable oil samples from Zhejiang Province of China, and none of the target compounds were detected.

Pursuant to section 8(d) of TSCA, EPA promulgated a model Health and Safety Data Reporting Rule. The section 8(d) model rule requires manufacturers, importers, and processors of listed chemical substances and mixtures to submit to EPA copies and lists of unpublished health and safety studies. Nonylphenol 30 EO (NP 30) is included on this list. Effective date: 3/29/96; Sunset date: 6/30/98.

Contaminant exposure in aqueous systems typically involves complex chemical mixtures. Given the large number of compounds present in the environment, it is critical to identify hazardous chemical interactions rapidly. The present study utilized a prototype for a novel high-throughput assay to quantify behavioral changes over time to identify chemical interactions that affect toxicity. The independent and combined effects of 2 chemicals, diazinon (an insecticide) and Nonylphenol 30 EO (NP 30) (a detergent metabolite), on the swimming behavior of the freshwater crustacean Daphnia pulex were examined. Cumulative distance and change in direction were measured repeatedly via optical tracking over 90 min. Exposure to low concentrations of diazinon (0.125-2 uM) or Nonylphenol 30 EO (NP 30) (0.25-4 uM) elicited significant concentration- and time-dependent effects on swimming behavior. Exposure to 0.5 uM Nonylphenol 30 EO (NP 30) alone did not significantly alter mean cumulative distance but did elicit a small, significant increase in mean angle, the measure of change in direction. When 0.5 uM Nonylphenol 30 EO (NP 30) was used in combination with diazinon (0.125-0.5 uM), it augmented the adverse impact of diazinon on the swimming behavior of Daphnia. Additionally, enhanced sensitivity to diazinon was observed in animals exposed to treated wastewater effluent for 24 hr prior to a diazinon challenge. The present experiments demonstrate that exposure to Nonylphenol 30 EO (NP 30) and complex chemical mixtures (e.g., treated wastewater) can enhance the toxicity of exposure to the insecticide diazinon.

Nonylphenol 30 EO (NP 30) is a widely diffused and stable environmental contaminant, originating from the degradation of alkyl phenol ethoxylates, common surfactants employed in several industrial applications. Due to its hydrophobic nature, Nonylphenol 30 EO (NP 30) can easily accumulate in living organisms, including humans, where it displays a wide range of toxic effects. Since the gastrointestinal tract represents the main route by which Nonylphenol 30 EO (NP 30) enters the body, the intestine may be one of the first organs to be damaged by chronic exposure to this pollutant through the diet. In the present study, we investigated the effects of Nonylphenol 30 EO (NP 30) on a human intestinal epithelial cell line (Caco-2 cells). We demonstrated that Nonylphenol 30 EO (NP 30) was cytotoxic to cells, as revealed by a decrease of the cell number and the decrement of mitochondrial functionality after 24 hr of treatment. Nonylphenol 30 EO (NP 30) also reduced the number of cells entering into S-phase and interfered with epidermal growth factor signaling, with consequent negative effects on cell survival. In addition, Nonylphenol 30 EO (NP 30) induced apoptosis, involving the activation of caspase-3, and triggered an endoplasmic reticulum-stress response, as revealed by over-expression of GRP78 (78 kDa glucose-regulated protein) and activation of XBP1 (X-box binding protein-1). Together, these findings support the hypothesis that prolonged exposure to Nonylphenol 30 EO (NP 30) through the diet may lead to local damage at the level of intestinal mucosa, with potentially negative consequences for intestinal homeostasis and functionality.

Exogenous substances altering the function of the endocrine system and exhibiting adverse health effects on the organism are defined as endocrine disruptors. Nonylphenol is one of the most abundant alkylphenol ethoxylate derivatives, being detected in food products. Diverse studies have classified nonylphenol as hazardous to the health, especially to male reproduction. This in vitro study aimed to examine the effects of Nonylphenol 30 EO (NP 30) on androstenedione and testosterone production as well as on the viability of Leydig cells of NMRI mice. The cells were cultured for 44 h with addition of 0.04; 0.2; 1.0; 2.5 and 5.0 ug/mL of Nonylphenol 30 EO (NP 30) and compared to the control. Quantification of testosterone and androstenedione directly from aliquots of the medium was performed by enzyme-linked immunosorbent assay. Cell viability was measured by the metabolic activity assay for mitochondrial functional activity. Androstenedione production significantly (P < 0.001) increased with 1.0; 2.5 and 5.0 ug/mL Nonylphenol 30 EO (NP 30). Although cAMP-stimulated testosterone production was not significantly affected by Nonylphenol 30 EO (NP 30), a tendency to attenuate the level of testosterone in the Leydig cells treated with 2.5 and 5.0 ug/mL Nonylphenol 30 EO (NP 30) was observed. The viability of mouse Leydig cells was slightly increased at the lowest doses of Nonylphenol 30 EO (NP 30) (0.04 and 0.2 ug/mL). We also observed an increase at higher concentrations of the substance (1.0; 2.5 and 5.0 ug/mL), but this increase was not significant. Further investigations are required to establish the biological significance and possible reproductive implications.

The uptake and effects of contaminants were measured in the insectivorous tree swallow (Tachycineta bicolor) at a wastewater treatment site. The study examined reproductive, immunological, and growth endpoints in tree swallows exposed to chlorinated hydrocarbon contaminants and to Nonylphenol 30 EO (NP 30) in wastewater lagoons at the Iona Wastewater Treatment Plant, Vancouver (BC, Canada). Clutch size was significantly lower in tree swallows breeding at Iona Island in 2000 and 2001 compared to the reference site. In 2000, fledging success was significantly lower and mean mass of nestling livers was significantly higher in the tree swallows breeding at the Iona Island Wastewater Treatment Plant. Additional factors that may influence reproductive success, such as parental provisioning and diet composition, did not differ significantly between sites. Levels of Nonylphenol 30 EO (NP 30) detected in sediment and insects were elevated at the Iona Island Wastewater Treatment Plant (2000: lagoon sediment 82,000 ng/g dry weight, insects 310 ng/g wet weight; 2001: lagoon sediment 383,900 ng/g dry weight, insects 156 ng/g wet weight) compared to the reference site (2000: pond sediment 1,100 ng/g dry weight, insects not sampled; 2001: pond sediment 642 ng/g dry weight, insects 98 ng/g wet weight). These results indicate that tree swallows might be a useful indicator species for exposure to Nonylphenol 30 EO (NP 30) at wastewater treatment sites; however, further work is necessary to determine the extent of uptake and effects of Nonylphenol 30 EO (NP 30) in riparian insectivorous birds.

The present study investigated in vivo and in vitro effects of environmental relevant concentrations of Nonylphenol 30 EO (NP 30) (100-750 ng/L) on the reproduction of rainbow trout (Oncorhynchus mykiss). To determine the effect of Nonylphenol 30 EO (NP 30) on semen quality rainbow trout were exposed to three concentrations of Nonylphenol 30 EO (NP 30) in a flow-through system during the spawning period (60 days). At an estimated Nonylphenol 30 EO (NP 30) concentration of 750 ng/L semen production was completely inhibited, at 280 and 130 ng/L the semen production was significantly reduced in comparison to the control. Sperm density, sperm motility and sperm fertility were not affected. Also the development of embryos and larvae at the end of yolk sac stage was affected by Nonylphenol 30 EO (NP 30). At estimated Nonylphenol 30 EO (NP 30) exposure levels of 280 and 750 ng/L the percentage of eyed stage embryos was slightly but significantly lower (2-4%) than at 130 ng/L Nonylphenol 30 EO (NP 30) and in the control. At Nonylphenol 30 EO (NP 30) concentrations of 750 ng/L only 23.8 +/- 1.2% of the larvae survived to the end of the yolk sac stage, at 280 ng/L 53.7 +/- 8.2%, at 130 ng/L 73.8 +/- 1.5%, and in the control 70.9 +/- 1.8%. Sperm motility was not affected by Nonylphenol 30 EO (NP 30) as sperm motility rate, swimming velocity, swimming pattern and motility duration were similar in water and in water containing of 100, 250, or 750 ng/L Nonylphenol 30 EO (NP 30). Incubation of eggs in physiological saline solution containing of 100, 250, or 750 ng/L Nonylphenol 30 EO (NP 30) did not change their fertilizability in comparison to the control. Therefore, Nonylphenol 30 EO (NP 30) did not affect the egg viability. Also the fertilization process (sperm egg contact) was not influenced by Nonylphenol 30 EO (NP 30) as the fertilization rate (percentage of hatched larvae) was similar to the control when eggs were fertilized in water containing of 100, 250, or 750 ng/L Nonylphenol 30 EO (NP 30).

Laboratory studies have suggested that some alkylphenols and pesticides elicit developmental toxicity to crustaceans. The purpose of the present study was to evaluate the possibility that the alkylphenol degradation product Nonylphenol 30 EO (NP 30) is embryotoxic to the crustacean Daphnia magna through its known ability to interfere with the metabolic elimination of testosterone. Direct exposure of maternal daphnids to testosterone caused developmental abnormalities in neonates that consisted of partial arrest of early embryonic development and abnormalities in shell spine and first antennae development. Exposure of maternal daphnids to concentrations of Nonylphenol 30 EO (NP 30) also produced developmental abnormalities though the profile of abnormalities was distinct from that observed throughout the testosterone concentration-response curve. Thus, Nonylphenol 30 EO (NP 30) is a developmental toxicant in daphnids, but its toxicity is not consistent with that elicited by elevated testosterone accumulation. Further experiments demonstrated that testosterone was directly toxic to developing embryos, and the maternal organism can serve as the vector for this toxicity. In contrast, neither direct embryo exposure nor early maternal exposure to Nonylphenol 30 EO (NP 30) elicited embryotoxicity consistent with that observed during continuous maternal and gestational exposure. Thus, Nonylphenol 30 EO (NP 30) is not directly embryotoxic at these exposure levels, but rather toxicity is mediated by maternal influences during gestation. The threshold concentration for the occurrence of developmental abnormalities (approximately 44 ug/L) indicates that typical environmental concentrations of Nonylphenol 30 EO (NP 30) pose no imminent hazard with respect to developmental toxicity. However, these effects do occur at sufficiently low levels to warrant evaluation of the relative susceptibility of other crustacean species to this previously uncharacterized mode of toxicity.

Nonylphenol 30 EO (NP 30)'s production and use as a heat and UV costabilizer in plastics, and in the manufacture of alkylphenol ethoxylates may result in its release to the environment through various waste streams. A major source of Nonylphenol 30 EO (NP 30) in the environment is the degradation of these alkylphenol ethoxylates. If released to air, a vapor pressure of 8.18X10-4 mm Hg at 25 °C indicates Nonylphenol 30 EO (NP 30) will exist solely as a vapor in the atmosphere. Vapor-phase Nonylphenol 30 EO (NP 30) will be degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals; the half-life for this reaction in air is estimated to be 7.5 hours. Nonylphenol 30 EO (NP 30) does not absorb at wavelengths >290 nm and, therefore, is not expected to be susceptible to direct photolysis by sunlight. If released to soil, Nonylphenol 30 EO (NP 30) is expected to have no mobility based upon Koc values of 6900-53,300. Volatilization from moist soil surfaces is expected based upon an estimated Henry's Law constant of 3.4X10-5 atm-cu m/mole. However, adsorption to soil is expected to attenuate volatilization. Nonylphenol 30 EO (NP 30) is not expected to volatilize from dry soil surfaces based upon its vapor pressure. Nonylphenol 30 EO (NP 30) is expected to biodegrade rapidly in soil based on degradation of >90% in 20 days; however, the field dissipation half-life of Nonylphenol 30 EO (NP 30) in soils treated with centrifuge dried biosolids and lagoon dried biosolids was 257 and 248 days, respectively. If released into water, Nonylphenol 30 EO (NP 30) is expected to adsorb to suspended solids and sediment based upon the reported Koc values. Based on the biodegradation of Nonylphenol 30 EO (NP 30) in seawater of about 50% after 58 days, Nonylphenol 30 EO (NP 30) is expected to biodegrade in the aqueous environment. Volatilization from water surfaces is expected based upon this compound's estimated Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 1.8 and 17 days, respectively. However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 1.3-9.6 years if adsorption is considered. BCFs of 15-1300 measured in a variety of fish suggest bioconcentration in aquatic organisms is low to very high depending on the species. Hydrolysis is not expected to be an important environmental fate process since this compound lacks functional groups that hydrolyze under environmental conditions (pH 5 to 9). Occupational exposure to Nonylphenol 30 EO (NP 30) may occur through dermal contact with this compound at workplaces where Nonylphenol 30 EO (NP 30) is produced or used. Monitoring data indicate that the general population may be exposed to Nonylphenol 30 EO (NP 30) mainly via ingestion of fish or seafood that have accumulated Nonylphenol 30 EO (NP 30).

Nonylphenol 30 EO (NP 30)'s production and use as a heat and UV stabilizer in plastics(1), and in the manufacture of alkylphenol ethoxylates(2) may result in its release to the environment through various waste streams(SRC). A major source of Nonylphenol 30 EO (NP 30) in the environment is the degradation of these alkylphenol ethoxylates(3).

Based on a classification scheme(1), Koc values of 6900-53,300(2-4) indicate that Nonylphenol 30 EO (NP 30) is expected to be immobile in soil(SRC). Volatilization of Nonylphenol 30 EO (NP 30) from moist soil surfaces is expected(SRC) given an estimated Henry's Law constant of 3.4X10-5 atm-cu m/mole(SRC), based upon its vapor pressure, 8.18X10-4 mm Hg(5), and water solubility, 7 mg/L(6). However, adsorption to soil is expected to attenuate volatilization(SRC). Nonylphenol 30 EO (NP 30) is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(5). Nonylphenol 30 EO (NP 30) is expected to biodegrade rapidly in soil based on degradation of >90% in 20 days(6); however, the field dissipation half-life of Nonylphenol 30 EO (NP 30) in soils treated with centrifuge dried biosolids and lagoon dried biosolids was 257 and 248 days, respectively(7).

According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), Nonylphenol 30 EO (NP 30), which has a vapor pressure of 8.18X10-4 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase Nonylphenol 30 EO (NP 30) is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7.5 hours(SRC), calculated from its rate constant of 5.2X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Nonylphenol 30 EO (NP 30) does not absorb at wavelengths >290 nm(4) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

 Biodegradation of Nonylphenol 30 EO (NP 30) in seawater at a concentration of 11 ug/L was initially slow but after four weeks at 11 °C, the degradation rate increased and after 58 days, about 50% of the initial Nonylphenol 30 EO (NP 30) was present(1). Seawater and the presence of sediment did not increase the biodegradation rate, with approximately 60% of the initial Nonylphenol 30 EO (NP 30) remaining after 58 days(1). The concentration of Nonylphenol 30 EO (NP 30) in grey water samples was reduced from 0.8-38 ug/L to less than reporting limit to 3.5 ug/L under aerobic conditions(2). Nonylphenol 30 EO (NP 30) decomposed rapidly in soil with rates of 1.953 and 49.72 mg/kg/day at starting concentrations of 10 and 500 mg/kg, respectively; >90% was degraded within 10 and 20 days, respectively(3). In soil, incubated for 58 days at 20 °C in the dark, Nonylphenol 30 EO (NP 30) biodegraded at a rate of 0.58/day with a half-life of 1.4 days(4).

The rate constant for the vapor-phase reaction of Nonylphenol 30 EO (NP 30) with photochemically-produced hydroxyl radicals has been estimated as 5.2X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 7.5 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Nonylphenol 30 EO (NP 30) is not expected to undergo hydrolysis in the environment due to the lack of functional groups that hydrolyze under environmental conditions(2). Nonylphenol 30 EO (NP 30) does not absorb at wavelengths >290 nm(3) and, therefore, is not expected to be susceptible to direct photolysis by sunlight(SRC).

The Henry's Law constant for Nonylphenol 30 EO (NP 30) is estimated as 3.4X10-5 atm-cu m/mole(SRC) derived from its vapor pressure, 8.18X10-4 mm Hg(1), and water solubility, 7 mg/L(2). This Henry's Law constant indicates that Nonylphenol 30 EO (NP 30) is expected to volatilize from water surfaces(3). Based on this Henry's Law constant, the volatilization half-life from a model river (1 m deep, flowing 1 m/sec, wind velocity of 3 m/sec)(3) is estimated as 1.8 days(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(3) is estimated as 17 days(SRC). However, volatilization from water surfaces is expected to be attenuated by adsorption to suspended solids and sediment in the water column. The estimated volatilization half-life from a model pond is 1.3-9.6 years if adsorption is considered(4). Nonylphenol 30 EO (NP 30)'s estimated Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Nonylphenol 30 EO (NP 30) is not expected to volatilize from dry soil surfaces(SRC) based upon its vapor pressure(1).

SURFACE WATER: Whole water samples from the lower Tennessee River below the Calvert City, Kentucky chemical complex had Nonylphenol 30 EO (NP 30) concentrations of 325 ppb(1). Nonylphenol 30 EO (NP 30) has been qualitatively identified in Mill Creek in Georgia(2). Nonylphenol 30 EO (NP 30) was detected at 0.510-1.200 ug/L in 29% of samples from 18 streams in north-central and northwestern Arkansas, samples were collected March, April and August of 2004(3). Nonylphenol 30 EO (NP 30) was detected at 860 and 620 ng/L in surface water samples collected 2.1 and 10 km downstream from a waste water effluent point on the Redwood River, MN; it was detected at 240 ng/L in samples collected upstream(4). Seawater samples collected 2008 and 2009 from 5 sites in Morro Bay, CA contained Nonylphenol 30 EO (NP 30) at 0.1-0.9 ug/L(5). Surface water samples collected in 2002 from 6 locations of Cootes Paradise, Ontario, Canada contained Nonylphenol 30 EO (NP 30) at <0.01-0.258 ug/L(6).

The concentration of Nonylphenol 30 EO (NP 30) in 30 anaerobically and 8 aerobically stabilized sludge samples was 0.45-2.53 and 0.08-0.5 g/kg, respectively(1). Nonylphenol 30 EO (NP 30) has been detected in effluents from the nonferrous metals industry (3 ng/uL extract) and the organic chemicals industry (187 ng/uL extract) in the US(2). Nonylphenol 30 EO (NP 30) has been qualitatively identified in a textile finishing plant effluent from North Carolina(3). Nonylphenol 30 EO (NP 30) was detected at 220 ng/L in effluent samples collected from a waste water treatment plant on the Redwood River, MN(4). The mean concentrations of Nonylphenol 30 EO (NP 30) in final effluent from a water reclamation facility in Los Angeles, CA was 124 ng/L in samples collected Oct of 2009(5). Effluent samples collected in 2002 from a wastewater treatment plant in Ontario, Canada contained Nonylphenol 30 EO (NP 30) at 0.286 ug/L(6).

Nonylphenol 30 EO (NP 30) was detected in 72% of sediment samples collected in 1989 from 30 US rivers at <2.9-2960 ug/kg with an average of 162 ug/kg(1). Sediment samples collected 2008 and 2009 from 5 sites in Morro Bay, CA contained Nonylphenol 30 EO (NP 30) at not detected to 157 ng/g dry weight(2). Nonylphenol 30 EO (NP 30) was detected at 100 and 140 ug/kg in sediment samples collected 2.1 and 10 km downstream from a waste water effluent point on the Redwood River, MN; it was not detected (detection limit 100 ug/kg) in samples collected upstream(3). Nonylphenol 30 EO (NP 30) was detected at <0.01-1.75 ug/g in 21 surface sediment samples collected 2001-2002 from 6 locations of Cootes Paradise, Ontario, Canada(4). The mean concentration of Nonylphenol 30 EO (NP 30) was 190 and 130 ng/g dry weight in sediment samples collected Nov 2003 from Tai-shi and Chi-ku, Taiwan, respectively(5).

Nonylphenol 30 EO (NP 30) was detected in 35 of 75 household food detergents purchased from major supermarkets and local stores in Taiwan at not detected to 76.3 ng/g. Porcelain, glass and melamine dishware washed at varying temperatures and cleaning times contained Nonylphenol 30 EO (NP 30) residues of <0.18-2.38, <0.18-3.71 and <0.18-1.32 ug/L, respectively(1).

NIOSH (NOES Survey 1981-1983) has statistically estimated that 16,739 workers (3822 of these are female) were potentially exposed to Nonylphenol 30 EO (NP 30) in the US(1). Occupational exposure to Nonylphenol 30 EO (NP 30) may occur through dermal contact with this compound at workplaces where Nonylphenol 30 EO (NP 30) is produced or used. Monitoring data indicate that the general population may be exposed to Nonylphenol 30 EO (NP 30) mainly via ingestion of fish or seafood that has accumulated Nonylphenol 30 EO (NP 30)(SRC).

Nonylphenol 30 EO (NP 30) was detected in 51% of 371 urine samples collected in the US with a median concentration of <0.1 ug/L(1). Nonylphenol 30 EO (NP 30) was detected in adipose, liver and brain tissue of eleven autopsy patients in 2002 in Antwerp, Belgium at <0.004-0.161, <0.003-1.401 and <0.004-0.009 ng/g wet weight, respectively(2). In hair samples collected from 42 people residing in Pomerania, Poland, Nonylphenol 30 EO (NP 30) was detected at 5.4-23,829.5 ng/g dry weight(3). Nonylphenol 30 EO (NP 30) was detected in three Japanese human milk samples at 0.65-1.4 ng/g(4).