pyrrole

H226 (10.7%): Flammable liquid and vapor [Warning Flammable liquids]

H302 (89.3%): Harmful if swallowed [Warning Acute toxicity, oral]

P210, P233, P240, P241, P242, P243, P264, P270, P280, P301+P317, P303+P361+P353, P330, P370+P378, P403+P235, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 1442 reports by companies from 11 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

H226: Flammable liquid and vapor [Warning Flammable liquids]

P210, P233, P240, P241, P242, P243, P280, P303+P361+P353, P370+P378, P403+P235, and P501 (click each P-code to see the statement)

FOAM, CARBON DIOXIDE, DRY CHEMICAL.

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.

0.32 [mg/m3]

3.5 [mg/m3]

21 [mg/m3]

IN VIEW OF THE COMPOUND'S RELATIVELY LOW TOXICITY, ORDINARY HANDLING PRECAUTIONS INCLUDING USE OF GLOVES & GOOD VENTILATION ARE ADEQUATE TO PREVENT INJURY.

Colorless liquid with an agreeable odor like chloroform; Darkens on standing if oxygen not completely removed; [Merck Index] Yellowish or brown liquid; Turns brown when polymerized by light; [Hawley] Hygroscopic; [HSDB] Colorless liquid; [MSDSonline]

Colourless to yellowish liquid; Nutty, sweet, warm, ethereal aroma

Colorless liquid when fresh

Yellowish or brown oil

Agreeable empyreumatic odor resembling that of chloroform

Burning, pungent taste

129.7 °C

130.00 to 131.00 °C. @ 760.00 mm Hg

130-131 °C

129.7 °C @760 [mm Hg]

-23.4 °C

102 °F (39 °C) (CLOSED CUP)

Soluble in alcohol, ether and dilute acids. Also soluble in most organic chemicals.

Water solubility: 4.5X10+4 mg/l @ 25 °C

45 mg/mL at 25 °C

Soluble in most fixed oils; Slightly soluble in water

Soluble (in ethanol)

0.9698 @ 20 °C

0.955-0.975

0.9698 @ 20°C

2.31 (Air= 1)

8.36 [mmHg]

8.35 mm Hg @ 25 dec C

8.35 [mm Hg] @25 °C

log Kow = 0.75

Henry's Law constant = 1.80X10-5 atm-cu m/mol @ 25 °C

DARKENS ON STANDING WITH EXPOSURE TO AIR.

WHEN HEATED TO DECOMPOSITION IT EMITS HIGHLY TOXIC FUMES OF NITROXIDES.

4.1123X10-3 Pa.s @ 249.74K

-2.2418X10+9 J/kmol

10.79 kcla/mol @ 25 °C

4.3079X10+2 N/m @ 249.74K

Index of refraction: 1.5085 @ 20 °C/D

1.507-1.510

pKa= 17.5

pKa = -3.80 (protonated form) (conjugate acid)

Polymerizes under influence of acids and glycols; soln in dil hydrogen chloride yield pyrrole red, an amorphous, orange-colored substance

Decomposes in acid; Conversion factors: 1 mg/l= 3.64 ppm; 1 ppm= 2.74 mg/cu m

Hydroxyl radical rate constant = 1.1X10-10 cu m/molc-sec @ 25 °C

Hygroscopic

... CAN REACT WITH OXIDIZING MATERIALS.

Violent reaction with 2-nitrobenzaldehyde.

Neurotoxin - Other CNS neurotoxin

Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation.

LC50 (rat) = 2,270 mg/m3/4h

LD50 Mouse sc 61 mg/kg

LD50 Mouse ip 98 mg/kg

...PERSONS WITH ABNORMAL RESPIRATORY, CIRCULATORY OR LIVER CONDITIONS SHOULD NOT BE EXPOSED TO THIS SUBSTANCE.

IT HAS A DEPRESSANT ACTION ON THE CENTRAL NERVOUS SYSTEM AND, IN SEVERE INTOXICATION, IS INJURIOUS TO THE LIVER.

NO CASES OF OCCUPATIONAL DISEASE DUE TO PYRROLE HAVE BEEN REPORTED; HOWEVER TESTS INDICATE THAT IT HAS A MODERATE CUMULATIVE TOXICITY.

INTRAPERITONEAL INJECTIONS OF LARGE DOSES INTO DOGS CAUSED CONVULSIONS & LIVER INJURY. PYRROLE GENERALLY CAUSES DISCOLORATION OF URINE, & LUNG & LIVER INJURY IN MAMMALS. DEATH FOLLOWING LARGE DOSES IS ACCOMPANIED BY ACUTE EMPHYSEMA & PULMONARY STASIS.

Exposure to the gamma-diketone, 2,5-hexanedione, results in the accumulation of neurofilaments within the distal axon and is associated with acceleration of neurofilament transport within the proximal axon. The epsilon-amino groups of lysyl residues react with 2,5-hexanedione forming pyrrole adducts, followed by pyrrole-mediated protein crosslinking. Both reaction steps have been proposed as mechanisms causing neurofilament accumulation and acceleration of transport. In order to assess the importance of steps on neurofilament transport, we compared transport in the optic system of rats exposed to 2,5-hexanedione and 3-acetyl-2,5-hexanedione, a non-toxic analog of 2,5-hexanedione which forms pyrroles but does not crosslink proteins. Control, 2,5-hexanedione-treated, and 3-acetyl-2,5-hexanedione-treated rats received intraoptic injections of (35S)-methionine and were exposed to saline, 2,5-hexanedione, or 3-acetyl-2,5-hexanedione by intraperitoneal injections before and during the period of neurofilament transport. Neurofilament triplet proteins in the optic nerve and tract were identified by polyacrylamide gel electrophoresis followed by fluorography. The rate of neurofilament transport was accelerated in 2,5-hexanedione-treated animals over that of controls. However, despite higher levels of protein-bound pyrroles in 3-acetyl-2,5-hexanedione-treated animals, the rate of transport was indistinguishable from that of controls. These findings indicate that pyrrole formation alone is not sufficient to cause acceleration of neurofilament transport.

Glutathione S-transferase expression was examined in hepatic cytosol from rats and rabbits treated with 4-picoline, pyrrole, pyridine, pyrazine, imidazole, or piperidine using enzymatic activity, SDS-PAGE, and immunoblot analyses and the results were compared to those obtained with phenobarbital and 3-methylcholanthrene. SDS-PAGE and immunoblot analyses of hepatic cytosol prepared from rats treated with pyrazine revealed the induction of class alpha (Ya and Yc) and mu (Yb) bands with a corresponding 2.4-fold increase in metabolic activity using 1-chloro-2,4-dinitrobenzene as substrate. A new class alpha band migrating in the region of the Yc band was observed in the SDS-PAGE and detected in the immunoblot of cytosol from pyrrole-treated rats, whereas treatment with 4-picoline, imidazole, or piperidine failed to alter the expression of the major classes of glutathione S-transferase isozymes in this species. SDS-PAGE and immunoblot analyses of rabbit hepatic cytosol revealed a unique species-dependent difference in the expression of glutathione S-transferases. While phenobarbital and 3-methylcholanthrene induce class alpha and mu glutathione S-transferase expression in rat hepatic cytosol, one of the most interesting observations was that neither of these agents stimulated glutathione S-transferase expression in the rabbit. Immunoblot analysis of cytosol isolated from 4-picoline-treated rabbits using glutathione S-transferase class alpha-specific IgG showed the appearance of a novel class alpha 28-kDa glutathione S-transferase band and the concomitant disappearance of a class alpha 29-kDa glutathione S-transferase band. SDS-PAGE and immunoblot analyses showed that treatment of rabbits with pyrrole,pyrazine, imidazole, or piperidine resulted in the disappearance of this class alpha 29-kDa glutathione S-transferase band with no detectable expression of the class alpha 28-kDa glutathione S-transferase band; the level of the class alpha 29-kDa band was unaffected by pyridine treatment. In contrast, immunoblot analyses of hepatic cytosol revealed that a 25.5-kDa class mu glutathione S-transferase band disappeared following treatment with pyridine, but was unaffected by treatment other than nitrogen heterocycles. The Vmax of glutathione conjugation to the substrate 1-chloro-2,4-dinitrobenzene decreased by 52, 36, 59, 41, 37, and 32% in hepatic cytosol isolated from 4-picoline, pyrrole-, pyridine, pyrazine-, imidazole-, and piperidine-treated rabbits, respectively. The results suggest that nitrogen heterocycles differ in their ability to modulate glutathione-S-transferase isozyme expression in rat and rabbit hepatic tissue and that rabbit hepatic glutathione S-transferases are refractory to induction by agents such as pyrazine, phenobarbital, or 3-methylcholanthrene and hence these xenobiotics do not appear to be bifunctional inducers in this species.

The effect was studied of such mutagens as 3-amino-1-dimethyl-5H-pyridol(4,3-b)indole, N-methyl-N'-nitro-N-nitrosoguanidine, 2-(2-furyl)-3-(5-nitro-2-furyl)-acrylamide, 5-hydroxymethyl-2-furfural (HMF) and pyrrole on the viability and activity of some enzymes of a human histiocytic lymphoma cell line, U-937, cultured in a serum-free medium. Incubation of U-937 with the mutagens for 12 hr at approx 37 °C in the serum-free medium reduced the viability of the U-937 cells. Especially, 3-amino-1-dimethyl-5H-pyridol(4,3-b)indole and N-methyl-N'-nitro-N-nitrosoguanidine reduced it markedly. 3-Amino-1-dimethyl-5H-pyridol(4,3-b)indole, N-methyl-N'-nitro-N-nitrosoguanidine, 2-(2-furyl)-3-(5-nitro-2-furyl)-acrylamide and 5-hydroxymethyl-2-furfural were also found to decrease the formation of formazan in the U-937 cells. All the mutagens slightly increased the activity of a drug-metabolizing enzyme, NADPH-cytochrome c reductase, in the cells. They also caused a variation of such enzyme activities in the cells as glutamic oxaloacetic transaminase, catalase and alkaline phosphatase. Leakage of the activities of NADPH-cytochrome c reductase and glutamic oxaloacetic transaminase from the U-937 cells into the culture medium was also observed, especially when the cells were treated with high concentration of 3-amino-1-dimethyl-5H-pyridol(4,3-b)indole, N-methyl-N'-nitro-N-nitrosoguanidine and 2-(2-furyl)-3-(5-nitro-2-furyl)-acrylamide. No marked effect of 3-amino-1-dimethyl-5H-pyridol(4,3-b)indole and N-methyl-N'-nitro-N-nitrosoguanidine on the activity of beta-galactosidase was observed.

For more Non-Human Toxicity Excerpts (Complete) data for PYRROLE (7 total), please visit the HSDB record page.

Pyrrole's production and presence in creosote and in drug manufacturing may result in its release to the environment through various waste streams. If released to air, a vapor pressure of 8.35 mm Hg at 25 °C indicates pyrrole will exist solely as a vapor in the ambient atmosphere. Vapor-phase pyrrole 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 4 days. Pyrrole does not absorb light in the environmental UV spectrum, and is not expected to directly photolyze. If released to soil, pyrrole is expected to have high mobility based upon an estimated Koc of 61. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 1.80X10-5 atm-cu m/mole. Pyrrole may potentially volatilize from dry soil surfaces based upon its vapor pressure. If released into water, pyrrole is not expected to adsorb to suspended solids and sediment in the water column based upon the estimated Koc. Pyrrole does not readily undergo biodegradation in water unless there exists bacteria that have had previous exposure to pyrrole. Given this need for acclimation, the decomposition of pyrrole may be very slow. Volatilization from water surfaces is expected to be an important fate process based upon this compound's Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 42 hours and 368 hours, respectively. An estimated BCF of 2 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to occur due to the lack of hydrolyzable functional groups. Occupational exposure to pyrrole may occur through inhalation, and dermal contact with this compound at workplaces where pyrrole is produced or used. The general population may be exposed to pyrrole through the consumption of food and use of creosote. (SRC)

Pyrrole's production and presence in creosote(1), chemical intermediate in drug manufacturing(2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 61(SRC), determined from a log Kow of 0.75(2) and a regression-derived equation(3), indicates that pyrrole is expected to have high mobility in soil(SRC). Volatilization of pyrrole from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 1.8X10-5 atm-cu m/mole(4). The potential for volatilization of pyrrole from dry soil surfaces may exist(SRC) based upon a vapor pressure of 8.35 mm Hg(5). Pyrrole does not readily undergo biodegradation in water unless there exists bacteria that have had previous exposure to pyrrole. Given this need for acclimation, the decomposition of pyrrole may be very slow(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 61(SRC), determined from a log Kow of 0.75(2), indicates that pyrrole is not expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from water sources is expected(3) based upon a Henry's Law constant of 1.80X10-5 atm-cu m/mole(4). Volatilization half-lives for a model river and model lake are 42 hrs and 368 hrs, respectively(SRC), using an estimation method(3). According to a classification scheme(5), an estimated BCF of 2(3,SRC) from a log Kow of 0.75(2) suggests the potential for bioconcentration in aquatic organisms is low. Experiments have shown that pyrrole is actually degraded by gasoline-adapted ground water cultures when present as a single substrate. Adaption time was 480 hrs and degradation time was 600 hrs(6). Pyrrole was not degraded in a mixture of compounds in water after 1100-1300 hrs at 10 °C and at a concentration of 0.2-1 mg/l(6).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pyrrole, which has a vapor pressure of 8.35 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase pyrrole 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 4 days(SRC) from its rate constant of 1X10-10 cu cm/molecule sec(3). In a comparison of room temperature rate constants and loss rates of selected organics in the presence of 7.2X10+11 molecule/cu cm of ozone, 5X10+5 molecule/cu cm of hydroxyl radicals, and 2.4X10+8 molecules/cu cm of NO3 radicals, pyrrole displayed the following rate constants: 1.6X10-17 cu cm/molecule sec with a loss rate of 1 day, 1.2X10-11 cu cm/molecule sec with a loss rate of 5.2 days, and 4.9X10-11 cu cm/molecule sec with a loss rate of 1000 days, respectively(4).

AEROBIC: Pyrrole was not degraded in a mixture of compounds in water after 1100-1300 hrs at 10 °C and at a concentration of 0.2-1 mg/l. Experiments have shown that pyrrole is actually degraded by gasoline-adapted ground water cultures when present as a single substrate. Adaption time was 480 hrs and degradation time was 600 hrs. Pyrrole inhibits benzene biodegradation strongly even at pyrrole concentrations of 100-200 ug/l(1). Degradation of pyrrole seems to be enhanced with the concomitant degradation of other compounds in an aqueous environment. No degradation of pyrrole was observed under denitrifying conditions during 846 days of incubation(2). In an aerobic enrichment culture that originated from groundwater at a creosote-contaminated aquifer in Fredensbury Denmark, pyrrole was completely removed after 49 days. It is suggested that microorganisms have to adapt to pyrrole before they can begin to degrade it and that the lag phase can be very long(3).

ANAEROBIC: Anaerobic research of pyrrole using primary digestive sludge, having an average inflow of 100 cu m/day and a mean retention time of 20 days, displayed negative gas production during the first 11 weeks of incubation. This corresponds to no biodegradation of pyrrole under anaerobic conditions(1).

The rate constant for the vapor-phase reaction of pyrrole with photochemically-produced hydroxyl radicals is 1X10-10 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 4 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Pyrrole is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2) nor to directly photolyze due to the lack of absorption in the environmental UV spectrum (>290 nm). A rate constant of 8.71X10+9 mole-1 sec-1 with hydroxyl radicals in aqueous solution was estimated for pyrrole using structure-reactivity relationships (SRR) and linear free-energy relationships (LFER)(3). The -log of the rate constant of pyrrole reacting with nitrate radical in the gas phase at 298 K is 10.338(4) with a half life of 3.62 sec(SRC) assuming a concentration of 1.5X10+13 in the ambient environment under dark conditions(5).

An estimated BCF of 2 was calculated for pyrrole(SRC), using a log Kow of 0.75(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low.

The Koc of pyrrole is estimated as approximately 61(SRC), using a log Kow of 0.75(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that pyrrole is expected to have high mobility in soil.

The Henry's Law constant for pyrrole is 1.8X10-5 atm-cu m/mole(1). This Henry's Law constant indicates that pyrrole is expected to volatilize from water surfaces(2). 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)(2) is estimated as approximately 42 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as approximately 368 hours(SRC). Pyrrole's Henry's Law constant(1) indicates that volatilization from moist soil surfaces may occur(SRC). The potential for volatilization of pyrrole from dry soil surfaces may exist(SRC) based upon a vapor pressure of 8.35 mm Hg(3).

GROUNDWATER: Pyrrole was detected in 1 of 5 groundwater samples collected from Fredericia(Jutland) Denmark in 1992 at a concentration of 0.22 ug/l(1). Pyrrole is introduced into groundwater through the use of creosote on wooden electric poles(2).

Results of a study of several sites show that prior to coal gasification by ground water, pyrrole was not detected (limits of detection were 0.1 ppb). However, once coal gasification began, pyrrole was detected at 208 ppm in Hanna, Wyoming and 111 ppm Gillete, Wyoming. Pyrrole was not detected from low-Btu gasification of Rosebud coal but was detected at 23 ppm from an in situ oil shale process (limits of detection were 0.1 ppb)(1). Two retort wastewaters selected for study were produced from January to May, 1979 in the modified in situ retort 6 at the Occidental Oil Shale, Inc. facility at Logan Wash, CO. In the condensate retort water, 4.9 mg/l of pyrrole was detected while no pyrrole was detected at the process retort water (detection limits not specified)(2). Pyrrole was detected from shale oil wastewaters used to cool hot spent shale, both in gas condensate water and process retort water units not specified(3).

Pyrrole is a constituent of creosote which is a compound used as a wood preservative, especially in electric poles. Due to this, pyrrole may be found in soil in locations where creosote has been used(1).

SOURCE DOMINATED: Pyrrole was detected at <1 ng/ml of air above 1 ml of water in 10 ml samples from two process retort wastewaters collected at Laramie Energy Technology Center during May 1982 and at the Logan Wash site of Occidental Oil Shale Inc. during December 1987; it was also detected in the gas-condensate retort wastewaters at 3.1 and 5.0 ng/ml of air above 1 ml of water at both sites(1). Pyrrole has been found in stock emission during incineration of municipal waste units not specified(2). URBAN/SUBURBAN: Pyrrole was not detected in ambient air at either Logan Wash, CO or at Boulder, CO(1).

Pyrrole has been detected in "popped" popcorn at a level of 26 ug/kg in a dry capture method and 44 ug/kg in a wet capture method(1). Fresh chicken breast with bone was cut into 1.5 inch cubes, coated with flour and fried in Fri-al shortening. During a 48 hour period in which the chicken was fried, pyrrole was detected (detection level not specified)(2).

Occupational exposure to pyrrole may occur through inhalation and dermal contact with this compound at workplaces where pyrrole is produced or used. The general population may be exposed to pyrrole via ingestion of food, and dermal contact with this compound and creosote containing pyrrole. (SRC)

Pyrrole's production and presence in creosote and in drug manufacturing may result in its release to the environment through various waste streams. If released to air, a vapor pressure of 8.35 mm Hg at 25 °C indicates pyrrole will exist solely as a vapor in the ambient atmosphere. Vapor-phase pyrrole 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 4 days. Pyrrole does not absorb light in the environmental UV spectrum, and is not expected to directly photolyze. If released to soil, pyrrole is expected to have high mobility based upon an estimated Koc of 61. Volatilization from moist soil surfaces is expected to be an important fate process based upon a Henry's Law constant of 1.80X10-5 atm-cu m/mole. Pyrrole may potentially volatilize from dry soil surfaces based upon its vapor pressure. If released into water, pyrrole is not expected to adsorb to suspended solids and sediment in the water column based upon the estimated Koc. Pyrrole does not readily undergo biodegradation in water unless there exists bacteria that have had previous exposure to pyrrole. Given this need for acclimation, the decomposition of pyrrole may be very slow. Volatilization from water surfaces is expected to be an important fate process based upon this compound's Henry's Law constant. Estimated volatilization half-lives for a model river and model lake are 42 hours and 368 hours, respectively. An estimated BCF of 2 suggests the potential for bioconcentration in aquatic organisms is low. Hydrolysis is not expected to occur due to the lack of hydrolyzable functional groups. Occupational exposure to pyrrole may occur through inhalation, and dermal contact with this compound at workplaces where pyrrole is produced or used. The general population may be exposed to pyrrole through the consumption of food and use of creosote. (SRC)

Pyrrole's production and presence in creosote(1), chemical intermediate in drug manufacturing(2) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 61(SRC), determined from a log Kow of 0.75(2) and a regression-derived equation(3), indicates that pyrrole is expected to have high mobility in soil(SRC). Volatilization of pyrrole from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 1.8X10-5 atm-cu m/mole(4). The potential for volatilization of pyrrole from dry soil surfaces may exist(SRC) based upon a vapor pressure of 8.35 mm Hg(5). Pyrrole does not readily undergo biodegradation in water unless there exists bacteria that have had previous exposure to pyrrole. Given this need for acclimation, the decomposition of pyrrole may be very slow(6).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 61(SRC), determined from a log Kow of 0.75(2), indicates that pyrrole is not expected to adsorb to suspended solids and sediment in water(SRC). Volatilization from water sources is expected(3) based upon a Henry's Law constant of 1.80X10-5 atm-cu m/mole(4). Volatilization half-lives for a model river and model lake are 42 hrs and 368 hrs, respectively(SRC), using an estimation method(3). According to a classification scheme(5), an estimated BCF of 2(3,SRC) from a log Kow of 0.75(2) suggests the potential for bioconcentration in aquatic organisms is low. Experiments have shown that pyrrole is actually degraded by gasoline-adapted ground water cultures when present as a single substrate. Adaption time was 480 hrs and degradation time was 600 hrs(6). Pyrrole was not degraded in a mixture of compounds in water after 1100-1300 hrs at 10 °C and at a concentration of 0.2-1 mg/l(6).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), pyrrole, which has a vapor pressure of 8.35 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase pyrrole 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 4 days(SRC) from its rate constant of 1X10-10 cu cm/molecule sec(3). In a comparison of room temperature rate constants and loss rates of selected organics in the presence of 7.2X10+11 molecule/cu cm of ozone, 5X10+5 molecule/cu cm of hydroxyl radicals, and 2.4X10+8 molecules/cu cm of NO3 radicals, pyrrole displayed the following rate constants: 1.6X10-17 cu cm/molecule sec with a loss rate of 1 day, 1.2X10-11 cu cm/molecule sec with a loss rate of 5.2 days, and 4.9X10-11 cu cm/molecule sec with a loss rate of 1000 days, respectively(4).

AEROBIC: Pyrrole was not degraded in a mixture of compounds in water after 1100-1300 hrs at 10 °C and at a concentration of 0.2-1 mg/l. Experiments have shown that pyrrole is actually degraded by gasoline-adapted ground water cultures when present as a single substrate. Adaption time was 480 hrs and degradation time was 600 hrs. Pyrrole inhibits benzene biodegradation strongly even at pyrrole concentrations of 100-200 ug/l(1). Degradation of pyrrole seems to be enhanced with the concomitant degradation of other compounds in an aqueous environment. No degradation of pyrrole was observed under denitrifying conditions during 846 days of incubation(2). In an aerobic enrichment culture that originated from groundwater at a creosote-contaminated aquifer in Fredensbury Denmark, pyrrole was completely removed after 49 days. It is suggested that microorganisms have to adapt to pyrrole before they can begin to degrade it and that the lag phase can be very long(3).

ANAEROBIC: Anaerobic research of pyrrole using primary digestive sludge, having an average inflow of 100 cu m/day and a mean retention time of 20 days, displayed negative gas production during the first 11 weeks of incubation. This corresponds to no biodegradation of pyrrole under anaerobic conditions(1).

The rate constant for the vapor-phase reaction of pyrrole with photochemically-produced hydroxyl radicals is 1X10-10 cu cm/molecule-sec at 25 °C(1). This corresponds to an atmospheric half-life of about 4 days at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Pyrrole is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2) nor to directly photolyze due to the lack of absorption in the environmental UV spectrum (>290 nm). A rate constant of 8.71X10+9 mole-1 sec-1 with hydroxyl radicals in aqueous solution was estimated for pyrrole using structure-reactivity relationships (SRR) and linear free-energy relationships (LFER)(3). The -log of the rate constant of pyrrole reacting with nitrate radical in the gas phase at 298 K is 10.338(4) with a half life of 3.62 sec(SRC) assuming a concentration of 1.5X10+13 in the ambient environment under dark conditions(5).

An estimated BCF of 2 was calculated for pyrrole(SRC), using a log Kow of 0.75(1). According to a classification scheme(2), this BCF suggests the potential for bioconcentration in aquatic organisms is low.

The Koc of pyrrole is estimated as approximately 61(SRC), using a log Kow of 0.75(1) and a regression-derived equation(2). According to a classification scheme(3), this estimated Koc value suggests that pyrrole is expected to have high mobility in soil.

The Henry's Law constant for pyrrole is 1.8X10-5 atm-cu m/mole(1). This Henry's Law constant indicates that pyrrole is expected to volatilize from water surfaces(2). 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)(2) is estimated as approximately 42 hours(SRC). The volatilization half-life from a model lake (1 m deep, flowing 0.05 m/sec, wind velocity of 0.5 m/sec)(2) is estimated as approximately 368 hours(SRC). Pyrrole's Henry's Law constant(1) indicates that volatilization from moist soil surfaces may occur(SRC). The potential for volatilization of pyrrole from dry soil surfaces may exist(SRC) based upon a vapor pressure of 8.35 mm Hg(3).

GROUNDWATER: Pyrrole was detected in 1 of 5 groundwater samples collected from Fredericia(Jutland) Denmark in 1992 at a concentration of 0.22 ug/l(1). Pyrrole is introduced into groundwater through the use of creosote on wooden electric poles(2).

Results of a study of several sites show that prior to coal gasification by ground water, pyrrole was not detected (limits of detection were 0.1 ppb). However, once coal gasification began, pyrrole was detected at 208 ppm in Hanna, Wyoming and 111 ppm Gillete, Wyoming. Pyrrole was not detected from low-Btu gasification of Rosebud coal but was detected at 23 ppm from an in situ oil shale process (limits of detection were 0.1 ppb)(1). Two retort wastewaters selected for study were produced from January to May, 1979 in the modified in situ retort 6 at the Occidental Oil Shale, Inc. facility at Logan Wash, CO. In the condensate retort water, 4.9 mg/l of pyrrole was detected while no pyrrole was detected at the process retort water (detection limits not specified)(2). Pyrrole was detected from shale oil wastewaters used to cool hot spent shale, both in gas condensate water and process retort water units not specified(3).

Pyrrole is a constituent of creosote which is a compound used as a wood preservative, especially in electric poles. Due to this, pyrrole may be found in soil in locations where creosote has been used(1).

SOURCE DOMINATED: Pyrrole was detected at <1 ng/ml of air above 1 ml of water in 10 ml samples from two process retort wastewaters collected at Laramie Energy Technology Center during May 1982 and at the Logan Wash site of Occidental Oil Shale Inc. during December 1987; it was also detected in the gas-condensate retort wastewaters at 3.1 and 5.0 ng/ml of air above 1 ml of water at both sites(1). Pyrrole has been found in stock emission during incineration of municipal waste units not specified(2). URBAN/SUBURBAN: Pyrrole was not detected in ambient air at either Logan Wash, CO or at Boulder, CO(1).

Pyrrole has been detected in "popped" popcorn at a level of 26 ug/kg in a dry capture method and 44 ug/kg in a wet capture method(1). Fresh chicken breast with bone was cut into 1.5 inch cubes, coated with flour and fried in Fri-al shortening. During a 48 hour period in which the chicken was fried, pyrrole was detected (detection level not specified)(2).

Occupational exposure to pyrrole may occur through inhalation and dermal contact with this compound at workplaces where pyrrole is produced or used. The general population may be exposed to pyrrole via ingestion of food, and dermal contact with this compound and creosote containing pyrrole. (SRC)

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.