퍼옥시아세틸질산염

Triple point: -50 °C

Hydroxyl radical reaction rate constant = 1.0X10-13 cu cm/molec-sec at 25 °C

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The metabolic and pulmonary function responses were investigated in 32 non-smoking men and women (8 men and 8 women 18 to 26 years of age, and 8 men and 8 women 51 to 76 years of age) who were exposed for 2 hours to each of 8 conditions: (1) filtered air (FA), (2) 0.13 ppm peroxyacetyl nitrate (PAN), (3) 0.45 ppm ozone (O3), (4) 0.60 ppm nitrogen dioxide (NO2), (5) 0.13 ppm PAN + 0.45 ppm O3 (PAN/O3), (6) 0.13 ppm PAN + 0.60 ppm NO2 (PAN/NO2), (7) 0.60 ppm NO2 + 0.45 ppm O3 (NO2/O3), and (8) 0.13 ppm PAN + 0.60 ppm NO2 + 0.45 ppm O3 (PAN/NO2/O3). The subjects alternated 20-min periods of rest (n = 3) and cycle ergometer exercise (n = 3) at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Heart rate was monitored throughout each exposure, and VE was measured during the last 2 min of each exercise period. Exposure to FA, PAN, NO2, and PAN/NO2 had no effect on any measure of pulmonary or metabolic function. Ozone was primarily responsible for the pulmonary function effects observed. There was no significant difference between the responses to O3 exposure and the responses to the three O3 mixtures, indicating no interactions between the pollutants. ...

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that peroxyacetyl nitrate is expected to have very high mobility in soil(SRC). Volatilization of peroxyacetyl nitrate from moist soil surfaces is expected to be an important fate process(SRC) given a Henry's Law constant of 2.78X10-4 atm-cu m/mole(3). However, mobility and volatilization may be attenuated by the polar nature of this compound(SRC). Peroxyacetyl nitrate is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 29.2 mm Hg(4). Biodegradation data were not available(SRC, 2007).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 4(SRC), determined from a structure estimation method(2), indicates that peroxyacetyl nitrate is not expected to adsorb to suspended solids and sediment(SRC). Volatilization from water surfaces is expected(3) based upon a Henry's Law constant of 2.78X10-4 atm-cu m/mole(4). Using this Henry's Law constant and an estimation method(3), volatilization half-lives for a model river and model lake are 7 hours and 5 days, respectively(SRC). However, mobility and volatilization may be attenuated by the polar nature of this compound(SRC). According to a classification scheme(5), an estimated BCF of 3(SRC), from an estimated log Kow of -0.19(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Biodegradation data were not available(SRC, 2007).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), peroxyacetyl nitrate, which has a vapor pressure of 29.2 mm Hg at 25 °C(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase peroxyacetyl nitrate 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 380 days(SRC), calculated from its rate constant of 1.0X10-13 cu cm/molecule-sec at 25 °C(3). Peroxyacetyl nitrate is very stable at low temperatures but does decompose at higher temperatures to release NO2; whether photolysis can compete with thermal decomposition is still of interest(4). Peroxyacetyl nitrate exits in equilibrium with the radical intermediates from which it is formed, thereby existing as a sink or source depending on the concentration of the peroxyacetyl radical and NO2 in the atmosphere(5). When peroxyacetyl nitrate does react with NO, it will generate radicals which initiate additional hydrocarbon consumption and NO oxidation(5). Therefore, peroxyacetyl nitrate plays an important role in atmospheric chemistry and has a large effect on ozone formation(5). Peroxyacetyl nitrate was photolyzed readily when irradiated with light at wavelengths <300 nm(2) and therefore may be susceptible to direct photolysis by sunlight(SRC). The compound has been identified as one of the main components of photochemical smog throughout the planet(2).

/PLANTS/ The inhibitory effect of peroxyacetyl nitrate on the cyclic photophosphorylation of chloroplasts isolated from Black Valentine variety bean leaves (Phaseolis vulgaris L.) has been studied. Peroxyacetyl nitrate caused inhibition to photophosphorylation, in either the dark or the light, by affecting the chloroplast. Evidence is presented which suggests that peroxyacetyl nitrate could oxidize sulfhydryl groups on enzymes necessary for photophosphorylation. The inhibition to photophosphorylation caused by peroxyacetyl nitrate cannot be reversed by glutathione, even when added in large amounts ...

/PLANTS/ ... Peroxyacetyl nitrate (PAN) has a well-documented history as damaging to vegetation. There have been few long-term experimental studies despite the field evidence for damaging effects. Early studies in California have been followed by more recent data from east Asia, but there is still a dearth of information on the potential for effects of PAN and related peroxyacyl nitrates on vegetation typical of regions around tropical and sub-tropical cities where PAN pollution is increasingly important. ... Although reproductive processes (flowering, seed production) appear to be most sensitive, there have been no experimental studies on subsequent seed viability and the consequences at the ecosystem level of changes to plant phenology. ...

Peroxyacetyl nitrate has been identified as one of the main components of photochemical smog throughout the planet(1,6). The reaction of acetaldehyde with the OH free radical in urban atmospheres leads directly to the formation of the peroxyacetyl radical which in turn reacts with NO2 to form peroxyacetyl nitrate(2). In a field study conducted to assess the atmospheric impacts of ethanol fuel use, peroxyacetyl nitrate was shown to increase following the use of 10% ethanol fuel over the 1994 and 1995 winters in Albuquerque, NM as compared to summer levels in 1993, before the use of ethanol fuels(2). Peroxyacetyl nitrate concentrations in irradiated wood smoke from North Carolina oak species were 52 ppb (Apr 18), 174 ppb (Mar 7), and 232 ppb (Mar 28); NOx was added to burn chambers to a concentration of approx 0.6 ppm(3). The average air emission of peroxyacetyl nitrate from stationary sources in The Netherlands is 283 tons/yr(4). In a study evaluating the photochemical air pollution potential of representative 1996 America automobiles, peroxyacetyl nitrate was produced upon irradiation of exhaust from Chevelles not equipped with clean-air devices(5).

Using a structure estimation method based on molecular connectivity indices(1), the Koc of peroxyacetyl nitrate can be estimated to be 4(SRC). According to a classification scheme(2), this estimated Koc value suggests that peroxyacetyl nitrate is expected to have very high mobility in soil.

URBAN/SUBURBAN: Ambient levels of peroxyacetyl nitrate at four locations in the urban Los Angeles area sampled during a 2-week period from Aug 28 to Sept 13, 1993 ranged from 0.31 to 1.94 ppb (Long Beach), 0.14 to 1.61 ppb (Los Angeles), 0.53 to 2.96 ppb (Azusa), 0.81 to 7.30 (Claremont, Sept only); the overall highest level was 9.9 ppb, in Claremont(1). The average peroxyacetyl nitrate concentrations in the atmosphere of Alburquergue, NM during the winter months in 1994 and 1995 were 0.4 and 0.2 ppb, respectively(2). Average concentrations in downtown and suburban locations in Atlanta, GA taken during August, 1992 were 1.0 and 0.6 ppbv, respectively; on days when the ozone concentration exceeded 80 ppbv, concentrations were similar in both locations, 1.20 and 1.38 ppbv, respectively; at lower ozone concentrations, suburban peroxyacetyl nitrate levels were much lower(3). The daily mean level in the atmosphere of downtown Edmonton, Alberta, Canada from Dec 1982 to May 1984 was 0.6 ppb, with a high concentration of 7.5 ppb(4). The compound often persisted throughout the night in Edmonton, whereas it dissipated rapidly in Calgary, Canada(4). The average air concentration of peroxyacetyl nitrate in The Netherlands 0.4 ppb, based on measurements taken from June 1979 through March 1981(5). Daily average concentrations in Athens, Greece during Sept 18 through Oct 10, 1985 ranged from 0.9 to 0.27 ppb(6).

URBAN/SUBURBAN: 24 Hour average concentrations in ambient air of New Brunswick, NJ during 1978-1980 (ppb)(1). [Table#7255]

URBAN/SUBURBAN: Highest Ambient Levels of Peroxyacetyl Nitrate Concentrations (ppb) in Southern California and Other Urban Areas, 1985-1994(1). [Table#7256]

URBAN/SUBURBAN: Peroxyacetyl nitrate concentrations (ppb) in some European Cities(1). [Table#7257]

For more Atmospheric Concentrations (Complete) data for PEROXYACETYL NITRATE (6 total), please visit the HSDB record page.

/HUMAN EXPOSURE STUDIES/ The metabolic and pulmonary function effects were investigated in 10 nonsmoking, young adult men who were exposed for 2 hr (20 degrees C...) to 4 conditions: (1) filtered air (FA), (2) 0.30 ppm peroxyacetyl nitrate (PAN), (3) 0.45 ppm ozone (O3), and (4) 0.45 ppm O3 + 0.30 ppm PAN (PAN/O3). The subjects alternated 15-min periods of rest and 20-min periods of bicycle ergometer exercise at a work load predetermined to elicit a ventilatory minute volume (VE) of 27 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and postexposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Heart rate was monitored throughout the exposure, and (VE), oxygen uptake (VO2), respiratory rate (fR), and tidal volume (VT) were measured during the last 2 min of each exercise period. There were no changes in any variable consequent to FA or PAN exposure. The only metabolic changes to occur because of O3 and PAN/O3 exposure were a decrease in VT, a concomitant increase in fR, and consequently no change in VE. Both O3 and PAN/O3 induced significant (p < 0.05) decrements in FVC, FEV1.0, FEV2.0, FEV3.0, FEF25-75%, IC, ERV, and TLC. The decrements after PAN/O3 exposure averaged 10% greater than the decrements after O3 exposure. ...

/HUMAN EXPOSURE STUDIES/ The metabolic and pulmonary function responses were investigated in 32 non-smoking men and women (8 men and 8 women 18-26 years of age, and 8 men and 8 women 51-76 years of age) who were exposed for 2 hours to each of 8 conditions: (1) filtered air (FA), (2) 0.13 ppm peroxyacetyl nitrate (PAN), (3) 0.45 ppm ozone (O3), (4) 0.60 ppm nitrogen dioxide (NO2), (5) 0.13 ppm PAN + 0.45 ppm O3 (PAN/O3), (6) 0.13 ppm PAN + 0.60 ppm NO2 (PAN/NO2), (7) 0.60 ppm NO2 + 0.45 ppm O3 (NO2/O3), and (8) 0.13 ppm PAN + 0.60 ppm NO2 + 0.45 ppm O3 (PAN/NO2/O3). The subjects alternated 20-min periods of rest (n = 3) and cycle ergometer exercise (n = 3) at a work load predetermined to elicit a ventilatory minute volume (VE) of approximately 25 L/min (BTPS). Functional residual capacity (FRC) was determined pre- and post-exposure. Forced vital capacity (FVC) was determined before and after exposure, and 5 min after each exercise period. Heart rate was monitored throughout each exposure, and VE was measured during the last 2 min of each exercise period. Exposure to FA, PAN, NO2, and PAN/NO2 had no effect on any measure of pulmonary or metabolic function. Ozone was primarily responsible for the pulmonary function effects observed. There was no significant difference between the responses to O3 exposure and the responses to the three O3 mixtures, indicating no interactions between the pollutants. ...

/SIGNS AND SYMPTOMS/ In humans, the lowest level causing eye irritation was 0.64 mg/cu m for 2 hr.

/SIGNS AND SYMPTOMS/ Peroxyacetyl nitrate (PAN) is a ubiquitous air pollutant formed from NO(2) reacting with acetoxy radicals generated from ambient aldehydes in the presence of sunlight and ozone. It contributes to eye irritation associated with photochemical smog and is present in most urban air.

/ALTERNATIVE and IN VITRO TESTS/ Peroxyacetyl nitrate (PAN) ... induced apoptosis in human leukemia HL-60, human chronic myelogenous leukemia K-562, and mouse monocyte-macrophage RAW 264.7 cell lines. In the HL 60 cells, characteristic apoptosis morphology could be observed 4 hr after the cells were treated with 50 uM PAN. Exposure of HL-60 cells to increasing concentrations of PAN (from 1 uM to 100 uM) confirmed the concentration dependence of apoptosis as evidenced by DNA fragmentation in HL-60 cells, chromatin condensation by acridine-orange staining, and the appearance of the DNA apoptotic peak in flow cytometry. During apoptosis in HL-60 cells, 3-nitrotyrosine and 3,5-dinitrotyrosine were detected by high-performance liquid chromatography and liquid chromatography-mass spectrometry-mass spectrometry. ... Moreover, exogenous superoxide dismutase promoted PAN-induced apoptosis, and in contrast, a combination of superoxide dismutase and catalase suppressed this apoptosis. ... The formation of H2O2 produced from the dismutation of PAN-elicited superoxide anion contributed to the apoptotic mechanism in HL-60 cells through ROS pathways. ...

Peroxyacetyl nitrate is formed as a result of atmospheric photochemical reactions of hydrocarbons (typically resulting from industrial and domestic activities) in the presence of NOx(1,2). It is one of the Greenhouse Gases which contribute to global warming(2).

An estimated BCF of 3 was calculated in fish for peroxyacetyl nitrate(SRC), using an estimated log Kow of -0.19(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

The Henry's Law constant for peroxyacetyl nitrate is 2.78X10-4 atm-cu m/mole(1). This Henry's Law constant indicates that peroxyacetyl nitrate 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 7 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 5 days(SRC). Peroxyacetyl nitrate's Henry's Law constant indicates that volatilization from moist soil surfaces may occur(SRC). Peroxyacetyl nitrate is expected to volatilize from dry soil surfaces(SRC) based upon a vapor pressure of 29.2 mm Hg(3).

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male and female WIstar rats were exposed to peroxyacetyl nitrate (PAN) for 6 hours/day, 5 days/week for either 4 or 13 weeks. PAN concentrations used in the 4 week study were 0, 0.9, 4.1, or 11.8 ppm; concentrations used in the 13 week study were 0, 0.2, 1.0 or 4.6 ppm. In the 4 week study, exposure to 11.8 ppm caused elevated mortality, hematocrit values, red blood cell counts and lung weight. In addition, exposure resulted in abnormal behavior, growth retardation, severe inflammation, epithelial metaplasia and hyperplasia in the respiratory tract. Minimal behavioral disturbance, transient growth retardation, slightly increased lung weights and slight histopathological changes in the respiratory tract were noted at 4.1 ppm. No treatment related effects were noted at 0.9 ppm. Exposure to 4.6 ppm in the 13 week study resulted in changes similar to those found at 11.8 ppm in the 4 week study, with the exception that elevated mortality was not observed. No treatment-related effects exhibiting a dose-response were observed at 1.0 ppm.

/LABORATORY ANIMALS: Subchronic or Prechronic Exposure/ Male strain A mice were exposed to 74.3 mg/cu m (15 ppm) peroxyacetyl nitrate (PAN) for 6 hours/day, 5 days/week for 6 months. Toxic effects noted included hyperplastic tracheobronchitis, bronchiolitis, pneumonitis, bronchiolectasis, bronchiolarization of alveolar ducts, a focal interstitial fibrotic reaction and patchy centriacinar emphysema. Hyperplasia of the bronchial epithelium was also observed, and foci of squamous metaplasia were observed in the trachea and mainstem bronchi in approximately 50% of the PAN-exposed mice. ...

/GENOTOXICITY/ A series of experiments was conducted in which Chinese hamsters ... were exposed to peroxyacetyl nitrate (PAN) in air at concentrations of approximately 3 ppm for up to 1 month and then examined for somatic mutations and chromosomal aberrations. Mutations were assayed by measuring the frequency of thioguanine-resistant lung fibroblasts (isolated de novo and cultured). Chromosomal aberrations were assayed by measuring the frequency of micronuclei in either the bone marrow (polychromatic erythrocytes) or the lungs (binucleate lung fibroblasts cultured in the presence of cytochalasin B). ... Although in each experiment the mutation frequencies for the test animals were higher than the corresponding controls, /they/ were not significantly different from the concurrent negative controls (P > .05) or the historical controls, except for experiment C. In experiment C, there was a significant regression of mutation frequency versus dose (P < 0.001) if all of the historical controls for pooled animals are included at zero dose. No reproducible evidence of chromosomal breakage was found in either lung or bone marrow. Thus, although PAN has been found to be a bacterial mutagen, /the authors/ did not find statistically significant evidence of mutagenicity in vivo. The toxicity of PAN limited the exposure concentration that could be used. ...

/GENOTOXICITY/ Exposures of Salmonella typhimurium strain TA100 with and without S9 metabolic activation to low ppm levels of pure peroxyacetyl nitrate (PAN) in the gas phase were conducted. Measurements of the gas-phase PAN exposure concentration and the concentration of its decomposition products in surrogate test media led to a measured mutagenic activity of 34 +/- 5 revertants/umole. ...

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

Peroxyacetyl nitrate (PAN) decomposes in water generating hydrogen peroxide. Little is known of the mechanism of action, but oxidative stress is likely for PAN and its congeners.

Peroxyacetyl nitrate produces a unique signature mutation (a tandem GG to TT transversion) in Salmonella that is likely due to a GG intrastrand cross-link.

... peroxyacetyl nitrate ... formed in the atmosphere by reactions of nitrogen oxides, hydrocarbons, and sunlight

Formed in the atmosphere by reactions of nitrogen oxides, hydrocarbons, and sunlight.

The reaction of acetaldehyde with the OH free radical in urban atmospheres leads directly to the formation of the peroxyacetyl radical which in turn reacts with NO2 to form peroxyacetyl nitrate.

Peroxyacetyl nitrate exits in equilibrium with the radical intermediates from which it is formed, thereby existing as a sink or source depending on the concentration of the peroxyacetyl radical and NO2 in the atmosphere. This dissociation occurs with a lifetime of 30 minutes at 25 °C. At high NO2/NO ratios, peroxyacetyl nitrate is regenerated following each dissociation of peroxyacetyl nitrate molecule; however at NO2/NO = 3, a molecule is regenerated only one out of two dissociations; this is due to rapid reaction with NO which has a rate constant three times faster than the reaction with NO2. When peroxyacetyl nitrate does react with NO, it will generate radicals which initiate additional hydrocarbon consumption and NO oxidation.

Identified as one of the main components of photochemical smog throughout the planet