Potentiation by triorthotolyl phosphate of acrylate ester-induced alterations in respiration

Silver, E.H.; Leith, David; Murphy, Sheldon D.

doi:10.1016/0300-483x(81)90081-0

Cited by 27 publications

(10 citation statements)

References 8 publications

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“…This has previously been observed in rats (Altland et al, 1978) and is in accordance with observations on the hypothermic effects of inhalation of carbon monoxide and/or nicotine (Altland & Rattner, 1979;Lopez et al, 2003). In fact, inhalation of a wide range of xenobiotic substances such as ozone, acrylates, and formaldehyde (Watkinson et al, 2001;Jaeger & Gearhart, 1982;Silver et al, 1981) elicits a hypothermic response in rodents. The magnitude of this response is determined by the concentration of the xenobiotic, the mass of the animal, and environmental stress associated with, for example, restraint (Watkinson et al, 2003).…”

Section: Figsupporting

confidence: 89%

Stress and Hypothermia in Mice in A Nose-Only Cigarette Smoke Exposure System

Eijl

Oorschot

Olivier

et al. 2006

Inhalation Toxicology

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In nose-only exposure systems, animals need to be restrained inside a tube, which leads to stress. Stress is known to cause hyperthermia in rodents. Chronically repeated episodes of hyperthermia could be detrimental to animal health and influence results of nose-only exposure studies. Therefore we investigated whether hyperthermia occurred in male C57BL/6J mice that were restrained for increasing lengths of time, using nosepieces held at room temperature, preheated at 37• C, or thermostat controlled at different temperatures, with and without exposure to different concentrations of cigarette smoke. Body temperature, body weight, plasma corticosterone levels, and adrenal weights were recorded. Restraint using nosepieces at room temperature caused a time-dependent decrease in body temperature, which could be reversed by preheating the nosepieces to 37• C. Cigarette smoke dose-dependently caused an additional decrease, which was counteracted by controlling nosepiece temperature at 38• C. During 3 mo of exposure using heated nosepieces, ∆ body temperature remained constant. Body weight gain did not differ between smoke-exposed and room air-breathing animals exposed using either heated or roomtemperature nosepieces, but both groups gained significantly less weight, while adrenal weights were significantly and similarly increased, when compared to unrestrained littermates. Plasma corticosterone levels did not differ between the three groups. In conclusion, during restraint in nose-only exposure tubes with room temperature metal nosepieces, mice suffer a pronounced hypothermia. Preventing this by heating the nosepieces does not reduce the stress experienced by the animals.Nose-only exposure systems are widely used in inhalation studies on the effects of aerosols or gases on rodents. Cited ad-

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Section: Figsupporting

confidence: 89%

Stress and Hypothermia in Mice in A Nose-Only Cigarette Smoke Exposure System

Eijl

Oorschot

Olivier

et al. 2006

Inhalation Toxicology

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“…As measured by RD50, the rat is less sensitive than the mouse to the sensory irritation induced by many vapors (Bos et al, 1992). Silver et al (1981) measured breathing parameters in rats exposed to 500 ppm ethyl acrylate and noted a reduction of ~20% in breathing frequency. The current results are consistent with this report.…”

Section: Discussionmentioning

confidence: 99%

“…A pause during expiration was observed in the ethyl acrylateexposed animals. Target exposure concentrations were 600, 1000, and 1500 ppm and were selected based on the observation that 500 ppm produced only moderate respiratory depression in the rat (Silver et al, 1981), with the expectation that these concentrations would span the RD50 in the rat. Atmospheres were generated with the syringe pump system and analyzed by the gas chromatographic system described earlier.…”

Section: Ethyl Acrylate Rd50 Estimationmentioning

confidence: 99%

“…The RD50 for ethyl acrylate in mice is 315 ppm (De Ceaurriz et al, 1981). The RD50 in the rat is not known, but a moderate (~20%) reduction in breathing frequency has been reported to occur in this species during exposure to 500 ppm ethyl acrylate (Silver et al, 1981). The current study also included examination of the effects of ethyl acrylate on breathing frequency.…”

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confidence: 94%

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Sensory Nerve-Mediated Nasal Vasodilatory Response to Inspired Ethyl Acrylate

Morris

2002

Inhalation Toxicology

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The irritants acrolein, acetaldehyde, and acetic acid induce a rapid sensory nerve-mediated nasal vasodilatory response in the rat. The aim of the current study was to examine acute nasal sensory nerve-mediated acute responses to an irritant ester vapor, ethyl acrylate. For this purpose, the upper respiratory tract of the urethane-anesthetized male F344 rat was isolated by insertion of an endotracheal cannula, and ethyl acrylate-laden air was drawn continuously through that site at a flow rate of 100 ml/min for 50 min. Vascular function was monitored by measuring inert vapor (acetone) uptake throughout the exposure. Nasal flow resistance was also monitored during exposure, and plasma protein extravasation was measured by Evans blue dye leakage. At exposure concentrations of 100 to 400 ppm, ethyl acrylate induced a rapid nasal vasodilatory response, as indicated by increased acetone uptake rates. This response was maintained throughout the exposure. Changes in nasal flow resistance or in Evans blue dye leakage were not observed at these exposure concentrations. The vasodilatory response was diminished in animals pretreated with the sensory nerve toxin capsaicin, providing strong evidence that this response was sensory nerve mediated. Pretreatment with the carboxylesterase inhibitor bis-para-nitro-phenolphospahte at a dose sufficient to inhibit nasal carboxylesterase did not alter the response, suggesting that the parent ester, not the carboxylesterase metabolites, is primarily responsible for the sensory-nerve-mediated vasodilatory responses to this ester.

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“…It is not the release of acid that is decisive for the toxicity of short-chain acrylates and methacrylates, but the reactivity of the Michael system (alpha-beta unsaturated compounds) with nucleo-philic compounds such as glutathione (McCarthy and Witz 1997;McCarthy et al 1994;Silver et al 1981). …”

Section: Mechanism Of Actionmentioning

confidence: 99%

n ‐Butyl acrylate [MAK Value Documentation, 2017]

Hartwig

Arand²

2018

The MAK‐Collection for Occupational Health and Safety

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The German Commission for the Investigation of Health Hazards of Chemical Compounds in the Work Area has re‐evaluated the maximum concentration at the workplace (MAK value) of 2 ml/m 3 for n‐butyl acrylate. The critical effect in a two‐year inhalation study with rats was reserve cell hyperplasia with loss of ciliated or olfactory cells at the lowest concentration of 15 ml/m 3 . The lower confidence limit of the benchmark dose for an extra risk of 5% increase of the critical effect incidence (BMDL 05 ) of about 3 ml/m 3 , which had been calculated in the previous evaluations, was confirmed. Since 2014, the Commission uses an empirical approach to set MAK values for substances with critical effects on the upper respiratory tract or the eyes. Based on this approach, the equivalent concentration at the workplace is 1.5 ml/m 3 . However, studies in humans to investigate the sensory irritation of n‐butyl acrylate are lacking. As the structurally related ethyl acrylate possesses a RD 50 value as well as subchronic and chronic NOAECs similar to those of n‐butyl acrylate, the NOAEC of 2.5 ml ethyl acrylate/m 3 for sensory irritation in volunteers was used as a read‐across. As the MAK value for ethyl acrylate has been set at 2 ml/m 3 , the MAK value of 2 ml/m 3 for n‐butyl acrylate could be confirmed. In analogy to ethyl acrylate, the assignment of n‐butyl acrylate to Peak Limitation Category I and the excursion factor of 2 were confirmed. The NOAECs for developmental toxicity in rats and mice are sufficiently high so that damage to the embryo or foetus is unlikely when the MAK value is observed. Thus, n‐butyl acrylate continues to be classified in Pregnancy Risk Group C. The substance is marginally clastogenic in vitro but not in vivo and was not carcinogenic in a 2‐year inhalation study in rats. There are only a few cases of contact sensitization in humans but there are positive results in local lymph node assays. Data on airway sensitization are still not available. n‐Butyl acrylate continues to be designated with “Sh”. Skin absorption was calculated to contribute significantly to the systemic toxicity and n‐butyl acrylate is designated with an “H”.

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Potentiation by triorthotolyl phosphate of acrylate ester-induced alterations in respiration

Cited by 27 publications

References 8 publications

Stress and Hypothermia in Mice in A Nose-Only Cigarette Smoke Exposure System

Stress and Hypothermia in Mice in A Nose-Only Cigarette Smoke Exposure System

Sensory Nerve-Mediated Nasal Vasodilatory Response to Inspired Ethyl Acrylate

n ‐Butyl acrylate [MAK Value Documentation, 2017]

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