Inhalation Toxicity of Phosphine in the Rat: Acute, Subchronic, and Developmental

Newton, Paul E.; Schroeder, Raymond E.; Sullivan, Jeremiah B.; Busey, William M.; Banas, Deborah A.

doi:10.3109/08958379309034503

Cited by 21 publications

(23 citation statements)

References 5 publications

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“…The haematological variables we evaluated were within the normal range, consistent with other findings in humans,5 but in contrast to animal studies. 7 In spite of our small sample, the results of environmental monitoring showed that the exposures experienced by the fumigators in this study are far lower than those reported previously. 28 Although phosphine is a potent poison, our results show that it is possible to keep exposure to this fumigant at levels that do not present detectable health risks as measured by the genotoxicity biomarkers used in this study.…”

Section: Discussioncontrasting

confidence: 65%

“…[5][6][7] Within the state of New South Wales, Australia, Grain Corp is the government organisation responsible for about 85% of the commercial grain stores (about 270 sites, 500 individual stores), with 31 fumigators being responsible for all phosphine fumigation. During a normal year, there are about 170-200 fumigations with phosphine that occur mainly during summer months (December-March).…”

mentioning

confidence: 99%

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Evaluation of phosphine genotoxicity at occupational levels of exposure in New South Wales, Australia.

Barbosa¹,

Bonin²

1994

Occup Environ Med

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Phosphine has been claimed to cause chromosomal damage at exposures close to the current time weighted average exposure standard of 0'3 ppm (0.4 mg/m3). The current study involved 31 phosphine fumigators and 21 controls during the high fumigation season. All were volunteers and were evaluated for genotoxicity variables, including micronuclei in peripheral blood lymphocytes and urine mutagenicity. In parallel, all fumigators and 17 controls were evaluated--for full haematology, multiple biochemical analysis, whole blood organochlorines, and whole blood and serum cholinesterase activity. The results for-micronuclei showed no significant differences between fumigators and controls, but detected a strong association between age and increased frequency of micronuclei. Measurement of urine mutagenicity did not show any significant difference between fumigators and controls, but did show increased excretion of mutagens in smokers. All haematological and biochemical variables were within normal ranges, except for some nonspecific changes in biochemistry. At monitored occupational exposures of < 2-4 ppm/h our results show no association between phosphine exposure and genotoxic or toxicological effects in fiunigators. (Occup Environ Med 1994;51:700-705)

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Section: Discussioncontrasting

confidence: 65%

mentioning

confidence: 99%

Evaluation of phosphine genotoxicity at occupational levels of exposure in New South Wales, Australia.

Barbosa¹,

Bonin²

1994

Occup Environ Med

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“…Because of the previously reported repeated-dose lethality above approximately 5 ppm (Newton et al, 1993), the high exposure level for the chronic toxicity and oncogenicity study was set at 3 ppm with low and mid exposure levels of 0.3 and 1 ppm, respectively. In order not to exceed the lower explosive limit during exposure atmosphere generation, the phosphine was supplied as 1% in nitrogen (Scott Specialty Gases, South Plainfield, NJ).…”

Section: Exposure Levelsmentioning

confidence: 99%

“…Previous studies (Newton et al, 1993) have shown that repeated daily 6-h exposures were lethal if the concentration times time (C T) product of approximately 180 ppm h were exceeded. Repeat daily exposures to 5 ppm (Newton et al, 1993;Morgan et al, 1995) did not produce lethality after 2 wk of exposure, or a C T product well in excess of 180 ppm h. Repeat exposures to 7.5 ppm (Newton et al, 1993) had a median lethal time of 4 d, or a C T of 180 ppm h for Fischer 344 rats. Therefore, to stay below this apparent threshold for lethality from repeat exposures, the high exposure level was set, in conjunction with the U.S. Environmental Protection Agency (EPA), at 3 ppm.…”

Section: Chamber Monitoringmentioning

confidence: 99%

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A 2-Year Inhalation Study of Phosphine in Rats

Newton

Hilaski

Banas³

et al. 1999

Inhalation Toxicology

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Phosphine is a highly toxic gas used as a fumigant, a dopant in semiconductor manufacturing, and in the production of organophosphines. In a chronic toxicity and oncogenicity study of phosphine, 60 male and female F344 rats per group were exposed via whole-body inhalation for 6 h/ day, 5 days/ wk for up to 104 wk to mean concentrations of 0, 0.3, 1, or 3 ppm phosphine. Three parts per million was considered the maximum exposure level because of lethality seen at higher exposure levels in previous repeat dose studies. Ten rats per sex per group were sacrificed after 52 wk of exposure. Survivors were sacrificed after 104 wk of exposure. There were no phosphine-related effects seen on clinical observations, body weight, food consumption, hematology, clinical chemistry, urinalysis, or ophthalmology. There were no phosphine-related macroscopic findings or effect on absolute or relative organ weights. No histomorphologic alterations attributable to phosphine exposure were seen. In conclusion, under the conditions of this study, there were no treatment-related changes suggestive of a toxic or carcinogenic effect seen in rats following 52 wk or 2 yr of whole-body inhalation exposure to 0.3, 1, or 3 ppm phosphine. 702P. E. NEWTON ET AL. FIGURE 4. Mean body weights in male F344 rats during inhalation exposures to 0, 0.3, 1, or 3 ppm phosphine. 2-YEAR INHALATION PHOSPHINE STUDY 703FIGURE 5. Mean body weights in female F344 rats during inhalation exposures to 0, 0.3, 1, or 3 ppm phosphine.

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Aluminum

Dinman¹

2001

Patty's Toxicology

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Because of this element's electrochemical properties, its positvely charged ions form very tight chemical bonds with other anions such that dissociation is minimal in neutral or near‐neutral‐pH environments. Since most living organizations operate at or about such pH levels, by implication most naturally occurring aluminum compounds would display minimal potentials for cellular or subcellular interactions. Its binding forces, in addition to making this element available only recently (at the time of writing), has also meant that aluminum was relatively unavailable to the milieu intériur. However, since progressively more of the metal and its compounds came into common human use and commerce, ultimately its wide usage could be expected to eventually result in the possibility intimate human contact and finally, human health and hazard concerns. These events have indeed occurred so that aluminum and its possible association with neurological disorders became a prominent health issue of the late twentieth century. Because of the foregoing electrochemical physical realities, concerns have focused on the element's health effects per se, with little or attention directed at effects of aluminum compounds, such as chloride, phosphate, and sulfates. This should also not be unexpected, given their relative biological inavailability. Obviously, some aluminum compounds do ionize sufficient to lower pH in aqueous environments (e.g., aluminum chloride or phosphate) and act as simple irritants. However, most other aluminum compounds, as expected have had very little apparent biologic availability or effects, and thus are accorded little scientific attention as compounds per se. These facts are reflected in the content of contemporary biomedical literature. Although multiple aluminum compounds have been studied, few, if any, are studied except as they serve to “transport” aluminum into the body. The overwhelming majority represent interest in aluminum's effects alone rather than an individual compound's possible bioimpact. For these reasons, this chapter deals mainly with aluminum as an element and the most common prevalent form: the oxides. Since its other compounds as such are the subject of so little current investigation, these other compounds are considered separately later in this chapter.

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Inhalation Toxicity of Phosphine in the Rat: Acute, Subchronic, and Developmental

Cited by 21 publications

References 5 publications

Evaluation of phosphine genotoxicity at occupational levels of exposure in New South Wales, Australia.

Evaluation of phosphine genotoxicity at occupational levels of exposure in New South Wales, Australia.

A 2-Year Inhalation Study of Phosphine in Rats

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