Pulmonary pathology from inhalation of a complex mineral oil mist in dogs, rats, mice and gerbils

Stula, Edwin F.; Kwon, B. K.

doi:10.1080/0002889778507777

Cited by 23 publications

(6 citation statements)

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“…Lushbaugh et al (1950), Shoshkes et al (1950, Stula and Kwon (1978) and Osmitz et al (1987) all report this as the major histopathologic effect using a variety of animal species and exposure regimens. Lushbaugh et al (1950), Shoshkes et al (1950, Stula and Kwon (1978) and Osmitz et al (1987) all report this as the major histopathologic effect using a variety of animal species and exposure regimens.…”

Section: Discussionmentioning

confidence: 99%

Pulmonary Effects due to Subchronic Exposure to Oil Fog

et al. 1990

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Male and in some cases female rats were exposed to an oil fog generated by flash vaporization and subsequent condensation of light-weight lubricating oil. Exposures were for 3.5 h/d, 4d/wk for 13 wk. Males were exposed at concentrations of 1.5, 0.5, 0.2 or 0.0 mg/l (1500, 500, 200, and 0 mg/m3) and a particle size of approximately 1 micron (mass median aerodynamic diameter). A number of biologic endpoints were assessed the day after the last exposure and, in some cases, after a 4 wk recovery period. Effects of 1.5 mg/l on male and female rats were compared. Diffuse accumulation of macrophages in the alveoli was observed in all oil fog exposed groups. The degree of severity was concentration dependent. Histopathologic changes were more prominent in males than in females and represented the most notable gender-related differences. Histologic effects observed one day and 4 wk post exposure were similar. Minimal histopathologic changes and minimal increase in lavage fluid protein were the only effects observed at the 0.2 mg/l exposure level. There was a significant increase in lavage fluid protein, percent lavagable polymorphonuclear leukocytes and lung wet and dry weight following exposure to both 0.5 and 1.5 mg/l. At the highest exposure concentration effects on lung weights were still evident 4 wk post exposure. Pulmonary function endpoints including total lung capacity, vital capacity, residual volume, diffusing capacity to CO, compliance, and end expiratory volume (EEV) were unaffected by oil fog exposure with the exception of EEV in males exposed at the 1.5 mg/l level. All of the changes observed following oil fog exposure were consistent with a mild inflammatory edema.

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Section: Discussionmentioning

confidence: 99%

Pulmonary Effects due to Subchronic Exposure to Oil Fog

et al. 1990

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“…Both studies were conducted with SD rats. Two chronic (6-26 months) studies with a white mineral oil (25-30 carbon atoms, 95% naphthenic with 1-6 rings) (Wagner et al 1964) and with a fiber-yarn preparation (70% paraffinic mineral oil, 30% synthetic fiber adjuvants) plus 1000 ppm acetone (fiber solvent) in the test atmosphere were also evaluated (Stula and Kwon 1978). These studies used SD rats, mongrel dogs, CF and CAF/JAX mice, rabbits, Syrian hamsters, and gerbils.…”

Section: Evaluation Of the Inhalation Toxicity Of Pharmaceutical Whitmentioning

confidence: 99%

Mineral oil in food, cosmetic products, and in products regulated by other legislations

Pirow

Blume

Hellwig

et al. 2019

Critical Reviews in Toxicology

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For a few years, mineral oils and their potential adverse health effects have been a constant issue of concern in many regulatory areas such as food, cosmetics, other consumer products, and industrial chemicals. Analytically, two fractions can be distinguished: mineral oil saturated hydrocarbons (MOSH) and mineral oil aromatic hydrocarbons (MOAH). This paper aims at assessing the bioaccumulative potential and associated histopathological effects of MOSH as well as the carcinogenic potential of MOAH for consumer-relevant mineral oils. It also covers the absorption, distribution, metabolism, and excretion of MOSH and MOAH upon oral and dermal exposures. The use and occurrence of consumerrelevant, highly refined mineral oils in food, cosmetics and medicinal products are summarized, and estimates for the exposure of consumers are provided. Also addressed are the challenges in characterizing the substance identity of mineral oil products under REACH. Evidence from more recent autopsy and biopsy studies, along with information on decreasing food contamination levels, indicates a low risk for adverse hepatic lesions that may arise from the retention of MOSH in the liver. With respect to MOAH, at present there is no indication of any carcinogenic effects in animals dermally or orally exposed to highly refined mineral oils and waxes. Such products are used not only in cosmetics but also in medicinal products and as additives in food contact materials. The safety of these mineral oilcontaining products is thus indirectly documented by their prevalent and long-term use, with a simultaneous lack of clinical and epidemiological evidence for adverse health effects.

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“…No consistent difference in tumour incidence was observed in any of the species studied. Stula andKwon (1978, cited in Dalbey andBiles, 2003) studied the effects of inhalational exposure of mice and dogs to a fibre-finish oil with 70% unspecified paraffinic mineral base oil (Saybolt viscosity = ~50 at 38 °C) and other ingredients, including surfactants. Groups of 27 CAF 1 /JAX mice were exposed to aerosolised oil at 100 mg/m 3 together with 1 000 ppm acetone, to simulate conditions in acetate fibre production for 12 months.…”

Section: Mixturesmentioning

confidence: 99%

Scientific Opinion on Mineral Oil Hydrocarbons in Food

2012

EFS2

107

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Consumers are exposed to a range of mineral oil hydrocarbons (MOH) via food. Mineral oil saturated hydrocarbons (MOSH) consist of linear and branched alkanes, and alkyl-substituted cyclo-alkanes, whilst mineral oil aromatic hydrocarbons (MOAH) include mainly alkyl-substituted polyaromatic hydrocarbons. Products, commonly specified according to their physico-chemical properties, may differ in chemical composition depending on the oil source. Technical grade MOH contain 15 -35 % MOAH, which is minimised in food grade MOSH (white oils). Major sources of MOH in food are food packaging and additives, processing aids, and lubricants. Estimated MOSH exposure ranged from 0.03 to 0.3 mg/kg b.w. per day, with higher exposure in children. Specific production practices of bread and grains may provide additional MOSH exposure. Except for white oils, exposure to MOAH is about 20 % of that of MOSH. Absorption of alkanes with carbon number above C 35 is negligible. Branched and cyclic alkanes are less efficiently oxidised than n-alkanes. MOSH from C 16 to C 35 may accumulate and cause microgranulomas in several tissues including lymph nodes, spleen and liver. Hepatic microgranulomas associated with inflammation in Fischer 344 rats were considered the critical effect. The no-observed-adverse-effect level for induction of liver microgranulomas by the most potent MOSH, 19 mg/kg b.w. per day, was used as a Reference Point for calculating margins of exposure (MOEs) for background MOSH exposure. MOEs ranged from 59 to 680. Hence, background exposure to MOSH via food in 1 On request from the European Commission, Question No EFSA-Q-2010-00170, adopted on 3 May 2012. 2 SUMMARYFollowing a request from the European Commission, the EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) was asked to deliver a scientific opinion on mineral oil hydrocarbons (MOH) in Food. Mineral oil hydrocarbons occur in food both as a result of contamination and from various intentional uses in food production. In order to assess the need for possible regulatory measures as regards MOH in food, EFSA was requested to assess the risks related to their occurrence in food. More specifically, the opinion should evaluate whether new toxicity data are available and whether the current acceptable daily intakes (ADIs) are still applicable, explore whether certain classes (or subclasses) of MOH are more relevant due to their toxicity or to differences in the way they are metabolised by the human body, and identify the different background sources, other than from adulteration or misuse, of MOH occurrence in food. In addition a dietary exposure assessment was requested for the general population and for specific subgroups of the population (e.g. infants, children and people following specific diets), by taking into account the background occurrence of MOH in food. Included in the request was also to advise on MOH and food classes to be included if monitoring were to be set up for their presence in food.The scientific literature and other sources were s...

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Pulmonary pathology from inhalation of a complex mineral oil mist in dogs, rats, mice and gerbils

Cited by 23 publications

References 0 publications

Pulmonary Effects due to Subchronic Exposure to Oil Fog

Pulmonary Effects due to Subchronic Exposure to Oil Fog

Mineral oil in food, cosmetic products, and in products regulated by other legislations

Scientific Opinion on Mineral Oil Hydrocarbons in Food

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