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IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Chemical Agents and Related Occupations. Lyon (FR): International Agency for Research on Cancer; 2012. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 100F.)

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Chemical Agents and Related Occupations.

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Mineral oils were considered by previous IARC Working Groups in 1983 and 1987 (IARC, 1984, 1987). Since that time new data have become available, which have been incorporated in this Monograph, and taken into consideration in the present evaluation.

1. Exposure Data

1.1. Identification of the agent

Mineral oils (also known as base oils, mineral base oils or lubricant base oils) are chemical substances prepared from naturally occurring crude petroleum oil. Crude oil is distilled first at atmospheric pressure and then under high vacuum to yield vacuum distillates and residual fractions that can be further refined to mineral oils. Mineral oils refined from petroleum crude oils are complex and variable mixtures of straight and branched-chain paraffinic, naphthenic (cycloparaffinic), and aromatic hydrocarbons having carbon numbers of 15 or more and boiling points in the range of 300–600°C (IARC, 1984).

Mineral oils are described by several dozen generic “petroleum stream” Chemical Abstracts Service (CAS) numbers. Many mineral oils may have more than one CAS number because different refiners submitted slightly different descriptions for similar refining streams when CAS numbers were being assigned (both in the United States of America and Europe) (CONCAWE, 1997).

The hydrocarbon composition and physical characteristics of a mineral oil depend on both the composition of the original crude oil and the processes used during refining (e.g. solvent extraction, hydro-treatment) (CONCAWE, 1997). Production processes of mineral oils have changed substantially over time (IARC, 1987; Tolbert, 1997). In the past, many mineral oils were only mildly refined and contained significant levels of polycyclic aromatic hydrocarbons (PAHs). Acid treatment was initially used to remove PAHs and other impurities and to improve the technical properties of the finished oils. In recent decades, acid treatment has largely been replaced by extensive refining with solvent extraction and/or hydro-treatment, which has further reduced the level of PAHs and other contaminants. Mineral oils have been produced by means of the severe hydro-treatment procedure since the 1960s (Kane et al., 1984; Mackerer et al., 2003). Regulatory pressures in the USA further encouraged the move to highly refined mineral oils in the mid-1980s (Woskie et al., 2003).

There are several assays that can be used to determine if a mineral oil is highly or severely refined (Mackerer et al., 2003). Two useful short-term assays that are widely used by mineral-oil manufacturers are the modified Ames test (ASTM, 1996) and the IP346 assay (Institute for Petroleum, 1985, 1993; CONCAWE, 1994). The modified Ames test measures the amount of extractable mutagenic activity in a mineral-oil sample; mineral oils with a mutagenicity index ≤ 1.0 in this assay are considered highly or severely refined. The IP346 assay measures the amount of material extractable in dimethyl sulfoxide (DMSO): mineral oils with a DMSO-extractable content < 3% in the IP346 assay are considered highly or severely refined. Naphthenic mineral oils tend to have higher non-mutagenic DMSO extractables and some naphthenic oils can give a false-positive result in the IP346 assay. The modified Ames test can give conclusive results if the outcome of the IP346 assay is high.

1.2. Uses

A wide variety of mineral oil-containing products including lubricants as well as products intended for non-lubricant purposes are manufactured for different applications. Lubricant products include engine oils, transmission fluids, gear oils, hydraulic fluids, as well as metalworking fluids (also known as metal-removal fluids). Metalworking fluids may be different from other mineral oil-containing products due to the types of additives used, the additive treatment rates, and contaminants – including those of microbial origin – that are associated with use. “Non-lubricant” products include agricultural spray oils, printing inks, tyre oils, etc. Oil mists or aerosols can arise from the use of mineral oil both as lubricant and as non-lubricant. In practice, oil aerosols may be generated by several mechanisms such as aeration, contact with a fast-moving surface, or by heating. Important applications associated with potential generation of oil aerosols are metal-working, textile machinery, rock drills, aerosol lubrication, agriculture sprays, concrete mould release agents, corrosion preventatives, printing inks, rubber extenders, lubricant-blending in open processes, and applications in food and pharmaceutical preparations (CONCAWE, 1986; Urbanus et al., 2003; ACGIH, 2007). The particle size of the mists, aerosols or fogs is likely to differ for each of these processes (IARC, 1984).

1.3. Human exposure

1.3.1 Occupational exposure

There are several occupational environments in which an oil mist can be generated. In these situations the opportunities for dermal exposure or inhalation exposure, with concomitant ingestion, are substantial. Such occupations include metalworking, printing-press operating, and cotton- and jute-spinning (Tolbert, 1997). According to the US National Occupational Exposure Survey (1981–83), approximately 1 million workers (including approximately 390,000 women) in the USA were potentially exposed to mineral oil (NIOSH, 1990).

A small number of studies have evaluated respiratory morbidity from exposure to mineral-oil mist among newspaper pressmen, marine engineers, cable oilers, and tunnel blasters. Mineral-oil aerosol concentrations in these studies ranged from approximately 0.3 mg/m3 (Bakke et al., 2001) to about 3 mg/m3 (Skyberg et al., 1992; Svendsen & Hilt, 1997, 1999; Bukowski, 2003). Values of up to >20 mg/m3 were recorded in earlier studies (Goldstein et al., 1970).

Ambient mineral-oil mist concentrations were measured in the engine rooms of ships: the typical lubricating oil (b.p. 300–700°C) is a solvent-refined mineral oil containing paraffins, cycloparaffins, aromatic hydrocarbons, and additives. The air concentrations of oil mist in the engine rooms of different ships varied from not detectable to 0.53 mg/m3 (mean 0.24 mg/m3). The levels of hydrocarbons varied from 0.2 to 14.5 mg/m3 (Svendsen & Børresen, 1999). [The level of refinement of these oils was not reported.]

1.3.2. Non-occupational exposure

The non-occupationally involved general population may be exposed to mineral oils through ingestion of contaminated foodstuffs. In a study conducted in Switzerland, Grob et al. (2001) analysed mineral oil in the fat or in a raw extract from animal feed or foodstuffs. The average concentration in the feed was 100 mg/kg, with a maximum of 1000 mg/kg, 25 mg/kg in animal body fat (maximum, 150 mg/kg) and 30 mg/kg in the fat phase of eggs (maximum, 80 mg/kg). Paraffin oil is used for feed production, which may account for part of the contamination problem (e.g. in eggs). [The level of refinement of these mineral oils was not reported.]

2. Cancer in Humans

2.1. Introduction

Mineral oils comprise a diverse set of agents used for a wide range of industrial operations. There is evidence that mineral oils vary in their potential to cause cancer with the degree of treatment or processing. Hydro-treatment and solvent extraction reduce the PAH content, and thus the carcinogenicity of the oils. Untreated and mildly treated oils have been classified as Group-1 carcinogens, with sufficient evidence from studies in humans that mineral oils (containing various additives and impurities) that have been used in occupations such as mule-spinning, metal machining and jute-processing are carcinogenic to humans.

A major challenge in making an overall assessment of the carcinogenicity of mineral oils is this diversity in processing, with incomplete information on the extent of processing in specific industrial applications. Mineral oils are typically used as part of a complex mixture for such applications as metalworking, lubrication, and cooling. The additional processing and combining with other agents makes attribution of risk specifically to mineral oils difficult (Woskie et al., 2003).

2.2. Cancer of the skin/scrotum

The evidence from a series of case reports and case series for skin cancer, particularly of the scrotum, over the period from the early 1900s through the 1960s, was reviewed in IARC Monograph Volume 34 (IARC, 1984). Five large case series of mule-spinners had been reported, each with over 100 scrotal cancers (Green, 1910; Southam & Wilson, 1922; Henry & Irvine, 1936; Henry, 1947), with sizable numbers of cases in other exposed populations. Despite the inherent limitations in case series as a source of information, the numbers of cases observed, the rarity of scrotal cancer, and the intensity of the direct exposure of the skin in these jobs during that time period render these case series highly informative. Scrotal cancer is virtually pathognomonic for occupational exposure, in part as a result of these historical case series.

Over the intervening period since the 1960s nothing has challenged the assessment of sufficient evidence of human carcinogenicity based on the historical evidence pertaining to skin cancer. In a cohort of 792 Swedish metalworkers exposed to oil mist there were four cases of scrotal cancer, all among 242 men employed as turners, versus 0 expected overall (Järvholm et al., 1981). The same group (Järvholm et al., 1985) reported on a cohort of 682 bearing-ring industry workers and found working as a lathe operator to be associated with scrotal cancer (four observed, 0.3 expected, P < 0.001). Zhao et al. (2005) studied a cohort of 5049 male aerospace workers in the USA and found a significantly increased risk for skin melanoma (see Table 2.1 available at Case series indicative of an increased risk for scrotal cancer continue to be published based on historical exposures. Pressmen working in a wax-manufacturing department in an oil refinery in the USA had a marked excess of scrotal cancer based on 11 cases in men working >10 years during the period 1937–56, which corresponds to a crude rate of 806 per 100,000 relative to a general population rate estimated at 0.15 per 100,000 (Hendricks et al., 1959). Tool setters and tool fitters in the West Midlands area of England showed notably elevated risk for scrotal cancer over the period 1936–1976 (Waldron et al., 1984).

Several epidemiological studies were able to detect the expected increased risk for skin cancer in general, or scrotal cancer in particular, but since these cancers are rarely fatal, studies based on cancer mortality were of limited use to address the question. Roush et al. (1982) studied squamous-cell carcinoma of the scrotum in a case–control study in Connecticut, USA, among men diagnosed between 1935 and 1973 (see Table 2.2 available at Occupations associated with exposure to cutting oils, including tool or machine setters, screw-machine operators, machinists, and machine operators, were examined and showed an odds ratio of 10.5 (95%CI: 4.0–36.9).

2.3. Other cancers

The more rigorous epidemiological studies pertain to the occupations in which mineral oils are used in various formulations and in different degrees, including metal workers, machinists, jute workers, and others. Given the time period and setting, the mineral oils studied were likely to be highly treated. At the time of the previous IARC Monograph there were several studies of workers in these industries, mostly based solely on job title and industry of employment and limited in detail regarding exposure (IARC, 1984). Exposure to mineral oil was inferred based solely on job title or self-reported exposure. Whereas dermal exposure is the primary route of exposure for skin/scrotal cancer, for other sites and under improved hygienic conditions, aerosols are of equal or greater concern.

Focusing on studies that made attempts to address exposure to mineral oil directly, there has been sporadic and inconsistent support for an association with bladder cancer (Ugnat et al., 2004; Friesen et al., 2009; see Table 2.3 available at and Table 2.4 at, stomach cancer (Zhao et al., 2005; see Table 2.5 at and Table 2.6 at, rectal cancer (Gerhardsson de Verdier et al., 1992; Eisen et al., 2001; see Table 2.7 at and Table 2.8 at, pancreatic cancer (Yassi et al., 2003), sinonasal cancers (Roush et al., 1980), laryngeal cancer (Ahrens et al., 1991; Eisen et al., 1992), and lung cancer (Rønneberg et al., 1988; Acquavella et al., 1993; see Table 2.9, available at and Table 2.10 at Individual studies have suggested that mineral oil may be related to a range of other cancers, including those of the larynx and pancreas, based on studies of metal-workers and related manufacturing occupations. For each of these, however, there are studies of equal or higher quality that do not show associations, and in many cases there are inconsistent results within the same study across exposure indices. There have been varyious interpretations of the strength of the evidence linking exposure to metalworking fluids to a range of cancer sites (Tolbert, 1997; Calvert et al., 1998; Mirer, 2003; Savitz, 2003). The diversity in exposures to other agents, including synthetic oils and contaminants, and the presence of accompanying unrelated occupational exposures make the relevance of many studies tenuous in the assessment of the carcinogenic hazards of exposures to mineral oils.

Lung cancer is the most extensively investigated cancer in these occupations. While there are several studies supporting an association with exposed workers in certain occupations (Coggon et al., 1984; Rønneberg et al., 1988; Acquavella et al., 1993; Droste et al., 1999; Zhao et al., 2005), the exposures are not generally to mineral oils alone, given the use of other compounds in the metal-working trade (see Table 2.9, online), the most detailed study did not show an association (Schroeder et al., 1997; Eisen et al., 2001), and smoking was not controlled for in some of the studies that did show an association (Coggon et al., 1984; Zhao et al., 2005; see Table 2.10 online).

The case–control studies have typically been better able to address confounding, whereas the cohort studies have tended to examine exposure in more detail. However, even in the most sophisticated studies, it was not possible to isolate highly-treated from untreated or mildly-treated oils, nor are mineral oils used in isolation from other agents. As noted in several reviews (Tolbert, 1997; Woskie et al., 2003), in metal-working there is concomitant exposure to a range of chemicals including biocides, metal dusts, and by-products of oil heating. Even in the study of the Michigan automobile-manufacturing workers – the most detailed study of metal-workers – the authors identified categories of exposure to straight-chain and soluble lubricating fluids, but were not able to separate or characterize mineral-oil exposures in particular (Eisen et al., 1992).

2.4. Synthesis

There is consistent evidence that untreated or mildly-treated mineral oils cause cancer of the skin, specifically of the scrotum, in humans. The association is highly unlikely to be due to chance, bias, or confounding, given the large case series, supportive epidemiological studies, the rarity of scrotal cancer, and the intensity of exposure during the period of interest.

There were insufficient data regarding cancer at other sites to draw conclusions on the carcinogenicity in humans for untreated, mildly-treated, or highly-treated mineral oils. Recent studies did address highly-treated mineral oils, but were limited in their assessment of this agent, instead addressing all aspects of the work environment. Exposure to mineral oils in metal-working and other industries has not been easy to assess, and other agents of concern are known to be present in such work environments. Given these limitations in assessing exposure to mineral oils, and the lack of consistency in study findings by cancer site, the evidence for carcinogenicity of highly-treated mineral oils remains insufficient to draw conclusions.

3. Cancer in Experimental Animals

Petroleum-derived base oils and formulated products have been tested for their potential carcinogenicity in mice and other experimental animals, by skin application, in feeding studies, by inhalation exposure, and by subcutaneous and intra-peritoneal injection. In IARC Monograph Volume 33 (IARC, 1984), the Working Group divided petroleum materials into eight classes plus two subclasses (6.2, 7.2) based on the extent of refinement. Class 8 covers petroleum-derived materials not otherwise classified, and this category is not considered in this Monograph. This categorization scheme is still useful and applied here despite the fact that the terminology used to describe the material tested in recent studies may not be easily conducive to allocate it to a given class. Table 3.1 presents the most representative animal cancer bioassays with mineral oils evaluated in IARC Monograph Volume 33 (IARC, 1984), as well as studies published since that time.

Table 3.1. Carcinogenicity studies of mineral oils in experimental animals.

Table 3.1

Carcinogenicity studies of mineral oils in experimental animals.

3.1. Earlier studies

Vacuum-distillate fractions [class 1], either naphthenic or paraffinic in nature, produced a significant skin-tumour response. De-waxing of these distillates did not appreciably alter their activity (Halder et al., 1984; IARC, 1984; Kane et al., 1984). Early studies demonstrated that both light and heavy fractions of paraffinic oils induced benign and malignant skin tumours (Twort & Ing, 1928). De-waxed paraffinic distillates induced both benign and malignant skin tumours in mouse skin (Gradiski et al., 1983). Jute-batching oil induced benign and malignant skin tumours and promoted tumours in mice pre-treated with 7,12-dimethylbenz[a]anthacene (Roe et al., 1967).

Acid-treated oils [class 2] of either naphthenic or paraffinic origin, induced benign and malignant skin-tumour responses (Twort & Lyth, 1939; Bingham et al., 1965; Bingham & Horton, 1966), unless severe acid treatment had been applied (Twort & Lyth, 1939).

Solvent-refined oils (raffinates) [class 3], either naphthenic or paraffinic in nature, generally did not produce skin tumours (Gradiski et al., 1983). However, in one study skin application of solvent-extracted paraffinic oil induced one malignant tumour, which suggests possible skin tumour-inducing activity (Doak et al., 1983).

Hydro-treated oils [class 4], principally paraffinic in nature, induced a moderate incidence of skin tumours when treatment of the distillates was mild (Halder et al., 1984; Kane et al., 1984), while no tumour was induced by severely hydro-treated oils. The combination of mild hydro-treatment and solvent extraction appears to reduce or eliminate skin tumorigenicity.

White oils and petrolatums [class 5], which are produced from oils that have undergone the most severe acid and/or hydro-treatment, showed no activity in the skin-tumour bioassay (Doak et al., 1983). Single subcutaneous injection of three different grades of medicinal petrolatum into mice induced no treatment-related tumours during the following 18 months (Oser et al., 1965). Similarly, a lifetime study in rats involving subcutaneous injection of liquid paraffin and yellow petrolatum did not show local tumours, except a single osteosarcoma near the site of yellow petrolatum injection (Schmähl & Reiter, 1953). Intra-peritoneal injection of two highly refined food-grade mineral oils into certain strains of mice induced plasma-cell neoplasms and reticulum-cell sarcomas (Potter & Boyce, 1962; Bober et al., 1976). Mice receiving repeated intra-peritoneal injections of liquid paraffin developed peritoneal reticulum-cell sarcomas, plasma-cell leukaemia, myeloid leukaemia and lymphocytic leukaemia (Rask-Nielsen & Ebbesen, 1965). In two feeding studies in which three different samples of medicinal-grade petrolatum and liquid paraffin were fed to rats for two years at either 2% or 5% of the diet, no significant increase in tumour incidence was observed (Schmähl & Reiter, 1953; Oser et al., 1965). Although the experimental design was considered inadequate and the exposure period was short, inhalation of light white naphthenic aerosol (100 mg/m3) by mice, rats, hamsters, and rabbits from 6–13 months did not produce a significant increase in tumours in any of the species tested (Wagner et al., 1964).

Solvent extracts [class 6.1], which are by-products of solvent refining and sometimes called aromatic oils, induced a significant increase in incidence of skin tumours (Gradiski et al., 1983). The same response was produced with highly concentrated aromatic extracts of medicinal-grade petrolatums (Kane et al., 1984).

High-boiling fractions from catalytically cracked oils [class 6.2] – also classified as aromatic oils – induced increasing numbers of skin tumours in mice with increasing boiling-ranges above 370°C. Further fractionation established that the activity is maximal for oils boiling at 500–520°C and is concentrated in the aromatic fraction of the oils. High-boiling, catalytically cracked oils also produced skin tumours in rabbits and monkeys (Smith et al., 1951). Additional studies confirmed the increased tumorigenic activity of oils with boiling ranges 370–500°C. Promoting activity was also detected for some oil fractions in mice and rabbits (Shubik & Saffiotti, 1955; Saffiotti & Shubik, 1963).

Unused gasoline-engine oil [class 7.1] applied in several studies to mouse skin did not give a tumorigenic response with the exception of one single tumour (Saffiotti & Shubik, 1963; Kane et al., 1984). Mice exposed via inhalation to unused diesel-engine oil for 11 months exhibited no increase in tumour incidence (Lushbaugh et al., 1950). In contrast, unused cutting oils (also class 7.1), which are often formulated products consisting of blends of base oils and chemical additives, produced skin tumours (Gilman & Vesselinovitch, 1955; Jepsen et al., 1977).

Used gasoline-engine oil [class 7.2] had stronger tumorigenic activity than unused oil; solvent extraction of polyaromatic hydrocarbons almost eliminated the tumorigenic activity (Grimmer et al., 1982a). Similarly, used cutting oil [also class 7.2] tended to be more active than a comparable, unused oil (Gilman & Vesselinovitch, 1955; Jepsen et al., 1977).

3.2. Studies published since the previous evaluation (IARC, 1984)

Studies conducted since IARC Monograph Volume 33 (IARC, 1984) show a marked improvement in experimental design and reporting, and confirmed previous findings. Exposure to batching oil [class 1] induced benign and malignant skin tumours and promoted tumour formation in mice pre-treated with urethane (Mehrotra et al., 1987; 1988). Subsequent studies with the same oil reported only benign tumours in mice treated with jute-batching oil, which occurred with and without pre-treatment with 7,12-dimethylbenz[a]anthacene (Agarwal et al., 1985). Additionally, in mice treated dermally with fractions of the same jute-batching oil for 40 weeks, the PAH-containing fractions induced tumours only when treatment was followed by 12-O-tretradecanoylphorbol-13-acetate (Agarwal et al., 1988). Unrefined naphthenic crude oil applied to the skin of mice induced papillomas and carcinomas (McKee et al., 1989). Dietary exposure to liquid paraffin did not induce an increased tumour incidence (Shoda et al., 1997).

Both mild and severe hydro-treatments of naphthenic oils [class 4] eliminate the tumorigenicity, which is associated with a decrease in PAH content (McKee et al., 1989). Despite the association, PAH content alone was not considered predictive of carcinogenicity.

Most tumours observed after exposure to white oils and petrolatums [class 5] produced from oils that have undergone the most severe acid and/or hydrogen treatment, were papillomas and to a lesser extent squamous cell carcinomas (Nessel et al., 1998, 1999).

4. Other relevant data

4.1. Humans

A group of 31 male glassmakers (smokers and non-smokers) and a group of suitably matched controls exposed to aerosols of mineral oils were examined for chromosomal abnormalities in peripheral blood lymphocytes. Chromosomal damage, including chromatid breaks, chromosome breaks, and chromosome exchanges (di-centrics and reciprocal translocations) were increased in the exposed workers compared with controls (Srám et al., 1985).

Workers from a cold-rolling steel plant (smokers and non-smokers) exposed to mineral oils were examined for mutagenic activity in the urine by means of Salmonella typhimurium strain TA98 in the presence of an exogenous source of metabolic activation. There was a significant difference in urinary mutagenicity between the exposed workers and the controls. While among non-smokers the mutagenic activity was not increased in exposed compared with unexposed workers, the overall results suggested a synergistic effect of smoking and exposure to mineral oils (Pasquini et al., 1985).

Overall, there is weak evidence on the mechanism underlying the effects of exposures to mineral oils in humans. This evidence is based on genotoxic (mutagenic) activity of mineral oils in bacteria and a single cytogenetic study of glassworkers exposed to aerosols of mineral oils.

4.2. Experimental systems

Samples of vacuum distillates (class 1), solvent-refined oils (class 3), hydro-treated oils (class 4), used hardening oil (class 7.2) and used crankcase oils (class 7.2) were mutagenic in Salmonella typhimurium in the presence and absence (class 7.2 only) of an exogenous source of metabolic activation. Samples of a white oil (class 5), a refined steel-hardening oil (class 7.1) and of unused crankcase oils (class 7.1) were not mutagenic in S. typhimurium strain TA98 in the presence or absence of exogenous metabolic activation (IARC, 1984, 1987).

Naphthenic distillates (raw or acid-treated) were tested for mutagenicity in the S. typhimurium assay in the presence and absence of an exogenous source of metabolic activation. With metabolic activation, both untreated and acid-treated naphthenic distillates were mutagenic. The naphthenic distillates contained approximately 12% (w/w) polycyclic aromatic hydrocarbons (Granella & Clonfero, 1991). A series of 15 high-viscosity mineral oils obtained from naphthenic distillates, including used, recycled and pooled oils, were examined for mutagenic activity in the S. typhimurium assay with strains TA98 and TA100 in the presence and absence of an exogenous source of metabolic activation. Four of the samples (three acid-treated naphthenic oils and one recycled fraction of a used oil) showed significant mutagenic activity in the presence metabolic activation (Granella et al., 1995).

An extensive evaluation of the mutagenic activities of 13 mineral oils obtained from various processes was conducted with a modified S. typhimurium assay. The modification consisted of extracting the mineral-oil samples with dimethyl sulfoxide and increasing the concentrations of both NADP+ and the liver post-mitochondrial fraction (S9). The mutagenic activities of the mineral-oil samples were significantly correlated with the amount of 3–7-ring polycyclic aromatic compounds for a subgroup of oil samples (Blackburn et al., 1984; Roy et al., 1988).

Six mineral-oil samples were evaluated in a S. typhimurium assay activated with washed liver microsomes from Aroclor-1254-induced rats. Five of the six samples were mutagenic. The results showed an empirical correlation between increasing mutagenicity index, carcinogenicity and the polycyclic aromatic hydrocarbon content of the oils (Brooks et al., 1995).

Three mineral-oil samples (N11, N1, and R1) and several fractions of the N1 oil – obtained from silica-gel column chromatography and high-performance liquid chromatography – were evaluated by means of 32P-postlabelling for their ability to form DNA adducts after a single dermal application on the skin of TO mice. Both the R1 and N1 oils had formed unidentified DNA adducts at 24 hours. The 2–3-ring fraction produced more adducts than the 4–6-ring fraction of N1. The adduct levels first increased and then decreased with time after treatment (Ingram et al., 2000).

5. Evaluation

There is sufficient evidence in humans for the carcinogenicity of untreated or mildly treated mineral oils. Untreated or mildly treated mineral oils cause cancer of the skin (observed in the scrotum).

There is sufficient evidence in experimental animals for the carcinogenicity of untreated vacuum distillates, acid-treated oils, and aromatic oils, including extracts from solvent treatment of distillates and the high-boiling fraction of catalytically cracked oils [classes 1, 2 and 6].

There is sufficient evidence in experimental animals for the carcinogenicity of mildly hydro-treated oils [class 4].

There is sufficient evidence in experimental animals for the carcinogenicity of used gasoline-engine oil [class 7.2].

There is weak evidence on the mechanism underlying the effects in humans of exposures to mineral oils. This evidence is based on genotoxic (mutagenic) activity of mineral oils in bacteria and a single cytogenetic study of glassworkers exposed to aerosols of mineral oils.

Untreated and mildly treated mineral oils are carcinogenic to humans (Group 1).


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