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We describe a patient with chronic actinic dermatitis whose photopatch tests revealed reactions to musk ketone and musk ambrette, both of which were found in his aftershave lotion. Minimal erythema doses of UVA and UVB were decreased. After initial unsuccessful treatment with PUVA therapy the patient was successfully treated with a combination of cyclosporine and PUVA.
BACKGROUND: Although photosensitivity disorders have been well described, their incidence in a referral institution had not been studied. OBJECTIVE: The purpose of this study was to evaluate the incidence of photosensitivity disorders, including photocontact dermatitis, in an academic medical center. METHODS: The results of the assessment of 203 consecutive patients, all of whom had phototests, referred for the evaluation of photosensitivity disorders during a 7.3-year period were reviewed. RESULTS: The mean age was 50 years, and 63% of the patients were women. The most frequent diagnoses were polymorphous light eruption (26% of the total patient population), chronic actinic dermatitis (17%), photoallergic contact dermatitis (8%), systemic phototoxicity to therapeutic agents (7%), and solar urticaria (4%). Positive photopatch reactions, patch test reactions, or both were observed in 40 (29%) of the 138 tested patients. The frequencies of the positive photopatch test reactions were sunscreens (57%), fragrances (18%), and antimicrobial agents (13%). Of the positive patch test responses, fragrances elicited 47% of the total positive reactions, followed by sunscreens (39%) and antimicrobial agents (7%). CONCLUSION: Polymorphous light eruption, chronic actinic dermatitis, and photoallergic contact dermatitis were the most frequently made diagnoses. Sunscreens, fragrances, and antimicrobial agents were the most common clinically relevant photoallergens and allergens.
Female B6C3F1 mice plus male and female Fischer 344/N rats were gavaged with allyl isovalerate (AIV) in corn oil at 0, 31, 62, or 125 (mice) and 0, 31, 62, 125, or 250 (rats) mg/kg body weight for five daily exposures per week for a 2-week period. Hematologic, immunologic, and histopathologic studies were performed 48 to 72 hr following the final treatment. AIV exposure had no effect on hematology or bone marrow cellularity in mice or rats. AIV exposure at 250 mg/kg was toxic to rats causing reduced weight gain and hepatotoxicity. In vivo and in vitro studies revealed that pluripotent hematopoietic stem cells (CFU-S) and granulocyte-macrophage progenitors (CFU-GM) in the bone marrow were decreased in the treated mice. Hematopoietic suppression was correlated with the reduction in the hexose monophosphate shunt metabolism of bone marrow cells but the Embden-Meyerhof pathway and tricarboxylic acid pathway enzymes did not appear to be affected. Examination of host resistance following Plasmodium and Listeria challenge did not demonstrate significant differences between treated and control mice, nor were there other effects on the immune system. This suggests that the myelotoxic effects were minimal and of a degree that would not alter host resistance.
The noninvasive mouse ear swelling assay (MESA) for contact allergy testing was evaluated using fragrance components and complex fragrance mixtures. The test materials represented weak sensitizers and nonsensitizers. Two versions of the MESA were investigated. Both were noninvasive and utilized only topical abdominal dosing and ear challenge with single applications in BALB/cBy mice. The vit A MESA differed from the regular MESA only in that mice were maintained on a diet with 17-fold higher levels of vitamin A (vit A) acetate beginning 3 weeks prior to induction. Sensitization reactions were determined by measuring the mean increase in ear swelling over baseline at 24, 48 and 72 hr postexposure. Irritation dose-response curves facilitated choosing a high nonirritating challenge dose. Sensitization dose-response curves were developed for cinnamaldehyde (CINN) and a complex fragrance mixture, F-16. From these curves, the SD50 was determined. This value represents the dose which sensitized half the animals and serves to rank the potency of compounds for allergic contact dermatitis and to compare values among different assays. The SD50 for CINN was 21.6% while the SD50vit A for F-16 was 26.6%. The other fragrance, isoeugenol (ISOE), and fragrance mixtures, F-07 and F-22, were also found to be weak sensitizers in the MESA and vit A MESA. The results in the MESA for CINN and ISOE were in the range observed with guinea pig test protocols but showed that the MESA was more sensitive than human test protocols. Two of the fragrance mixtures tested in the MESA gave comparable results in the Buehler guinea pig assay. However, the third (F-22) was negative in the Buehler assay and the MESA, but positive in the vit A MESA. The results of this work with weak sensitizers and the companion study (Thorne et al., 1991) with potent sensitizers at low doses illustrate that the noninvasive MESA is as sensitive as many standard guinea pig assays. In addition, it is easier and much less expensive to perform. The vit A MESA has the sensitivity and predictive power needed to test compounds and mixtures for contact sensitizing potency.
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The percutaneous absorption of two cosmetic fragrance materials, safrole and cinnamyl anthranilate, as well as of cinnamic alcohol and cinnamic acid, has been measured at occluded and non-occluded application sites. Absorption values were determined in the rhesus monkey in vivo. Absorption through human skin was measured by using excised skin in diffusion cells. Because of the insolubility in water of safrole and cinnamyl anthranilate, a nonionic surfactant solution (6% oleth 20) was used in the receptor chamber of the diffusion cell in order to facilitate the partitioning of the compounds from the skin into the receptor fluid. The relative volatility of the compounds was determined in order to aid in the interpretation of the absorption results. The greatest difference between in vivo and in vitro absorption values occurred with safrole, which was the least well absorbed and the most volatile compound. Cinnamic acid absorption through non-occluded human skin (17.8 +/- 4.9%, mean +/- SEM) was significantly lower than through monkey skin (38.6 +/- 8.3%). The values for absorption through human and monkey skin did not differ significantly for cinnamyl anthranilate (24.0 +/- 5.1% v. 26.1 +/- 2.3%) or cinnamic alcohol (33.9 +/- 7.3% v. 25.4 +/- 4.4%). Occlusion of the skin resulted in greater permeation of all of the compounds; a significant difference in permeability between the two types of skin occurred only with safrole. The fragrances were absorbed well, but their volatility must be considered in a toxicity evaluation. There was reasonable agreement between the values obtained from the studies of the human skin in vitro and the monkey skin in vivo.
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Musk ketone, musk xylene, musk tibetene and moskene, synthetic musks used in fragrances, were applied dermally to rats in daily doses of 240 (musk ketone and musk xylene only), 75, 24 or 7.5 mg/kg body weight for 90 days. The chemically related musk ambrette, a known neurotoxin in rats, was used as a positive control. While musk ambrette was clearly neurotoxic and caused testicular atrophy, as had been previously reported, the other compounds tested caused neither effect. The only effects of application of these materials were some organ weight changes at the higher doses, but these were not associated with histopathological changes in any of the tissues. The no-effect levels were: musk ketone, 75 mg/kg for males and females; musk xylene, 75 mg/kg for males and 24 mg/kg for females; moskene, 24 mg/kg for males and 75 mg/kg (highest dose administered) for females; and musk tibetene, 75 mg/kg (highest dose) for males and females.
The efficacy of a lymph node cell proliferation assay in the guinea pig as a first stage screening method of predicting sensitizing potentials of chemicals was studied by using several haptens. Animals were sensitized by a single 24-hr occlusive patch (24 cp), intradermal injection (id) and a combination of id and 24 cp, at a concentration used for guinea pig conventional contact hypersensitivity assay methods. Control animals were treated with vehicle(s) only. Suspensions of the lymph node cells (LNC) were individually prepared and cultured with [3H]methyl thymidine ([3H]TdR). [3H]TdR incorporation was measured and a stimulation index (SI) was calculated as a ratio of the mean [3H]TdR incorporation in sensitized animals and the mean [3H]TdR incorporation in control animals. LNC sensitized by 24 cp with 2,4-dinitrochlorobenzene proliferated maximally and significantly at day 5, whereas this occurred at day 7 after id sensitization. Significant LNC proliferation and high SI values were obtained successively by a combination of 24 cp and id. Moreover, strongly sensitizing chemicals increased significant LNC proliferation (SI > 2.0); weakly to moderately sensitizing chemicals also induced significant LNC proliferation (SI = 1.3-1.7). On the other hand, a primary irritant, sodium dodecyl sulfate, failed to encourage LNC proliferation (SI approximately 1.0).
The percutaneous absorption of the fragrance fixative musk xylol was measured in vitro in human and hairless guinea pig skin. For comparison, musk xylol was applied to skin in an oil-in-water emulsion or the volatile solvent, methanol. After 24 hr, total absorption of musk xylol in hairless guinea pig skin was 55% from the emulsion vehicle and 45% from the methanol vehicle. With human skin, permeation of musk xylol from both vehicles decreased to 22% of the applied dose. When human studies were continued for an additional 6 days after skin surface washing, only 6% of the applied dose remained in skin. The data suggest that most of the absorbed musk xylol in skin at 24 hr will be systemically absorbed in vivo within 1 wk. Throughout the 24-hr absorption study, absorbed musk xylol was not metabolized. A permeability constant for musk xylol permeation through hairless guinea pig skin was determined by a modified procedure for the lipophilic compound. At each time point, some diffusion cells were terminated so that skin and receptor fluid levels could be determined. Under steady-state absorption the permeability constant was 6.86 x 10(-5) cm/hr. The amount of musk xylol penetrating skin from three types of cosmetic products was also calculated on the basis of actual conditions of use. Products that are applied to large areas of the body and remain on the skin for long periods will result in the greatest absorption of musk xylol.
Five nitro musk compounds widely used in cosmetics and detergents were examined for DNA-damaging and mutation-inducing properties. For this purpose two short-time assays were used, the SOS chromotest and the Salmonella/mammalian microsome test. Musk ambrette showed mutagenicity in Salmonella typhimurium TA 100 requiring metabolic activation by rat liver postmitochondrial supernatant (S9) but it lacked mutagenicity in the absence of S9 and genotoxicity in the SOS chromotest. Musk xylene, musk ketone, musk moskene and musk tibetene showed neither mutagenicity nor genotoxicity in the presence and absence of S9.
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We characterized the inducing effects of two musk analogues, musk xylene and musk ambrette, on phase I and phase II drug-metabolizing enzymes in rat liver and compared their effects with 3-methylcholanthrene, isosafrole and 2(3)-tertbutylhydroxyanisole (BHA) at 0.1 mmol/kg dose level. Musk xylene and isosafrole increased more efficiently the metabolic activation of 2-amino-6-methyldipyrido[1,2-a:3',2'-d]imidazole (Glu-P-1) to mutagen than that of benzo(a)pyrene. Musk ambrette increased both the activation of Glu-P-1 and benzo(a)pyrene to the same extent. Western blot analyses revealed that musk xylene, musk ambrette, isosafrole and BHA induced more strongly cytochrome P450 1A2 (CYP1A2) in microsomes than CYP1A1. 3-Methylcholanthrene induced CYP1A1 in preference to CYP1A2. On the other hand, all drugs except for 3-methylcholanthrene did not show remarkable increases in phase II enzyme activities, such as DT-diaphorase, glutathione S-transferase and UDP-glucuronyltransferase, at 0.1 mmol/kg dose level. These results show that musk xylene, musk ambrette, isosafrole and BHA at the dose level used in this study possess the potency to induce CYP1A2 without remarkable induction of CYP1A1 and phase II enzyme activities as observed for 3-methylcholanthrene, although they have been considered to induce both phase I and phase II drug-metabolizing enzymes at higher doses.
Bergamottin, which accounts for about two-thirds of the absorption of UVA and UVB light by bergamot oil, is shown to be fairly unstable on UV irradiation of solutions of bergamot oil (in ethanol-water, 80:20 (w/w)). Bergamottin photodegradation is partly inhibited by molecular oxygen and also by a cinnamate sunscreen acting as a triplet excited state quencher. On UV irradiation of bergamot oil, type II photodynamic properties, i.e. singlet oxygen production, are observed, which can be mainly attributed to the excitation of bergamottin by light. Therefore bergamottin can be considered as a potential photosensitizer in the photobiological activity of bergamot oil.
It is well known that odors affect behaviors and autonomic functions. Previous studies reported that some compounds in cedar wood essence induced behavioral changes including sedative effects. In the present study, we analyzed cardiovascular and respiratory functions while subjects were inhaling fumes of pure compound (Cedrol) which was extracted from cedar wood oil. Vaporized Cedrol (14.2+/-1.7 microg/l, 5 l/min) and blank air (5 l/min) were presented to healthy human subjects (n=26) via a face mask, while ECGs, heart rate (HR), systolic blood pressure (SBP), diastolic BP (DBP), and respiratory rates (RR) were monitored. Statistical analyses indicated that exposure to Cedrol significantly decreased HR, SBP, and DBP compared to blank air while it increased baroreceptor sensitivity. Furthermore, respiratory rate was reduced during exposure to Cedrol. These results, along with the previous studies reporting close relationship between respiratory and cardiovascular functions, suggest that these changes in respiratory functions were consistent with above cardiovascular alterations. Spectral analysis of HR variability indicated an increase in high frequency (HF) component (index of parasympathetic activity), and a decrease in ratio of low frequency to high frequency components (LF/HF) (index of sympathovagal balance) during Cedrol inhalation. Furthermore, Cedrol inhalation significantly decreased LF components of both SBP and DBP variability, which reflected vasomotor sympathetic activity. Taken together, these patterns of changes in the autonomic parameters indicated that Cedrol inhalation induced an increase in parasympathetic activity and a reduction in sympathetic activity, consistent with the idea of a relaxant effect of Cedrol.