Drug and Chemical Toxicology最新文献

{"title":"Exposure to cigarette smoke condensate has a differential effect on primary human melanocytes from light skin and dark skin.","authors":"Shilpi Goenka","doi":"10.1080/01480545.2026.2726177","DOIUrl":"https://doi.org/10.1080/01480545.2026.2726177","url":null,"abstract":"<p><p>Smoking causes pigmentation changes and skin aging, according to epidemiological research. Nicotine affected melanogenesis and increased oxidative stress in primary human melanocytes from darkly pigmented (DP) and lightly pigmented (LP) skin. However, research on the effects of cigarette smoke condensate (CSC) on primary human melanocytes from light and dark pigmentations in an <i>in vitro</i> culture over long-term durations is lacking. Herein, CSC was tested on LP and DP melanocytes for 6 days. CSC suppressed tyrosinase activity and lightened LP and DP pellets, indicating melanin production suppression. However, CSC increased melanocyte dendricity in LP cells at 25, 50, and 100 µg/mL doses, indicating melanin export. In DP cells, CSC biphasically increased dendricity at 25 µg/mL and decreased it at 50 µg/mL. In CSC-free cultures, LP cells exhibit complete dendricity recovery at 25 µg/mL, partial recovery at 50 µg/mL, and further augmentation at 100 µg/mL. Dendricity in DP cells were recovered only at 25 µg/mL, not at 50 µg/mL. In LP cells, CSC increased ROS production and SA-β-gal staining, but in DP cells, ROS decreased and no senescence was seen. The data show that CSC concentration and melanocyte pigmentation affect melanocyte damage, oxidative stress, and senescence. Melanocytes from LP skin are more susceptible to CSC damage than DP skin.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-17"},"PeriodicalIF":2.2,"publicationDate":"2026-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149220048","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preventive and post-exposure effects of apigenin against ochratoxin A-induced nephrotoxicity in rats: biochemical and histopathological evidence.","authors":"Areej A Eskandrani, Wafa S Alansari, Hussein S Mohamed","doi":"10.1080/01480545.2026.2743656","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743656","url":null,"abstract":"<p><p>Ochratoxin A (OTA) is a potent nephrotoxin commonly found in foods and feeds, with the kidney as its primary target organ. Apigenin (APG), a plant-derived flavonoid with antioxidant and anti-inflammatory properties, may counteract OTA-induced renal damage. This study evaluated the preventive and post-exposure recovery effects of APG against OTA-induced nephrotoxicity in rats. Sixty adult male Sprague-Dawley rats were assigned to five groups (<i>n</i> = 12): control; APG (20 mg/kg bw/day); OTA-contaminated diet (10 mg OTA/kg diet); APG + OTA preventive group; and OTA + APG post-exposure recovery group. Serum kidney function biomarkers, electrolytes, inflammatory and apoptotic markers, malondialdehyde (MDA), nitric oxide (NO), reduced glutathione (GSH), and superoxide dismutase (SOD) activity were measured. OTA induced nephrotoxicity, evidenced by elevated serum electrolytes, kidney function biomarkers, inflammatory and apoptotic markers, increased MDA and NO, decreased GSH and SOD activity, and renal tubular injury. APG treatment in both preventive and post-exposure recovery groups significantly reduced electrolytes, kidney injury, inflammatory and apoptotic markers, MDA, and NO, while increasing GSH and SOD activity compared with the OTA group; renal tubular lesions were also less apparent. In conclusion, APG attenuated OTA-induced nephrotoxicity, improving renal biomarkers, oxidative/nitrosative stress indices, inflammatory and apoptosis-related biomarkers, and renal histopathology. The preventive regimen showed greater overall improvement than post-exposure recovery; however, interpretation of the latter is limited by the absence of an OTA-recovery control group.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149215417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>In ovo</i> exposure to triphenyltin hydroxide induces genotoxicity, cytotoxicity and developmental toxicity in chick embryos, <i>Gallus gallus domesticus</i>.","authors":"Dipsanu Paul, Sweety Nath Barbhuiya, Sarbani Giri, Dharmeswar Barhoi","doi":"10.1080/01480545.2026.2747043","DOIUrl":"https://doi.org/10.1080/01480545.2026.2747043","url":null,"abstract":"<p><p>Triphenyltin hydroxide (TPTH) is a widely used agricultural fungicide and environmental pollutant well known for its potent toxicological potential. Despite this, its embryotoxic effects remain unexplored in avian models. This study presents a novel evaluation of TPTH's acute toxicity, genotoxicity, cytotoxicity, teratogenic potential, and enzymatic and tissue architectural potential using the <i>in ovo</i> chick embryo model. Fertilized chicken eggs were exposed to varying TPTH concentrations that further revealed a time-dependent median lethal dose (LD₅₀) decline from 547.37 µg/egg at 24 h to 395.74 µg/egg at 96 h. Later, evaluations using 1%, 5%, and 10% of the 96 h LD₅₀ demonstrated profound subcellular damage. The Hen's egg test for micronucleus (HET-MN) assay showed a significant dose-dependent induction of micronuclei, confirming genomic instability. Additionally, a reduced polychromatic to normochromatic erythrocyte (PCE/NCE) ratio indicated severe cytotoxicity and suppressed erythropoiesis. Morphometric assessments revealed teratogenic alterations, including heart tube failure, microcephaly, cranial edema, microphthalmia, localized hemorrhaging, and concentration-dependent growth retardation in body length, eye diameter, and limb elongation. Biochemical assessments revealed that TPTH triggers severe oxidative stress. This was supported by significant dose-dependent reductions in superoxide dismutase, catalase, and glutathione across major organs, alongside increased lipid peroxidation in the brain. Histopathological analysis also revealed severe toxicity. These findings validated that TPTH induces potent developmental toxicity through a cascade of genotoxic, cellular, enzymatic damage, and structural alterations, highlighting its extreme embryotoxic risks to avian populations and associated ecosystems.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-17"},"PeriodicalIF":2.2,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149179957","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced reproductive toxicity following combined exposure to ethinylestradiol and levonorgestrel: evidence of non-additive endocrine disruption in male rats.","authors":"Khaled Belhamzaoui, Faouzi Dahdouh, Mohamed-Réda Djebbar, Houria Berrebbah, Salha Amira Benatallah, Houssem Chenna","doi":"10.1080/01480545.2026.2743943","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743943","url":null,"abstract":"<p><p>Ethinylestradiol (EE2) and levonorgestrel (LNG) are synthetic hormones widely used in contraceptives and increasingly recognized as endocrine-disrupting contaminants. Although their individual reproductive effects are documented, their combined toxicity remains poorly understood. This study evaluated the sub-chronic reproductive toxicity of EE2 and LNG, administered alone or in combination, in male <i>Wistar</i> rats, with emphasis on potential non-additive endocrine-disrupting interactions. Animals were orally treated with EE2 (1 µg/kg bw), LNG (5 µg/kg bw), or both for four weeks. Individual exposures caused significant alterations in testicular weight, hormone levels, oxidative stress markers, and sperm quality, whereas epididymal weight was not significantly affected. In contrast, combined exposure markedly intensified these effects, causing severe spermatogenic impairment, near-complete sperm depletion, and major histological damage in testicular tissue. This enhanced toxicity was associated with increased lipid peroxidation, reduced antioxidant defenses, and marked suppression of testosterone, FSH, and LH levels, indicating disruption of the hypothalamic-pituitary-gonadal axis. Two-way factorial analysis confirmed statistically significant EE2 x LNG interactions for testicular weight, sperm concentration, sperm motility, LH and testosterone; in each case the observed combined effect was smaller than predicted by effect addition, indicating an infra-additive rather than synergistic interaction, consistent with a floor effect at these already substantial individual effect sizes. These findings highlight the importance of assessing combined endocrine disruptor exposures, as mixture effects modify reproductive toxicity in ways not predictable from single-compound data alone.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-14"},"PeriodicalIF":2.2,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental toxicity screening of methylene blue in a chick embryo in ovo model.","authors":"Alper Altınkaya, Mehmet Ali Eren, Tuba Bülbül, Vural Özdemir, Aziz Bülbül","doi":"10.1080/01480545.2026.2743591","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743591","url":null,"abstract":"<p><p>Methylene blue (MB) is a clinically important agent used for acquired methemoglobinemia and selected critical care indications, yet its effects during early embryogenesis remain poorly defined. This study evaluated developmental toxicity following in ovo MB exposure, characterized dose-dependent embryolethality, estimated the median lethal dose (LD50), and assessed developmental outcomes across a lower-dose range.An initial analytical cohort of 360 fertilized chicken eggs was allocated to two experimental phases. In the lethal-dose phase, MB was administered into the air chamber at doses 1, 2, 4, or 8 mg/kg. In the low-dose phase, MB was administered at doses of 0.067, 0.125, 0.250, or 0.500 mg/kg. Each phase included a sham-control group and a saline vehicle-control group. Embryonic mortality, developmental progression, relative embryo weight, crown-rump length, and hatch-related outcomes were recorded during incubation. Mortality data were analyzed using control-corrected probit regression. In the lethal-dose phase, mortality increased dose-dependently, reaching 23.3%, 43.3%, 90.0%, and 100.0% at 1, 2, 4, and 8 mg/kg, respectively. The estimated LD50 was 2.01 mg/kg, with a 95% confidence interval of 1.68-2.40 mg/kg. In the low-dose phase, MB concentrations from 0.067 to 0.500 mg/kg did not significantly affect mortality, relative embryo weight, or crown-rump length compared with controls. These findings indicate a steep lethal response to MB in this model, while 0.500 mg/kg may be regarded as a provisional no-observed-adverse-effect level (NOAEL) candidate under the present experimental conditions. Direct clinical extrapolation is limited because the in ovo model lacks maternal metabolism, placental transfer, and fetal clearance.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-9"},"PeriodicalIF":2.2,"publicationDate":"2026-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149165214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic impact of bisphenol A on retinal pigment epithelium: disturbed energy pathways and antioxidant response in ARPE-19 cells.","authors":"Tuba Tüylü Küçükkılınç, Ozan Kaplan, Seyhan Türk, Emine Koç, Emine Merve Yıldırım, Mustafa Çelebier","doi":"10.1080/01480545.2026.2697203","DOIUrl":"https://doi.org/10.1080/01480545.2026.2697203","url":null,"abstract":"<p><p>Bisphenol A (BPA) is a widely utilized endocrine-disrupting chemical that has been associated with metabolic dysregulation in various tissues. Nevertheless, its impact on ocular metabolism remains insufficiently understood. This study aims to investigate the metabolic effects of BPA exposure in ARPE-19 retinal pigment epithelial cells using untargeted metabolomics. ARPE-19 cells were exposed to 100 µM BPA for 24 hours, and cytotoxicity, intracellular reactive oxygen species (ROS) levels and glutathione metabolism parameters were identified. Metabolic alterations were analyzed utilizing liquid chromatography-quadrupole time-of-flight mass spectrometry (Q-TOF LC/MS). Principal component analysis (PCA), volcano plots, heatmaps, and pathway enrichment analysis were conducted to identify significantly altered metabolites and pathways. BPA exposure led to notable metabolic changes, including alterations in the tricarboxylic acid (TCA) cycle, β-oxidation, nucleoside metabolism, and amino acid metabolism. Key metabolite changes included increased levels of glutamine, pyroglutamic acid, anserine, and adenosine 2',3'-cyclic phosphate, suggesting oxidative stress and metabolic adjustment. Pathway analysis identified significant changes in arachidonic acid metabolism and pyrimidine metabolism, indicating oxidative stress and metabolic compensation due to BPA exposure. The findings underscore the metabolic risks of BPA exposure to retinal health and necessitate further validation through targeted metabolomics and in vivo studies.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166269","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential protective effects of nano-hydroxyapatite and vitamin-B12 against acrylamide-induced neurotoxicity in rat cerebella.","authors":"Zamzam Nasrallah Abdel-Moaty, Yahia A Amin, Rana A Ali, Ahmed Talaat Galal, Safaa El-Nahas, Basma Tito Abd Elhameed, Salwa M Ouies, Maha Abd-El Baki Ahmed","doi":"10.1080/01480545.2026.2743571","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743571","url":null,"abstract":"<p><strong>Background: </strong>Acrylamide (ACR) is a common industrial substance that is used in the manufacture of many laboratory materials, formed during food processing, and is known to cause neurotoxicity and brain damage. Protective substances such as Nano-hydroxyapatite and vitamin B12 (Vit.B12) may play a modulatory role in mitigating this neural damage. The current study aimed to investigate the neurotoxicity and brain damage induced by ACR exposure and the ameliorative effects of nano-hydroxyapatite and Vit.B12 against these neural toxic effects.</p><p><strong>Methods: </strong>Forty male rats were divided into four groups (10 for each): Control group received distilled water, ACR group received a daily dose of 10 mg/kg bw ACR, ACR+Nano-HA received ACR (10 mg/kg) plus nano-HA (150 mg/kg), and ACR+Vit.B12 group that received ACR (10 mg/kg) plus Vit.B12 (1 mg/kg) for 5 weeks. Oxidant/antioxidant biomarkers, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and malondialdehyde (MDA), were measured in blood. Histological investigations, Semithin sections, and an electron micrograph of the cerebellum were performed. Immunohistochemical staining with an anti-GFAP antibody was performed to determine the severity of astrocytosis.</p><p><strong>Results: </strong>ARC exposure caused cerebellar degeneration, significant reduced Purkinje cell numbers, significant decreased layers thickness, and significantly decreased antioxidant biomarkers, but markedly elevated oxidative stress biomarker levels. Moreover, marked histological alterations and astrocytosis were observed, as evidenced by the increased number of G-FAP immunopositive cells in cerebellar tissues compared with the other groups.</p><p><strong>Conclusion: </strong>Acrylamide exposure severely damages cerebellar tissue, primarily through oxidative stress. The combination of nano-hydroxyapatite and vitamin B12 provided neuroprotection, with vitamin B12 producing the most noticeable recovery.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-14"},"PeriodicalIF":2.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149134878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deciphering the toxicological impact of sublethal ethion exposed <i>Drosophila melanogaster</i> using classical and transcriptomics approaches.","authors":"Srishti Sharma, Sujata Mohanty","doi":"10.1080/01480545.2026.2743612","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743612","url":null,"abstract":"<p><p>Ethion insecticide is known for its neurotoxicity and due to its extensive usage, non- target species may suffer along with the targeted ones. Thus, its detrimental effects on non-target species need to be explored in depth. The present study aims to assess the ethion toxicity in non-target model <i>Drosophila melanogaster</i> using classical and molecular approaches. The two sublethal concentrations 1.25 and 1.88 ppm were selected based on the LC₅₀ value and were used throughout the experiments. The detrimental effect of ethion on various life history traits increased with higher concentration. The phenotypic observations s evidenced deformities in egg, larvae and adult. The histological analysis revealed larval brain degeneration, loss of eye- imaginal disk nuclear features and extensive tissue damage in gut and Malpighian tubules. The preliminary RNAseq data analysis revealed that the upregulated differentially expressed genes (DEGs) in response to ethion were mostly associated with growth and development (<i>TwdlM</i>, <i>TwdlL</i> and <i>Eip78C</i> etc.), neurological behavior (<i>ap, inaD</i>, <i>Galphaq</i>, <i>Rim</i>, <i>ple, ddc</i> etc.<i>)</i>, reproduction (<i>Cp15</i>, <i>Cp16</i>, <i>Cp7Fa</i>, <i>Cp7Fb</i>, <i>dec</i>, CG1077 etc.). Moreover, the downregulated DEGs are belong to the class of Mitochondrial Ribosomal Protein (MRP) gene family which regulate growth through mitochondrial translation and transcription. The top 25 hub genes among DEGs were found to have human orthologues, which are used as candidate genes in studying various human diseases. Thus, the study highlights attention to the concerning ecotoxicity and possible health hazards associated with insecticide usage especially to non-targets including humans.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-18"},"PeriodicalIF":2.2,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Praziquantel residue profile and integrated biomarker response-based risk assessment for Nile tilapia <i>Oreochromis niloticus</i>.","authors":"Arpan Ghorai, Thangapalam Jawahar Abraham, Arya Sen, Ranjit Kumar Nadella, Niladri Sekhar Chatterjee, Prasanna Kumar Patil","doi":"10.1080/01480545.2026.2743619","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743619","url":null,"abstract":"<p><p>As aquaculture intensifies, Nile tilapia <i>Oreochromis niloticus</i> is increasingly susceptible to parasitic infections. This study evaluated the safety and physiological effects of praziquantel (PQ) in tilapia. PQ was administered orally at 50 mg/kg (recommended dose) and 125 mg/kg biomass/day (supratherapeutic dose) for 3 days, and the effects were compared with a control group. Mortality in PQ-treated groups ranged from 0.67% to 4%. Plasma glucose increased dose-dependently on day 3 and returned to baseline in the recommended dose group by day 28 post-treatment. Calcium, chloride, and acetylcholinesterase levels decreased during dosing, with partial recovery observed subsequently. On day 3, reductions in erythrocyte, hemoglobin, and hematocrit levels were accompanied by increases in leucocyte and thrombocyte counts. The supratherapeutic dose group exhibited more pronounced cellular and nuclear alterations in erythrocytes. Oxidative stress biomarkers in liver and kidney tissues indicated organ-specific stress. Integrated Biomarker Response analysis revealed that a supratherapeutic dose induced greater biological disturbance<i>s</i>. At the recommended dose, PQ residues in muscle and skin reached below detectable levels within 2 days, supporting a 2-day withdrawal period for consumer safety. However, some biological instabilities persisted beyond this period, suggesting incomplete physiological recovery and therefore, residue clearance alone does not confirm complete biological safety.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-16"},"PeriodicalIF":2.2,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126899","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Absorption and toxicity of mineral oil after dermal and mucosal surface exposure: a review.","authors":"Niels Hadrup, Jorid B Sørli, Stephanie C Hammel, Anoop K Sharma","doi":"10.1080/01480545.2026.2743650","DOIUrl":"https://doi.org/10.1080/01480545.2026.2743650","url":null,"abstract":"<p><p>Dermal and mucosal surface exposure to mineral oils occurs in the occupational setting. To evaluate exposure levels at which toxicity occurs, we collected data on non-cancer toxicity of crude oil, refinery streams and refined mineral oils. This included extraction of no-observed-adverse-effect levels (NOAELs) and lowest-observed-adverse-effect levels (LOAELs). Concerning biokinetics, whole oils appear to have low skin penetration, while polycyclic aromatic hydrocarbon (PAH) fractions penetrate to a considerable extent. Concerning toxicity of crude oil, reported local effects in humans include skin rash and eczema. In animals, a LOAEL_{Skin irritation} was 0.4 mg/cm². Systemic effects of crude oils include a LOAEL_{Developmental effects} of 30 mg/kg body weight (bw). Concerning refinery streams, local effects of syntower bottoms showed a LOAEL_{Skin histopathology} of 0.1 mg/cm². Catalytically-cracked clarified oil had a LOAEL_Irritation of 3 mg/cm²; a systemic LOAEL on maternal body weight and developmental toxicity of clarified slurry oil was 1 mg/kg bw (NOAEL: 0.05 mg/kg bw). Systemic effects of refinery streams correlated with PAH content (mainly driven by one study). Concerning refined mineral oils, local effects reported in mechanics and metal workers include contact dermatitis, oil acne and nose and throat irritation (exposure involved used oils and other chemicals). A human LOAEL_{skin occlusion} of refined oil was 2 mg/cm²; in animals, skin irritation had LOAELs as low as 15 mg/cm² (NOAEL: 7.6 mg/cm²). Systemic effects of refined oils in rats included a LOAEL_{Depressed body weight} of 160 mg/kg bw. In conclusion, both local and systemic effects are observed after dermal exposure to mineral oils.</p>","PeriodicalId":11333,"journal":{"name":"Drug and Chemical Toxicology","volume":" ","pages":"1-18"},"PeriodicalIF":2.2,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}