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Article ; Online: Skin Sensitization Induction Risk Assessment of Common Ingredients in Commercially Available Cleansing Conditioners.

Monnot, Andrew D / Towle, Kevin M / Warshaw, Erin M / Fung, Ernest S / Novick, Rachel M / Paustenbach, Dennis J / Drechsel, Derek A

Dermatitis : contact, atopic, occupational, drug

2019 Volume 30, Issue 2, Page(s) 116–128

Abstract: Background: An essential step in ensuring the toxicological safety of cosmetic or personal care products is the evaluation of the skin sensitizing potential of product ingredients.: Objective: We used a standardized protocol from cosmetic trade ... ...

Abstract	Background: An essential step in ensuring the toxicological safety of cosmetic or personal care products is the evaluation of the skin sensitizing potential of product ingredients. Objective: We used a standardized protocol from cosmetic trade industry and consumer safety groups to evaluate the sensitization potential of ingredients in 3 commercially available cleansing conditioners. Methods: A total of 33 ingredients were evaluated. Each ingredient underwent (1) dermatological evaluation, (2) in silico analysis for irritation and sensitization potential, and (3) a literature evaluation to determine risk of sensitization. Consumer exposure level was compared with the weight-of-evidence no-expected sensitization induction level for the constituent. If a no-expected sensitization induction level for a specific ingredient was not available, the dermal sensitization threshold approach was used. A margin of safety was calculated for each constituent. Results: The margins of safety for all evaluated ingredients in the cleansing conditioners were greater than 1. Conclusions: This analysis indicates that exposure to the individual ingredients present in these cleansing conditioners would not be expected to induce dermal sensitization in a consumer under the examined exposure scenario.
MeSH term(s)	Adult ; Clinical Protocols ; Computer Simulation ; Consumer Product Safety/standards ; Dermatitis, Allergic Contact/etiology ; Female ; Hair Preparations/adverse effects ; Hair Preparations/toxicity ; Humans ; Risk Assessment ; Scalp Dermatoses/chemically induced ; Scalp Dermatoses/etiology ; Skin Care/adverse effects ; Skin Care/methods
Chemical Substances	Hair Preparations
Language	English
Publishing date	2019-04-08
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2144723-8
ISSN	2162-5220 ; 1532-8163 ; 1710-3568
ISSN (online)	2162-5220 ; 1532-8163
ISSN	1710-3568
DOI	10.1097/DER.0000000000000445
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Article ; Online: Historical evolution of regulatory standards for occupational and consumer exposures to industrial talc.

Drechsel, Derek A / Barlow, Christy A / Bare, Jennifer L / Jacobs, Neva F / Henshaw, John L

Regulatory toxicology and pharmacology : RTP

2017 Volume 92, Page(s) 251–267

Abstract: Talc has been used historically in a wide range of industrial applications and consumer products. The composition and purity of talc used for industrial purposes can vary greatly depending on the source and may contain asbestos minerals. The developing ... ...

Abstract	Talc has been used historically in a wide range of industrial applications and consumer products. The composition and purity of talc used for industrial purposes can vary greatly depending on the source and may contain asbestos minerals. The developing science associated with the health risks of asbestos had an effect on the talc industry throughout the 20th century. This review presents a detailed analysis of the evolution of regulatory standards impacting the use of industrial talc in the U.S. from the early 20th century through the 1990s. While it was recognized by the 1930s that airborne exposures to talc dust at high concentrations could cause lung disease, it was not until later that concerns were raised about the health risks associated with potential occupational exposures to asbestos from industrial talc. Regulatory agencies adopted occupational standards for industrial talc in the early 1970s, but the terminology used to define and characterize talc and other associated minerals varied between agencies. In addition, the complex and varying mineralogy of industrial talc led to inconsistent and imprecise interpretation of studies concerning health risk and occupational health standards among individual agencies.
MeSH term(s)	Air Pollutants, Occupational/chemistry ; Animals ; Asbestos/adverse effects ; Asbestos/chemistry ; Dust/analysis ; Humans ; Industry ; Occupational Exposure/analysis ; Occupational Health ; Talc/adverse effects ; Talc/chemistry
Chemical Substances	Air Pollutants, Occupational ; Dust ; Asbestos (1332-21-4) ; Talc (14807-96-6)
Language	English
Publishing date	2017-12-09
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	604672-1
ISSN	1096-0295 ; 0273-2300
ISSN (online)	1096-0295
ISSN	0273-2300
DOI	10.1016/j.yrtph.2017.12.005
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Article ; Online: Respiration-dependent H2O2 removal in brain mitochondria via the thioredoxin/peroxiredoxin system.

Drechsel, Derek A / Patel, Manisha

The Journal of biological chemistry

2010 Volume 285, Issue 36, Page(s) 27850–27858

Abstract: Mitochondrial reactive oxygen species (ROS) play an important role in both physiological cell signaling processes and numerous pathological states, including neurodegenerative disorders such as Parkinson disease. While mitochondria are considered the ... ...

Abstract	Mitochondrial reactive oxygen species (ROS) play an important role in both physiological cell signaling processes and numerous pathological states, including neurodegenerative disorders such as Parkinson disease. While mitochondria are considered the major cellular source of ROS, their role in ROS removal remains largely unknown. Using polarographic methods for real-time detection of steady-state H(2)O(2) levels, we were able to quantitatively measure the contributions of potential systems toward H(2)O(2) removal by brain mitochondria. Isolated rat brain mitochondria showed significant rates of exogenous H(2)O(2) removal (9-12 nmol/min/mg of protein) in the presence of substrates, indicating a respiration-dependent process. Glutathione systems showed only minimal contributions: 25% decrease with glutathione reductase inhibition and no effect by glutathione peroxidase inhibition. In contrast, inhibitors of thioredoxin reductase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H(2)O(2) removal rates in mitochondria by 80%. Furthermore, a 50% decrease in H(2)O(2) removal was observed following oxidation of peroxiredoxin. Differential oxidation of glutathione or thioredoxin proteins by copper (II) or arsenite, respectively, provided further support for the thioredoxin/peroxiredoxin system as the major contributor to mitochondrial H(2)O(2) removal. Inhibition of the thioredoxin system exacerbated mitochondrial H(2)O(2) production by the redox cycling agent, paraquat. Additionally, decreases in H(2)O(2) removal were observed in intact dopaminergic neurons with thioredoxin reductase inhibition, implicating this mechanism in whole cell systems. Therefore, in addition to their recognized role in ROS production, mitochondria also remove ROS. These findings implicate respiration- and thioredoxin-dependent ROS removal as a potentially important mitochondrial function that may contribute to physiological and pathological processes in the brain.
MeSH term(s)	Animals ; Brain/cytology ; Cell Line ; Cell Membrane Permeability ; Cell Respiration/drug effects ; Dopamine/metabolism ; Enzyme Inhibitors/pharmacology ; Hydrogen Peroxide/metabolism ; Hydrogen Peroxide/pharmacology ; Liver/cytology ; Male ; Metals/pharmacology ; Mitochondria/drug effects ; Mitochondria/enzymology ; Mitochondria/metabolism ; Peroxiredoxins/metabolism ; Polarography ; Rats ; Rats, Sprague-Dawley ; Thioredoxin-Disulfide Reductase/antagonists & inhibitors ; Thioredoxins/metabolism
Chemical Substances	Enzyme Inhibitors ; Metals ; Thioredoxins (52500-60-4) ; Hydrogen Peroxide (BBX060AN9V) ; Peroxiredoxins (EC 1.11.1.15) ; Thioredoxin-Disulfide Reductase (EC 1.8.1.9) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2010-06-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M110.101196
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Article ; Online: Chapter 21 Paraquat-induced production of reactive oxygen species in brain mitochondria.

Drechsel, Derek A / Patel, Manisha

Methods in enzymology

2009 Volume 456, Page(s) 381–393

Abstract: Paraquat (PQ) is a prototypical redox cycling agent commonly used experimentally to generate reactive oxygen species and oxidative stress. Recently, PQ has also come under investigation as a potential environmental neurotoxin associated with increased ... ...

Abstract	Paraquat (PQ) is a prototypical redox cycling agent commonly used experimentally to generate reactive oxygen species and oxidative stress. Recently, PQ has also come under investigation as a potential environmental neurotoxin associated with increased risk for neurodegenerative disease developing after chronic exposure. The interactions of PQ with mitochondria remain an important aspect of its toxicity, particularly in the brain, although the underlying mechanisms are relatively uncharacterized. Here, we describe the basic measurement of PQ-induced hydrogen peroxide (H(2)O(2)) production in isolated brain mitochondria by use of two independent methods, polarography and fluorometry. The advantages of the use of these two independent methods include the capability to validate results and overcoming limitations in the use of either method exclusively. These simplified in vitro techniques for measurement of mitochondrial-generated H(2)O(2) can be easily applied to other tissues and models.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidative Stress ; Paraquat/pharmacology ; Rats ; Reactive Oxygen Species/metabolism
Chemical Substances	Reactive Oxygen Species ; Paraquat (PLG39H7695)
Language	English
Publishing date	2009-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1557-7988
ISSN (online)	1557-7988
DOI	10.1016/S0076-6879(08)04421-2
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Article ; Online: Differential contribution of the mitochondrial respiratory chain complexes to reactive oxygen species production by redox cycling agents implicated in parkinsonism.

Drechsel, Derek A / Patel, Manisha

Toxicological sciences : an official journal of the Society of Toxicology

2009 Volume 112, Issue 2, Page(s) 427–434

Abstract: Exposure to environmental pesticides can cause significant brain damage and has been linked with an increased risk of developing neurodegenerative disorders, including Parkinson's disease. Bipyridyl herbicides, such as paraquat (PQ), diquat (DQ), and ... ...

Abstract	Exposure to environmental pesticides can cause significant brain damage and has been linked with an increased risk of developing neurodegenerative disorders, including Parkinson's disease. Bipyridyl herbicides, such as paraquat (PQ), diquat (DQ), and benzyl viologen (BV), are redox cycling agents known to exert cellular damage through the production of reactive oxygen species (ROS). We examined the involvement of the mitochondrial respiratory chain in ROS production by bipyridyl herbicides. In isolated rat brain mitochondria, H2O2 production occurred with the following order of potency: BV > DQ > PQ in accordance with their measured ability to redox cycle. H2O2 production was significantly attenuated in all cases by antimycin A, an inhibitor of complex III. Interestingly, at micromolar (< or = 300 microM) concentrations, PQ-induced H2O2 production was unaffected by complex I inhibition via rotenone, whereas DQ-induced H2O2 production was equally attenuated by inhibition of complex I or III. Moreover, complex I inhibition decreased BV-induced H2O2 production to a greater extent than with PQ or DQ. These data suggest that multiple sites within the respiratory chain contribute to H2O2 production by redox cycling bipyridyl herbicides. In primary midbrain cultures, H2O2 differed slightly with the following order of potency: DQ > BV > PQ. In this model, inhibition of complex III resulted in roughly equivalent inhibition of H2O2 production with all three compounds. These data identify a novel role for complex III dependence of mitochondrial ROS production by redox cycling herbicides, while emphasizing the importance of identifying mitochondrial mechanisms by which environmental agents generate oxidative stress contributing to parkinsonism.
MeSH term(s)	Animals ; Brain/drug effects ; Electron Transport ; Herbicides/toxicity ; Male ; Mitochondria/drug effects ; Oxidation-Reduction ; Parkinsonian Disorders/chemically induced ; Rats ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism
Chemical Substances	Herbicides ; Reactive Oxygen Species
Language	English
Publishing date	2009-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/kfp223
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Article: Respiration-dependent H₂O₂ Removal in Brain Mitochondria via the Thioredoxin/Peroxiredoxin System

Drechsel, Derek A / Patel, Manisha

Journal of biological chemistry. 2010 Sept. 3, v. 285, no. 36

2010

Abstract	Mitochondrial reactive oxygen species (ROS) play an important role in both physiological cell signaling processes and numerous pathological states, including neurodegenerative disorders such as Parkinson disease. While mitochondria are considered the major cellular source of ROS, their role in ROS removal remains largely unknown. Using polarographic methods for real-time detection of steady-state H₂O₂ levels, we were able to quantitatively measure the contributions of potential systems toward H₂O₂ removal by brain mitochondria. Isolated rat brain mitochondria showed significant rates of exogenous H₂O₂ removal (9-12 nmol/min/mg of protein) in the presence of substrates, indicating a respiration-dependent process. Glutathione systems showed only minimal contributions: 25% decrease with glutathione reductase inhibition and no effect by glutathione peroxidase inhibition. In contrast, inhibitors of thioredoxin reductase, including auranofin and 1-chloro-2,4-dinitrobenzene, attenuated H₂O₂ removal rates in mitochondria by 80%. Furthermore, a 50% decrease in H₂O₂ removal was observed following oxidation of peroxiredoxin. Differential oxidation of glutathione or thioredoxin proteins by copper (II) or arsenite, respectively, provided further support for the thioredoxin/peroxiredoxin system as the major contributor to mitochondrial H₂O₂ removal. Inhibition of the thioredoxin system exacerbated mitochondrial H₂O₂ production by the redox cycling agent, paraquat. Additionally, decreases in H₂O₂ removal were observed in intact dopaminergic neurons with thioredoxin reductase inhibition, implicating this mechanism in whole cell systems. Therefore, in addition to their recognized role in ROS production, mitochondria also remove ROS. These findings implicate respiration- and thioredoxin-dependent ROS removal as a potentially important mitochondrial function that may contribute to physiological and pathological processes in the brain.
Language	English
Dates of publication	2010-0903
Size	p. 27850-27858.
Publishing place	American Society for Biochemistry and Molecular Biology
Document type	Article
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Tier-based skin irritation testing of hair cleansing conditioners and their constituents.

Fung, Ernest S / Novick, Rachel M / Drechsel, Derek A / Towle, Kevin M / Paustenbach, Dennis J / Monnot, Andrew D

Cutaneous and ocular toxicology

2018 Volume 38, Issue 1, Page(s) 44–47

Abstract: Purpose/Aim: The U.S. Food and Drug Administration (FDA) does not require specific testing to demonstrate the safety of personal care and cosmetic products or their ingredients. Recently, there have been reports of skin irritation associated with the use ...

Abstract	Purpose/Aim: The U.S. Food and Drug Administration (FDA) does not require specific testing to demonstrate the safety of personal care and cosmetic products or their ingredients. Recently, there have been reports of skin irritation associated with the use of commercially available cleansing conditioners. The goal of this study was to implement a tier-based safety assessment to evaluate the skin irritation potential of six commercially available cleansing conditioners and their ingredients. Materials and methods: The first tier of testing utilized the Organization for Economic Co-operation and Development (OECD) QSAR Toolbox to perform an in silico evaluation of the skin irritation potential of the product ingredients, and the second tier of testing utilized an OECD in vitro guideline test to evaluate the skin irritation potential of each product. Results: Thirty-two ingredients were evaluated using the OECD QSAR Toolbox profiler for the tier one analysis; nine ingredients received a structural alert for skin irritation/corrosion. In the tier two in vitro analysis, the evaluated cleansing conditioner products were all classified as non-irritants. Conclusions: These results provide evidence that use of the evaluated commercially available cleansing conditioners would not be expected to cause skin irritation among consumers. Additionally, this study demonstrates that the presence of structural alerts does not always accurately predict the safety of a product, as focused tier-based testing is necessary to comprehensively evaluate a product. This study illustrates a tier-based safety assessment approach, applicable to a wide variety of health endpoints, which efficiently and adequately evaluates the safety of personal care and cosmetic products and their ingredients.
MeSH term(s)	Computer Simulation ; Consumer Product Safety ; Hair Preparations/chemistry ; Hair Preparations/classification ; Hair Preparations/toxicity ; Humans ; Quantitative Structure-Activity Relationship ; Risk Assessment ; Skin/drug effects ; Skin Irritancy Tests
Chemical Substances	Hair Preparations
Language	English
Publishing date	2018-11-26
Publishing country	England
Document type	Journal Article
ZDB-ID	605635-0
ISSN	1556-9535 ; 1556-9527 ; 0731-3829
ISSN (online)	1556-9535
ISSN	1556-9527 ; 0731-3829
DOI	10.1080/15569527.2018.1512610
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Article ; Online: Skin Sensitization Induction Potential From Daily Exposure to Fragrances in Personal Care Products.

Drechsel, Derek A / Towle, Kevin M / Fung, Ernest S / Novick, Rachel M / Paustenbach, Dennis J / Monnot, Andrew D

Dermatitis : contact, atopic, occupational, drug

2018 Volume 29, Issue 6, Page(s) 324–331

Abstract: Background: Many chemicals used for fragrance purposes in a diversity of products have allergenic potential. Based on such concerns, industry groups developed concentration limits for use of fragrance chemicals in personal care and cosmetic products.: ...

Abstract	Background: Many chemicals used for fragrance purposes in a diversity of products have allergenic potential. Based on such concerns, industry groups developed concentration limits for use of fragrance chemicals in personal care and cosmetic products. Objective: The aim of this study was to use a quantitative risk assessment to evaluate the potential for skin sensitization induction resulting from daily exposure to fragrance chemicals present in personal care and cosmetic products. Methods: Product-specific dermal consumer exposure levels were calculated based on product use data in US adult females and benchmarked against acceptable exposure levels based on reported no expected sensitization induction levels to determine a margin of safety for each fragrance under evaluation. Conclusions: The results demonstrate an increased risk of skin sensitization induction for several leave-on products (lipstick, solid antiperspirant, eye shadow, face cream) for most of the evaluated fragrance chemicals, particularly under high-use exposure scenarios. In contrast, rinse-off products (shampoo, conditioner, facial cleanser) were not associated with risk of skin sensitization induction. Because the approach was based on maximum use limits for fragrance chemicals with skin sensitization concerns, the results suggest these limits may not be protective, particularly in the United States.
MeSH term(s)	Antiperspirants/adverse effects ; Body Surface Area ; Consumer Product Safety ; Cosmetics/administration & dosage ; Cosmetics/adverse effects ; Dermatitis, Allergic Contact/etiology ; Female ; Hair Preparations/administration & dosage ; Hair Preparations/adverse effects ; Humans ; Mathematical Concepts ; Perfume/administration & dosage ; Perfume/adverse effects ; Risk Assessment ; Skin/drug effects ; Skin Cream/administration & dosage ; Skin Cream/adverse effects
Chemical Substances	Antiperspirants ; Cosmetics ; Hair Preparations ; Perfume
Language	English
Publishing date	2018-09-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2144723-8
ISSN	2162-5220 ; 1532-8163 ; 1710-3568
ISSN (online)	2162-5220 ; 1532-8163
ISSN	1710-3568
DOI	10.1097/DER.0000000000000412
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Article: Role of reactive oxygen species in the neurotoxicity of environmental agents implicated in Parkinson's disease.

Drechsel, Derek A / Patel, Manisha

Free radical biology & medicine

2008 Volume 44, Issue 11, Page(s) 1873–1886

Abstract: Among age-related neurodegenerative diseases, Parkinson's disease (PD) represents the best example for which oxidative stress has been strongly implicated. The etiology of PD remains unknown, yet recent epidemiological studies have linked exposure to ... ...

Abstract	Among age-related neurodegenerative diseases, Parkinson's disease (PD) represents the best example for which oxidative stress has been strongly implicated. The etiology of PD remains unknown, yet recent epidemiological studies have linked exposure to environmental agents, including pesticides, with an increased risk of developing the disease. As a result, the environmental hypothesis of PD has developed, which speculates that chemical agents in the environment are capable of producing selective dopaminergic cell death, thus contributing to disease development. The use of environmental agents such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, rotenone, paraquat, dieldrin, and maneb in toxicant-based models of PD has become increasingly popular and provided valuable insight into the neurodegenerative process. Understanding the unique and shared mechanisms by which these environmental agents act as selective dopaminergic toxicants is critical in identifying pathways involved in PD pathogenesis. In this review, we discuss the neurotoxic properties of these compounds with specific focus on the induction of oxidative stress. We highlight landmark studies along with recent advances that support the role of reactive oxygen and reactive nitrogen species from a variety of cellular sources as potent contributors to the neurotoxicity of these environmental agents. Finally, human risk and the implications of these studies in our understanding of PD-related neurodegeneration are discussed.
MeSH term(s)	Animals ; Humans ; Neurons/drug effects ; Neurons/metabolism ; Neurotoxins/toxicity ; Oxidative Stress ; Parkinson Disease/metabolism ; Reactive Oxygen Species/metabolism
Chemical Substances	Neurotoxins ; Reactive Oxygen Species
Language	English
Publishing date	2008-03-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2008.02.008
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Article ; Online: Risk Assessment of the Skin Sensitization Induction Potential of Kathon CG in Rinse-off and Leave-on Personal Care and Cosmetic Products.

Towle, Kevin M / Drechsel, Derek A / Warshaw, Erin M / Fung, Ernest S / Novick, Rachel M / Paustenbach, Dennis J / Monnot, Andrew D

Dermatitis : contact, atopic, occupational, drug

2018 Volume 29, Issue 3, Page(s) 132–138

Abstract: Background: Kathon CG is a commonly used cosmetic-grade preservative that contains active ingredients methylchloroisothiazolinone (MCI) and methylisothiazolinone (MI).: Objective: The aim of the study was to perform a skin sensitization induction ... ...

Abstract	Background: Kathon CG is a commonly used cosmetic-grade preservative that contains active ingredients methylchloroisothiazolinone (MCI) and methylisothiazolinone (MI). Objective: The aim of the study was to perform a skin sensitization induction risk assessment of daily exposure to Kathon CG after use of various personal care and cosmetic products. Methods: We calculated an estimated daily consumer exposure level for rinse-off and leave-on products using the amount of product applied per application, number of applications per day, a retention factor, the MCI/MI concentration, and body surface area values. We assumed that the products contained the maximum recommended safe concentration of MCI/MI: 15 ppm in rinse-off products and 7.5 ppm in leave-on products. We compared estimated consumer exposure levels with the no expected sensitization induction level for MCI/MI and applied sensitization assessment factors to calculate product-specific margins of safety (MOSs). Conclusions: The MOSs for rinse-off products ranged from 5 to 63, whereas the MOSs for leave-on products ranged from 0.03 to 1.49. Overall, our results provide evidence that some leave-on products containing the maximum recommended safe concentration of Kathon CG may increase the risk of sensitization induction due to exposure to MCI/MI. In contrast, rinse-off products were not associated with a potential increased risk of skin sensitization induction.
MeSH term(s)	Cosmetics/adverse effects ; Cosmetics/analysis ; Cosmetics/pharmacology ; Dermatitis, Allergic Contact/diagnosis ; Dermatitis, Allergic Contact/etiology ; Female ; Humans ; Preservatives, Pharmaceutical/adverse effects ; Preservatives, Pharmaceutical/analysis ; Preservatives, Pharmaceutical/pharmacology ; Risk Assessment ; Skin/drug effects ; Thiazoles/adverse effects ; Thiazoles/analysis ; Thiazoles/pharmacology
Chemical Substances	Cosmetics ; Preservatives, Pharmaceutical ; Thiazoles ; 2-methyl-4-isothiazolin-3-one (229D0E1QFA) ; Kathon 886 (55965-84-9) ; 5-chloro-2-methyl-4-isothiazolin-3-one (DEL7T5QRPN)
Language	English
Publishing date	2018-03-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2144723-8
ISSN	2162-5220 ; 1532-8163 ; 1710-3568
ISSN (online)	2162-5220 ; 1532-8163
ISSN	1710-3568
DOI	10.1097/DER.0000000000000359
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