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Resident Involvement in Policy-Making
As dermatology residents, we hear rumblings of the political aspects of medicine on the news, at conferences, or from our attending physicians. Most of us conveniently ignore them until after we graduate; however, once we start practicing, we may be shocked to discover just how much politics affect the practice of medicine. In this article, the role of the American Academy of Dermatology Association (AADA) in policy-making is discussed as well as some ways residents can be involved in the process and emphasize just how vital our participation is, even this early on in our careers.
Role of the AADA in Policy-Making
The AADA advocates on behalf of its members and dermatology patients with the US Congress, state legislatures, and regulatory agencies on issues of concern to the specialty and offers members several opportunities to become involved in advocacy at the state, national, and grassroots levels.1 The AAD provides several sources of information on the Web, including the Dermatology Advocacy Network (http://www.aad-dan.com/), which includes information on how to contact your member of Congress through the AADA; updates on activities and topics discussed at the AADA Legislative Conference (https://www.aad.org/meetings/legislative -conference) and information on how to participate in future conferences; resources on getting involved in advocacy at the grassroots level (https://www.aad.org /members/practice-and-advocacy/get-involved /grassroots-advocacy); and information on how to become involved with SkinPAC (https://www.skinpac.org/), the AADA’s political action committee (PAC). A PAC is organized for the purpose of advancing a particular legislative agenda, whatever the issue may be. SkinPAC ensures that the concerns of dermatologists and their patients are heard on Capitol Hill.
Opportunities for Resident Involvement
There are several ways residents can be involved in policy-making, including (1) attending the annual AADA Legislative Conference, which offers participants a unique opportunity to attend advocacy training sessions taught by health policy experts, discuss dermatology issues with colleagues, and become trusted and influential voices that members of Congress can rely on,1 (2) sending a letter to your state or federal officials through the AADA Dermatology Advocacy Network, (3) becoming a state advocacy leader, especially through your state’s PAC, and (4) reading the AAD’s bi-weekly Dermatology Advocate e-newsletter (https://www.aad.org /members/publications/dermatology-advocate), which includes information on congressional actions, federal agency and administration activities, state-level legislative and regulatory news, actions by private payers, and the AADA’s active engagement in these arenas. Also featured in the Dermatology Advocate e-newsletter is news and information about how members can get involved in advocacy efforts by the AADA and SkinPAC.
AADA Legislative Conference
The 2015 AADA Legislative Conference took place in September in Washington, DC. This conference offers a unique opportunity for residents to learn how federal legislation will impact the future of dermatology. The AADA awards several scholarships to residents who commit to one year of involvement in AADA grassroots advocacy.2 The AADA covers all expenses to attend the conference for each scholarship recipient, and residents are not required to have any political knowledge or experience in order to attend the conference or receive a scholarship. Advocacy training, which is offered by a panel of health policy experts, covers all aspects of the legislative process as well as information about the legislators themselves.
In addition to the opportunities to get involved on a national level through the AADA, most states also have their own PACs with which physicians can work on grassroots-level issues, such as advocating for state laws prohibiting minors under 18 years of age from using indoor tanning beds, or larger issues including the Medicare sustainable growth rate or global period codes. Additionally, some subspecialties also have their own advocacy groups, including the American Society for Dermatologic Surgery Association’s State-based Advocacy Network for Dermatology Surgery (http://asdsa.asds.net/ResidentStateAdvocacy.aspx).
The Importance and Influence of Involvement in Policy-Making
It has been shown that many residents are in fact interested in joining PACs that are relevant to their specialty after learning about the roles these committees play in policy-making but that time constraints and obligations of residency often interfere with their participation.3 As residents, involvement by our attending physicians plays a huge role. A recent study showed more resident involvement when faculty members set an example of civic involvement and PAC support.3
I was inspired to write this column by my residency program’s impressive involvement with SkinPAC last year as well as my own personal experience being an active advocate. During medical school, I helped testify for the Texas State Senate Committee on Health and Human Services in Austin about the risks of indoor tanning and witnessed the eventual ban on indoor tanning use by minors in the state of Texas, which came as a direct result of our advocacy and push for change. I used the University of Texas Medical Branch Dermatology Interest blog (of which I was the Editor during medical school) to help educate others on this issue, lay down the facts to be discussed in an organized and powerful way, and provide contact information for state legislators (http://digutmb.blogspot.com/2013/05 /act-now-tell-governor-perry-to-support.html).
Final Thoughts
As dermatology residents, a substantial amount of what we do in the routine care of our patients is influenced by policy decisions made by legislators at the state and federal levels, who often do not understand the impact their decisions have on our ability to effectively practice medicine. Learning about these issues now and becoming involved in efforts to affect change is something every resident can do, so get active!
Acknowledgement—I would like to thank the faculty members of the Department of Dermatology and Cutaneous Surgery at the University of South Florida, Tampa, for their active involvement in SkinPAC and the AADA Legislative Conference.
1. Get involved: AADA advocacy. American Academy of Dermatology Web site. https://www.aad.org /members/practice-and-advocacy//get-involved. Accessed September 21, 2015.
2. Resident scholarship to legislative conference. American Academy of Dermatology Web site. https://www.aad.org /education/awards-grants-and-scholarships/resident -scholarship-to-legislative-conference. Accessed October 19, 2015.
3. Shah RP, Froelich, JM, Weinstein SL, et al. Factors influencing resident participation in the AAOS Political Action Committee. Orthopedics. 2013;36:826-830.
As dermatology residents, we hear rumblings of the political aspects of medicine on the news, at conferences, or from our attending physicians. Most of us conveniently ignore them until after we graduate; however, once we start practicing, we may be shocked to discover just how much politics affect the practice of medicine. In this article, the role of the American Academy of Dermatology Association (AADA) in policy-making is discussed as well as some ways residents can be involved in the process and emphasize just how vital our participation is, even this early on in our careers.
Role of the AADA in Policy-Making
The AADA advocates on behalf of its members and dermatology patients with the US Congress, state legislatures, and regulatory agencies on issues of concern to the specialty and offers members several opportunities to become involved in advocacy at the state, national, and grassroots levels.1 The AAD provides several sources of information on the Web, including the Dermatology Advocacy Network (http://www.aad-dan.com/), which includes information on how to contact your member of Congress through the AADA; updates on activities and topics discussed at the AADA Legislative Conference (https://www.aad.org/meetings/legislative -conference) and information on how to participate in future conferences; resources on getting involved in advocacy at the grassroots level (https://www.aad.org /members/practice-and-advocacy/get-involved /grassroots-advocacy); and information on how to become involved with SkinPAC (https://www.skinpac.org/), the AADA’s political action committee (PAC). A PAC is organized for the purpose of advancing a particular legislative agenda, whatever the issue may be. SkinPAC ensures that the concerns of dermatologists and their patients are heard on Capitol Hill.
Opportunities for Resident Involvement
There are several ways residents can be involved in policy-making, including (1) attending the annual AADA Legislative Conference, which offers participants a unique opportunity to attend advocacy training sessions taught by health policy experts, discuss dermatology issues with colleagues, and become trusted and influential voices that members of Congress can rely on,1 (2) sending a letter to your state or federal officials through the AADA Dermatology Advocacy Network, (3) becoming a state advocacy leader, especially through your state’s PAC, and (4) reading the AAD’s bi-weekly Dermatology Advocate e-newsletter (https://www.aad.org /members/publications/dermatology-advocate), which includes information on congressional actions, federal agency and administration activities, state-level legislative and regulatory news, actions by private payers, and the AADA’s active engagement in these arenas. Also featured in the Dermatology Advocate e-newsletter is news and information about how members can get involved in advocacy efforts by the AADA and SkinPAC.
AADA Legislative Conference
The 2015 AADA Legislative Conference took place in September in Washington, DC. This conference offers a unique opportunity for residents to learn how federal legislation will impact the future of dermatology. The AADA awards several scholarships to residents who commit to one year of involvement in AADA grassroots advocacy.2 The AADA covers all expenses to attend the conference for each scholarship recipient, and residents are not required to have any political knowledge or experience in order to attend the conference or receive a scholarship. Advocacy training, which is offered by a panel of health policy experts, covers all aspects of the legislative process as well as information about the legislators themselves.
In addition to the opportunities to get involved on a national level through the AADA, most states also have their own PACs with which physicians can work on grassroots-level issues, such as advocating for state laws prohibiting minors under 18 years of age from using indoor tanning beds, or larger issues including the Medicare sustainable growth rate or global period codes. Additionally, some subspecialties also have their own advocacy groups, including the American Society for Dermatologic Surgery Association’s State-based Advocacy Network for Dermatology Surgery (http://asdsa.asds.net/ResidentStateAdvocacy.aspx).
The Importance and Influence of Involvement in Policy-Making
It has been shown that many residents are in fact interested in joining PACs that are relevant to their specialty after learning about the roles these committees play in policy-making but that time constraints and obligations of residency often interfere with their participation.3 As residents, involvement by our attending physicians plays a huge role. A recent study showed more resident involvement when faculty members set an example of civic involvement and PAC support.3
I was inspired to write this column by my residency program’s impressive involvement with SkinPAC last year as well as my own personal experience being an active advocate. During medical school, I helped testify for the Texas State Senate Committee on Health and Human Services in Austin about the risks of indoor tanning and witnessed the eventual ban on indoor tanning use by minors in the state of Texas, which came as a direct result of our advocacy and push for change. I used the University of Texas Medical Branch Dermatology Interest blog (of which I was the Editor during medical school) to help educate others on this issue, lay down the facts to be discussed in an organized and powerful way, and provide contact information for state legislators (http://digutmb.blogspot.com/2013/05 /act-now-tell-governor-perry-to-support.html).
Final Thoughts
As dermatology residents, a substantial amount of what we do in the routine care of our patients is influenced by policy decisions made by legislators at the state and federal levels, who often do not understand the impact their decisions have on our ability to effectively practice medicine. Learning about these issues now and becoming involved in efforts to affect change is something every resident can do, so get active!
Acknowledgement—I would like to thank the faculty members of the Department of Dermatology and Cutaneous Surgery at the University of South Florida, Tampa, for their active involvement in SkinPAC and the AADA Legislative Conference.
As dermatology residents, we hear rumblings of the political aspects of medicine on the news, at conferences, or from our attending physicians. Most of us conveniently ignore them until after we graduate; however, once we start practicing, we may be shocked to discover just how much politics affect the practice of medicine. In this article, the role of the American Academy of Dermatology Association (AADA) in policy-making is discussed as well as some ways residents can be involved in the process and emphasize just how vital our participation is, even this early on in our careers.
Role of the AADA in Policy-Making
The AADA advocates on behalf of its members and dermatology patients with the US Congress, state legislatures, and regulatory agencies on issues of concern to the specialty and offers members several opportunities to become involved in advocacy at the state, national, and grassroots levels.1 The AAD provides several sources of information on the Web, including the Dermatology Advocacy Network (http://www.aad-dan.com/), which includes information on how to contact your member of Congress through the AADA; updates on activities and topics discussed at the AADA Legislative Conference (https://www.aad.org/meetings/legislative -conference) and information on how to participate in future conferences; resources on getting involved in advocacy at the grassroots level (https://www.aad.org /members/practice-and-advocacy/get-involved /grassroots-advocacy); and information on how to become involved with SkinPAC (https://www.skinpac.org/), the AADA’s political action committee (PAC). A PAC is organized for the purpose of advancing a particular legislative agenda, whatever the issue may be. SkinPAC ensures that the concerns of dermatologists and their patients are heard on Capitol Hill.
Opportunities for Resident Involvement
There are several ways residents can be involved in policy-making, including (1) attending the annual AADA Legislative Conference, which offers participants a unique opportunity to attend advocacy training sessions taught by health policy experts, discuss dermatology issues with colleagues, and become trusted and influential voices that members of Congress can rely on,1 (2) sending a letter to your state or federal officials through the AADA Dermatology Advocacy Network, (3) becoming a state advocacy leader, especially through your state’s PAC, and (4) reading the AAD’s bi-weekly Dermatology Advocate e-newsletter (https://www.aad.org /members/publications/dermatology-advocate), which includes information on congressional actions, federal agency and administration activities, state-level legislative and regulatory news, actions by private payers, and the AADA’s active engagement in these arenas. Also featured in the Dermatology Advocate e-newsletter is news and information about how members can get involved in advocacy efforts by the AADA and SkinPAC.
AADA Legislative Conference
The 2015 AADA Legislative Conference took place in September in Washington, DC. This conference offers a unique opportunity for residents to learn how federal legislation will impact the future of dermatology. The AADA awards several scholarships to residents who commit to one year of involvement in AADA grassroots advocacy.2 The AADA covers all expenses to attend the conference for each scholarship recipient, and residents are not required to have any political knowledge or experience in order to attend the conference or receive a scholarship. Advocacy training, which is offered by a panel of health policy experts, covers all aspects of the legislative process as well as information about the legislators themselves.
In addition to the opportunities to get involved on a national level through the AADA, most states also have their own PACs with which physicians can work on grassroots-level issues, such as advocating for state laws prohibiting minors under 18 years of age from using indoor tanning beds, or larger issues including the Medicare sustainable growth rate or global period codes. Additionally, some subspecialties also have their own advocacy groups, including the American Society for Dermatologic Surgery Association’s State-based Advocacy Network for Dermatology Surgery (http://asdsa.asds.net/ResidentStateAdvocacy.aspx).
The Importance and Influence of Involvement in Policy-Making
It has been shown that many residents are in fact interested in joining PACs that are relevant to their specialty after learning about the roles these committees play in policy-making but that time constraints and obligations of residency often interfere with their participation.3 As residents, involvement by our attending physicians plays a huge role. A recent study showed more resident involvement when faculty members set an example of civic involvement and PAC support.3
I was inspired to write this column by my residency program’s impressive involvement with SkinPAC last year as well as my own personal experience being an active advocate. During medical school, I helped testify for the Texas State Senate Committee on Health and Human Services in Austin about the risks of indoor tanning and witnessed the eventual ban on indoor tanning use by minors in the state of Texas, which came as a direct result of our advocacy and push for change. I used the University of Texas Medical Branch Dermatology Interest blog (of which I was the Editor during medical school) to help educate others on this issue, lay down the facts to be discussed in an organized and powerful way, and provide contact information for state legislators (http://digutmb.blogspot.com/2013/05 /act-now-tell-governor-perry-to-support.html).
Final Thoughts
As dermatology residents, a substantial amount of what we do in the routine care of our patients is influenced by policy decisions made by legislators at the state and federal levels, who often do not understand the impact their decisions have on our ability to effectively practice medicine. Learning about these issues now and becoming involved in efforts to affect change is something every resident can do, so get active!
Acknowledgement—I would like to thank the faculty members of the Department of Dermatology and Cutaneous Surgery at the University of South Florida, Tampa, for their active involvement in SkinPAC and the AADA Legislative Conference.
1. Get involved: AADA advocacy. American Academy of Dermatology Web site. https://www.aad.org /members/practice-and-advocacy//get-involved. Accessed September 21, 2015.
2. Resident scholarship to legislative conference. American Academy of Dermatology Web site. https://www.aad.org /education/awards-grants-and-scholarships/resident -scholarship-to-legislative-conference. Accessed October 19, 2015.
3. Shah RP, Froelich, JM, Weinstein SL, et al. Factors influencing resident participation in the AAOS Political Action Committee. Orthopedics. 2013;36:826-830.
1. Get involved: AADA advocacy. American Academy of Dermatology Web site. https://www.aad.org /members/practice-and-advocacy//get-involved. Accessed September 21, 2015.
2. Resident scholarship to legislative conference. American Academy of Dermatology Web site. https://www.aad.org /education/awards-grants-and-scholarships/resident -scholarship-to-legislative-conference. Accessed October 19, 2015.
3. Shah RP, Froelich, JM, Weinstein SL, et al. Factors influencing resident participation in the AAOS Political Action Committee. Orthopedics. 2013;36:826-830.
Allergic Contact Dermatitis for Residents
Allergic contact dermatitis (ACD) is a common inflammatory skin condition that affects more than 14 million Americans each year.1 It has been estimated that the economic burden of ACD is nearly $3 billion per year due to school absences, work time lost, and medical expenditures.1,2 In fact, skin diseases rank second to traumatic injuries as the most common type of occupational disease.3 As dermatology residents, we will encounter many patients with ACD, a potentially debilitating skin condition. In this column, I will discuss the different types of ACD as well as their differential diagnoses and management options according to the American Academy of Allergy, Asthma & Immunology’s updated practice parameter for contact dermatitis.4 The 2015 American Contact Dermatitis Society (ACDS) Allergen of the Year and the ACDS’s Contact Allergen Management Program also will be discussed.
Clinical Presentation and Pathophysiology
Allergic contact dermatitis is a widespread skin condition characterized by erythematous and pruritic skin lesions that occur after contact with external stimuli.5 It is caused by a type IV, T cell–mediated, delayed hypersensitivity reaction in which a foreign substance comes into contact with the skin and forms an antigen complex that subsequently leads to sensitization. Upon reexposure to the antigen, the sensitized T cells induce an inflammatory cascade causing the skin changes associated with ACD. Clinical presentations of ACD include vesicles and bullae with distinct angles, lines, and borders.6
Differential Diagnosis
In contrast to ACD, irritant contact dermatitis (the more common form of contact dermatitis) is a non–immune-modulated skin reaction that occurs when an individual is exposed to a substance that causes irritation and damage to the keratinocytes.6,7 It can be an acute reaction to a household cleaning product or a chronic reaction to soap if the patient has had exposure to the product for a prolonged period of time.7 The clinical presentation of irritant contact dermatitis includes dry and fissured skin with less distinct borders and negative patch test results.6
Some other skin diseases that should be considered in the differential diagnosis for suspected ACD include atopic dermatitis, dyshidrotic eczema, inverse psoriasis, latex allergy, palmoplantar psoriasis, scabies, and tinea pedis.5 When ACD is suspected, our diagnostic approach as dermatology residents should be based on a combination of the following factors: the clinical features of the skin reaction (eg, morphology, location, symptoms), the patient’s history of exposure to an alleged allergen and lack of exposure after treatment and/or avoidance, patch test results, laboratory test results, and/or histopathologic examination to exclude other disorders with similar clinical features.8
Management
Localized acute lesions of ACD can be successfully treated with mid- or high-potency topical steroids such as triamcinolone 0.1% or clobetasol 0.05%. If an extensive area of the skin (>20%) is affected, systemic steroid therapy often is required, generally offering relief within 12 to 24 hours. Caution should be taken when prescribing oral prednisone, such as for poison ivy, as it should be tapered over a few weeks to prevent rebound dermatitis. If treatment fails and the diagnosis or specific allergen remains unknown, patch testing should be performed.3,5
Updated Practice Parameter
Practice parameters for contact dermatitis were updated in 2015, as commissioned by the Joint Task Force on Practice Parameters, to address recent advances in the field of contact dermatitis and the most recommended methods for diagnosis and management based on the current scientific literature.4 Prior to this update, the most recent recommendations were from 2006.3
Since the publication of the original practice parameter, new questions have been addressed related to emerging clinical problems such as preoperative screening and postimplantation patch testing for metal allergy in patients undergoing joint replacement surgery. In the updated practice parameter, statements have been added that more comprehensively address evaluation and management of occupational contact dermatitis.4 The potential benefits and limitations of drug patch testing in patients with maculopapular rashes, erythroderma, and nonimmediate cutaneous reactions also have been addressed. New summary statements have been included that make recommendations on the management of ACD, particularly avoidance and prevention.4
ACDS Allergen of the Year
The purpose of this “award” is to recognize the agents that cause the most remarkable clinical effects, those that draw less attention, or those that exhibit exposure patterns that have changed. The ACDS’s 2015 Allergen of the Year is formaldehyde, an inexpensive biocidal preservative used in a wide range of products such as tissue specimen and cadaveric preservation solutions, nail polish, hair-smoothing treatments, and wrinkle-free fabrics.9
Formaldehyde-releasing preservatives (FRPs) are among the leading contact allergens and are found in many personal hygiene products, medications, and household cleansers.8 Specific sources of FRPs include shampoos, bodywashes, hand soaps, lotions, creams, baby wipes, mascara, disinfectants, fabric softeners, topical wart remedies, adhesives, and tissue specimen preservation solutions.10-13 According to de Groot et al,14 the US Food and Drug Administration’s Voluntary Cosmetic Registration Program database has estimated that approximately 20% of personal hygiene products and cosmetics contain an FRP, with imidazolidinyl urea as the most common.
It is important for patients to be aware of sources of formaldehyde exposure and understand that many products containing formaldehyde or FRPs may not list this information on their labels. In fact, one study reported that 33% of 67 moisturizers evaluated did not have proper labeling with regard to their formaldehyde/FRP content.15
Contact Allergen Management Program
During medical school I served as the Dermatology Interest Group Contact Dermatitis Awareness Chair at the University of Texas Medical Branch (Galveston, Texas) and was fortunate to have attended the annual meeting of the ACDS where I learned about the ACDS Contact Allergen Management Program (CAMP), an online resource for dermatologists to access that provides patients a printout list of allergen and cross-reactivity information for more than 1200 products (http://www.contactderm.org/i4a/pages/indexcfm?pageID=3489). This information helps consumers to choose the right products based on their allergies.
Final Thoughts
A thorough review of a patient’s medical history and, if needed, skin patch testing can identify the responsible allergen and initiate an appropriate avoidance plan for the patient. With appropriate avoidance, patients can achieve resolution of their dermatitis and prevent further episodes to substantially improve their quality of life and decrease health care costs.1 If left untreated, ACD can evolve from an acute form to a subacute form and eventually chronic eczematous dermatitis or progression to systemic disease.16,17 Allergic contact dermatitis can negatively impact an individual’s health-related quality of life, particularly in social functioning and psychological well-being.18,19 Therefore, it is pertinent in our role as dermatology residents to recognize ACD before its progression to a chronic state.
1. Bickers DR, Lim HW, Margolis D, et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006;55:490-500.
2. Jacob SE. The lanolin-wool wax alcohol update. The Dermatologist. February 2014;22. http://www.the-dermatologist.com/content/lanolin-wool-wax-alcohol-update. Accessed June 26, 2015.
3. Beltrani VS, Bernstein IL, Cohen DE, et al. Contact dermatitis: a practice parameter [published correction appears in Ann Allergy Asthma Immunol. 2006;97:819]. Ann Allergy Asthma Immunol. 2006;97(3, suppl 2):S1-S38.
4. Fonacier L, Bernstein DI, Pacheco K, et al. Contact dermatitis: a practice parameter—update 2015. J Allergy Clin Immunol Pract. 2015;3(suppl 3):S1-S39.
5. Usatine R, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82:249-255.
6. Usatine RP. Contact dermatitis. In: Usatine RP, Smith M, Mayeaux EJ Jr, et al, eds. Color Atlas of Family Medicine. New York, NY: McGraw-Hill; 2009. http://accessmedicine.mhmedical.com/content.aspx?bookid=378&Sectionid=40419504. Accessed June 26, 2015.
7. Vazirnia A, Jacob SE. Review of ACDS’ allergen of the year 2010-2015. The Dermatologist. November 2014;22. http://www.the-dermatologist.com/content/review-acds%E2%80%99-allergen-od-year-2000-2015. Accessed June 26, 2015.
8. Yiannias J. Clinical features and diagnosis of allergic contact dermatitis. UpToDate Web site. http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-allergic-contact-dermatitis?source=search_result&search=allergic+contact+dermatitis&selectedTitle=2~142#. Updated May 20, 2014. Accessed June 18, 2015.
9. Pontén A, Bruze M. Formaldehyde. Dermatitis. 2015;26:3-6.
10. Maier LE, Lampel HP, Bhutani T, et al. Hand dermatitis: a focus on allergic contact dermatitis to biocides. Dermatol Clin. 2009;27:251-264.
11. Marks JG, Elsner P, DeLeo VA. Contact & Occupational Dermatology. 3rd ed. St. Louis, MO: Mosby; 2002.
12. Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 6th ed. Hamilton, ON: BC Decker Inc; 2008.
13. Sasseville D. Hypersensitivity to preservatives. Dermatol Ther. 2004;17:251-263.
14. de Groot AC, White IR, Flyvholm MA, et al. Formaldehyde-releasers in cosmetics: relationship to formaldehyde contact allergy. part 1. characterization, frequency and relevance of sensitization, and frequency of use in cosmetics. Contact Dermatitis. 2010;62:2-17.
15. Rastogi SC. Analytical control of preservative labeling on skin creams. Contact Dermatitis. 2000;43:339-343.
16. Hsu JW, Matiz C, Jacob SE. Nickel allergy: localized, id, and systemic manifestations in children. Pediatr Dermatol. 2011;28:276-280.
17. Salam TN, Fowler JF Jr. Balsam-related systemic contact dermatitis. J Am Acad Dermatol. 2001;45:377-381.
18. Kiebert G, Sorensen SV, Revicki D, et al. Atopic dermatitis is associated with a decrement in health-related quality of life. Int J Dermatol. 2002;41:151-158.
19. Hutchings CV, Shum KW, Gawkrodger DJ. Occupational contact dermatitis has an appreciable impact on quality of life. Contact Dermatitis. 2001;45:17-20.
Allergic contact dermatitis (ACD) is a common inflammatory skin condition that affects more than 14 million Americans each year.1 It has been estimated that the economic burden of ACD is nearly $3 billion per year due to school absences, work time lost, and medical expenditures.1,2 In fact, skin diseases rank second to traumatic injuries as the most common type of occupational disease.3 As dermatology residents, we will encounter many patients with ACD, a potentially debilitating skin condition. In this column, I will discuss the different types of ACD as well as their differential diagnoses and management options according to the American Academy of Allergy, Asthma & Immunology’s updated practice parameter for contact dermatitis.4 The 2015 American Contact Dermatitis Society (ACDS) Allergen of the Year and the ACDS’s Contact Allergen Management Program also will be discussed.
Clinical Presentation and Pathophysiology
Allergic contact dermatitis is a widespread skin condition characterized by erythematous and pruritic skin lesions that occur after contact with external stimuli.5 It is caused by a type IV, T cell–mediated, delayed hypersensitivity reaction in which a foreign substance comes into contact with the skin and forms an antigen complex that subsequently leads to sensitization. Upon reexposure to the antigen, the sensitized T cells induce an inflammatory cascade causing the skin changes associated with ACD. Clinical presentations of ACD include vesicles and bullae with distinct angles, lines, and borders.6
Differential Diagnosis
In contrast to ACD, irritant contact dermatitis (the more common form of contact dermatitis) is a non–immune-modulated skin reaction that occurs when an individual is exposed to a substance that causes irritation and damage to the keratinocytes.6,7 It can be an acute reaction to a household cleaning product or a chronic reaction to soap if the patient has had exposure to the product for a prolonged period of time.7 The clinical presentation of irritant contact dermatitis includes dry and fissured skin with less distinct borders and negative patch test results.6
Some other skin diseases that should be considered in the differential diagnosis for suspected ACD include atopic dermatitis, dyshidrotic eczema, inverse psoriasis, latex allergy, palmoplantar psoriasis, scabies, and tinea pedis.5 When ACD is suspected, our diagnostic approach as dermatology residents should be based on a combination of the following factors: the clinical features of the skin reaction (eg, morphology, location, symptoms), the patient’s history of exposure to an alleged allergen and lack of exposure after treatment and/or avoidance, patch test results, laboratory test results, and/or histopathologic examination to exclude other disorders with similar clinical features.8
Management
Localized acute lesions of ACD can be successfully treated with mid- or high-potency topical steroids such as triamcinolone 0.1% or clobetasol 0.05%. If an extensive area of the skin (>20%) is affected, systemic steroid therapy often is required, generally offering relief within 12 to 24 hours. Caution should be taken when prescribing oral prednisone, such as for poison ivy, as it should be tapered over a few weeks to prevent rebound dermatitis. If treatment fails and the diagnosis or specific allergen remains unknown, patch testing should be performed.3,5
Updated Practice Parameter
Practice parameters for contact dermatitis were updated in 2015, as commissioned by the Joint Task Force on Practice Parameters, to address recent advances in the field of contact dermatitis and the most recommended methods for diagnosis and management based on the current scientific literature.4 Prior to this update, the most recent recommendations were from 2006.3
Since the publication of the original practice parameter, new questions have been addressed related to emerging clinical problems such as preoperative screening and postimplantation patch testing for metal allergy in patients undergoing joint replacement surgery. In the updated practice parameter, statements have been added that more comprehensively address evaluation and management of occupational contact dermatitis.4 The potential benefits and limitations of drug patch testing in patients with maculopapular rashes, erythroderma, and nonimmediate cutaneous reactions also have been addressed. New summary statements have been included that make recommendations on the management of ACD, particularly avoidance and prevention.4
ACDS Allergen of the Year
The purpose of this “award” is to recognize the agents that cause the most remarkable clinical effects, those that draw less attention, or those that exhibit exposure patterns that have changed. The ACDS’s 2015 Allergen of the Year is formaldehyde, an inexpensive biocidal preservative used in a wide range of products such as tissue specimen and cadaveric preservation solutions, nail polish, hair-smoothing treatments, and wrinkle-free fabrics.9
Formaldehyde-releasing preservatives (FRPs) are among the leading contact allergens and are found in many personal hygiene products, medications, and household cleansers.8 Specific sources of FRPs include shampoos, bodywashes, hand soaps, lotions, creams, baby wipes, mascara, disinfectants, fabric softeners, topical wart remedies, adhesives, and tissue specimen preservation solutions.10-13 According to de Groot et al,14 the US Food and Drug Administration’s Voluntary Cosmetic Registration Program database has estimated that approximately 20% of personal hygiene products and cosmetics contain an FRP, with imidazolidinyl urea as the most common.
It is important for patients to be aware of sources of formaldehyde exposure and understand that many products containing formaldehyde or FRPs may not list this information on their labels. In fact, one study reported that 33% of 67 moisturizers evaluated did not have proper labeling with regard to their formaldehyde/FRP content.15
Contact Allergen Management Program
During medical school I served as the Dermatology Interest Group Contact Dermatitis Awareness Chair at the University of Texas Medical Branch (Galveston, Texas) and was fortunate to have attended the annual meeting of the ACDS where I learned about the ACDS Contact Allergen Management Program (CAMP), an online resource for dermatologists to access that provides patients a printout list of allergen and cross-reactivity information for more than 1200 products (http://www.contactderm.org/i4a/pages/indexcfm?pageID=3489). This information helps consumers to choose the right products based on their allergies.
Final Thoughts
A thorough review of a patient’s medical history and, if needed, skin patch testing can identify the responsible allergen and initiate an appropriate avoidance plan for the patient. With appropriate avoidance, patients can achieve resolution of their dermatitis and prevent further episodes to substantially improve their quality of life and decrease health care costs.1 If left untreated, ACD can evolve from an acute form to a subacute form and eventually chronic eczematous dermatitis or progression to systemic disease.16,17 Allergic contact dermatitis can negatively impact an individual’s health-related quality of life, particularly in social functioning and psychological well-being.18,19 Therefore, it is pertinent in our role as dermatology residents to recognize ACD before its progression to a chronic state.
Allergic contact dermatitis (ACD) is a common inflammatory skin condition that affects more than 14 million Americans each year.1 It has been estimated that the economic burden of ACD is nearly $3 billion per year due to school absences, work time lost, and medical expenditures.1,2 In fact, skin diseases rank second to traumatic injuries as the most common type of occupational disease.3 As dermatology residents, we will encounter many patients with ACD, a potentially debilitating skin condition. In this column, I will discuss the different types of ACD as well as their differential diagnoses and management options according to the American Academy of Allergy, Asthma & Immunology’s updated practice parameter for contact dermatitis.4 The 2015 American Contact Dermatitis Society (ACDS) Allergen of the Year and the ACDS’s Contact Allergen Management Program also will be discussed.
Clinical Presentation and Pathophysiology
Allergic contact dermatitis is a widespread skin condition characterized by erythematous and pruritic skin lesions that occur after contact with external stimuli.5 It is caused by a type IV, T cell–mediated, delayed hypersensitivity reaction in which a foreign substance comes into contact with the skin and forms an antigen complex that subsequently leads to sensitization. Upon reexposure to the antigen, the sensitized T cells induce an inflammatory cascade causing the skin changes associated with ACD. Clinical presentations of ACD include vesicles and bullae with distinct angles, lines, and borders.6
Differential Diagnosis
In contrast to ACD, irritant contact dermatitis (the more common form of contact dermatitis) is a non–immune-modulated skin reaction that occurs when an individual is exposed to a substance that causes irritation and damage to the keratinocytes.6,7 It can be an acute reaction to a household cleaning product or a chronic reaction to soap if the patient has had exposure to the product for a prolonged period of time.7 The clinical presentation of irritant contact dermatitis includes dry and fissured skin with less distinct borders and negative patch test results.6
Some other skin diseases that should be considered in the differential diagnosis for suspected ACD include atopic dermatitis, dyshidrotic eczema, inverse psoriasis, latex allergy, palmoplantar psoriasis, scabies, and tinea pedis.5 When ACD is suspected, our diagnostic approach as dermatology residents should be based on a combination of the following factors: the clinical features of the skin reaction (eg, morphology, location, symptoms), the patient’s history of exposure to an alleged allergen and lack of exposure after treatment and/or avoidance, patch test results, laboratory test results, and/or histopathologic examination to exclude other disorders with similar clinical features.8
Management
Localized acute lesions of ACD can be successfully treated with mid- or high-potency topical steroids such as triamcinolone 0.1% or clobetasol 0.05%. If an extensive area of the skin (>20%) is affected, systemic steroid therapy often is required, generally offering relief within 12 to 24 hours. Caution should be taken when prescribing oral prednisone, such as for poison ivy, as it should be tapered over a few weeks to prevent rebound dermatitis. If treatment fails and the diagnosis or specific allergen remains unknown, patch testing should be performed.3,5
Updated Practice Parameter
Practice parameters for contact dermatitis were updated in 2015, as commissioned by the Joint Task Force on Practice Parameters, to address recent advances in the field of contact dermatitis and the most recommended methods for diagnosis and management based on the current scientific literature.4 Prior to this update, the most recent recommendations were from 2006.3
Since the publication of the original practice parameter, new questions have been addressed related to emerging clinical problems such as preoperative screening and postimplantation patch testing for metal allergy in patients undergoing joint replacement surgery. In the updated practice parameter, statements have been added that more comprehensively address evaluation and management of occupational contact dermatitis.4 The potential benefits and limitations of drug patch testing in patients with maculopapular rashes, erythroderma, and nonimmediate cutaneous reactions also have been addressed. New summary statements have been included that make recommendations on the management of ACD, particularly avoidance and prevention.4
ACDS Allergen of the Year
The purpose of this “award” is to recognize the agents that cause the most remarkable clinical effects, those that draw less attention, or those that exhibit exposure patterns that have changed. The ACDS’s 2015 Allergen of the Year is formaldehyde, an inexpensive biocidal preservative used in a wide range of products such as tissue specimen and cadaveric preservation solutions, nail polish, hair-smoothing treatments, and wrinkle-free fabrics.9
Formaldehyde-releasing preservatives (FRPs) are among the leading contact allergens and are found in many personal hygiene products, medications, and household cleansers.8 Specific sources of FRPs include shampoos, bodywashes, hand soaps, lotions, creams, baby wipes, mascara, disinfectants, fabric softeners, topical wart remedies, adhesives, and tissue specimen preservation solutions.10-13 According to de Groot et al,14 the US Food and Drug Administration’s Voluntary Cosmetic Registration Program database has estimated that approximately 20% of personal hygiene products and cosmetics contain an FRP, with imidazolidinyl urea as the most common.
It is important for patients to be aware of sources of formaldehyde exposure and understand that many products containing formaldehyde or FRPs may not list this information on their labels. In fact, one study reported that 33% of 67 moisturizers evaluated did not have proper labeling with regard to their formaldehyde/FRP content.15
Contact Allergen Management Program
During medical school I served as the Dermatology Interest Group Contact Dermatitis Awareness Chair at the University of Texas Medical Branch (Galveston, Texas) and was fortunate to have attended the annual meeting of the ACDS where I learned about the ACDS Contact Allergen Management Program (CAMP), an online resource for dermatologists to access that provides patients a printout list of allergen and cross-reactivity information for more than 1200 products (http://www.contactderm.org/i4a/pages/indexcfm?pageID=3489). This information helps consumers to choose the right products based on their allergies.
Final Thoughts
A thorough review of a patient’s medical history and, if needed, skin patch testing can identify the responsible allergen and initiate an appropriate avoidance plan for the patient. With appropriate avoidance, patients can achieve resolution of their dermatitis and prevent further episodes to substantially improve their quality of life and decrease health care costs.1 If left untreated, ACD can evolve from an acute form to a subacute form and eventually chronic eczematous dermatitis or progression to systemic disease.16,17 Allergic contact dermatitis can negatively impact an individual’s health-related quality of life, particularly in social functioning and psychological well-being.18,19 Therefore, it is pertinent in our role as dermatology residents to recognize ACD before its progression to a chronic state.
1. Bickers DR, Lim HW, Margolis D, et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006;55:490-500.
2. Jacob SE. The lanolin-wool wax alcohol update. The Dermatologist. February 2014;22. http://www.the-dermatologist.com/content/lanolin-wool-wax-alcohol-update. Accessed June 26, 2015.
3. Beltrani VS, Bernstein IL, Cohen DE, et al. Contact dermatitis: a practice parameter [published correction appears in Ann Allergy Asthma Immunol. 2006;97:819]. Ann Allergy Asthma Immunol. 2006;97(3, suppl 2):S1-S38.
4. Fonacier L, Bernstein DI, Pacheco K, et al. Contact dermatitis: a practice parameter—update 2015. J Allergy Clin Immunol Pract. 2015;3(suppl 3):S1-S39.
5. Usatine R, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82:249-255.
6. Usatine RP. Contact dermatitis. In: Usatine RP, Smith M, Mayeaux EJ Jr, et al, eds. Color Atlas of Family Medicine. New York, NY: McGraw-Hill; 2009. http://accessmedicine.mhmedical.com/content.aspx?bookid=378&Sectionid=40419504. Accessed June 26, 2015.
7. Vazirnia A, Jacob SE. Review of ACDS’ allergen of the year 2010-2015. The Dermatologist. November 2014;22. http://www.the-dermatologist.com/content/review-acds%E2%80%99-allergen-od-year-2000-2015. Accessed June 26, 2015.
8. Yiannias J. Clinical features and diagnosis of allergic contact dermatitis. UpToDate Web site. http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-allergic-contact-dermatitis?source=search_result&search=allergic+contact+dermatitis&selectedTitle=2~142#. Updated May 20, 2014. Accessed June 18, 2015.
9. Pontén A, Bruze M. Formaldehyde. Dermatitis. 2015;26:3-6.
10. Maier LE, Lampel HP, Bhutani T, et al. Hand dermatitis: a focus on allergic contact dermatitis to biocides. Dermatol Clin. 2009;27:251-264.
11. Marks JG, Elsner P, DeLeo VA. Contact & Occupational Dermatology. 3rd ed. St. Louis, MO: Mosby; 2002.
12. Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 6th ed. Hamilton, ON: BC Decker Inc; 2008.
13. Sasseville D. Hypersensitivity to preservatives. Dermatol Ther. 2004;17:251-263.
14. de Groot AC, White IR, Flyvholm MA, et al. Formaldehyde-releasers in cosmetics: relationship to formaldehyde contact allergy. part 1. characterization, frequency and relevance of sensitization, and frequency of use in cosmetics. Contact Dermatitis. 2010;62:2-17.
15. Rastogi SC. Analytical control of preservative labeling on skin creams. Contact Dermatitis. 2000;43:339-343.
16. Hsu JW, Matiz C, Jacob SE. Nickel allergy: localized, id, and systemic manifestations in children. Pediatr Dermatol. 2011;28:276-280.
17. Salam TN, Fowler JF Jr. Balsam-related systemic contact dermatitis. J Am Acad Dermatol. 2001;45:377-381.
18. Kiebert G, Sorensen SV, Revicki D, et al. Atopic dermatitis is associated with a decrement in health-related quality of life. Int J Dermatol. 2002;41:151-158.
19. Hutchings CV, Shum KW, Gawkrodger DJ. Occupational contact dermatitis has an appreciable impact on quality of life. Contact Dermatitis. 2001;45:17-20.
1. Bickers DR, Lim HW, Margolis D, et al. The burden of skin diseases: 2004 a joint project of the American Academy of Dermatology and the Society for Investigative Dermatology. J Am Acad Dermatol. 2006;55:490-500.
2. Jacob SE. The lanolin-wool wax alcohol update. The Dermatologist. February 2014;22. http://www.the-dermatologist.com/content/lanolin-wool-wax-alcohol-update. Accessed June 26, 2015.
3. Beltrani VS, Bernstein IL, Cohen DE, et al. Contact dermatitis: a practice parameter [published correction appears in Ann Allergy Asthma Immunol. 2006;97:819]. Ann Allergy Asthma Immunol. 2006;97(3, suppl 2):S1-S38.
4. Fonacier L, Bernstein DI, Pacheco K, et al. Contact dermatitis: a practice parameter—update 2015. J Allergy Clin Immunol Pract. 2015;3(suppl 3):S1-S39.
5. Usatine R, Riojas M. Diagnosis and management of contact dermatitis. Am Fam Physician. 2010;82:249-255.
6. Usatine RP. Contact dermatitis. In: Usatine RP, Smith M, Mayeaux EJ Jr, et al, eds. Color Atlas of Family Medicine. New York, NY: McGraw-Hill; 2009. http://accessmedicine.mhmedical.com/content.aspx?bookid=378&Sectionid=40419504. Accessed June 26, 2015.
7. Vazirnia A, Jacob SE. Review of ACDS’ allergen of the year 2010-2015. The Dermatologist. November 2014;22. http://www.the-dermatologist.com/content/review-acds%E2%80%99-allergen-od-year-2000-2015. Accessed June 26, 2015.
8. Yiannias J. Clinical features and diagnosis of allergic contact dermatitis. UpToDate Web site. http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-allergic-contact-dermatitis?source=search_result&search=allergic+contact+dermatitis&selectedTitle=2~142#. Updated May 20, 2014. Accessed June 18, 2015.
9. Pontén A, Bruze M. Formaldehyde. Dermatitis. 2015;26:3-6.
10. Maier LE, Lampel HP, Bhutani T, et al. Hand dermatitis: a focus on allergic contact dermatitis to biocides. Dermatol Clin. 2009;27:251-264.
11. Marks JG, Elsner P, DeLeo VA. Contact & Occupational Dermatology. 3rd ed. St. Louis, MO: Mosby; 2002.
12. Rietschel RL, Fowler JF Jr, eds. Fisher’s Contact Dermatitis. 6th ed. Hamilton, ON: BC Decker Inc; 2008.
13. Sasseville D. Hypersensitivity to preservatives. Dermatol Ther. 2004;17:251-263.
14. de Groot AC, White IR, Flyvholm MA, et al. Formaldehyde-releasers in cosmetics: relationship to formaldehyde contact allergy. part 1. characterization, frequency and relevance of sensitization, and frequency of use in cosmetics. Contact Dermatitis. 2010;62:2-17.
15. Rastogi SC. Analytical control of preservative labeling on skin creams. Contact Dermatitis. 2000;43:339-343.
16. Hsu JW, Matiz C, Jacob SE. Nickel allergy: localized, id, and systemic manifestations in children. Pediatr Dermatol. 2011;28:276-280.
17. Salam TN, Fowler JF Jr. Balsam-related systemic contact dermatitis. J Am Acad Dermatol. 2001;45:377-381.
18. Kiebert G, Sorensen SV, Revicki D, et al. Atopic dermatitis is associated with a decrement in health-related quality of life. Int J Dermatol. 2002;41:151-158.
19. Hutchings CV, Shum KW, Gawkrodger DJ. Occupational contact dermatitis has an appreciable impact on quality of life. Contact Dermatitis. 2001;45:17-20.
Yoga for Dermatologic Conditions
Regardless of its spiritual origins, yoga has become a popular way of reaching mind and body well-being with nearly 30 million people practicing regularly worldwide.1 Yoga, which is the combination of physical postures, controlled breathing, and meditation or mindfulness, has long been used in complementary and alternative medicine around the world and recently has gained popularity as a therapeutic practice, with nearly 14 million Americans reporting that yoga was recommended to them by a physician or therapist.2,3 Studies suggest that people who participate in even brief yoga programs may see improvements in anxiety, somatic stress and discomfort, health-related quality of life, and self-rated sleep quality, all benefits that can help medical conditions, especially those that are dermatologic in nature.4,5
Stress and Dermatologic Conditions
The interaction between the mind, skin, and body is well known. Research in psychoneuroimmunology, the interaction between psychological processes and the nervous and immune systems, has examined the role of neuropeptides, hormones, and neurotransmitters in psychodermatological disorders. The correlation between neuroimmunological pathways and skin inflammation is now well recognized, specifically the interactions between the brain and skin underlying many dermatological diseases (eg, acne, alopecia areata, various types of eczema and dermatitis, oral and genital herpes, hyperhidrosis, pruritus, psoriasis, rosacea, urticaria, warts, breaking or ridging of the nails).6-9
Two biological systems are known to be affected by the systemic stress response: (1) the hypothalamic-pituitary-adrenal axis, which regulates the release of adrenocorticotropin, ß-endorphin, and cortisol, and (2) the sympathoadrenal medullary system, which regulates the release of catecholamines (eg, epinephrine, norepinephrine).7 Cortisol and catecholamines have been shown to have potent effects on the immune system as well as the inflammatory response.9 Additionally, it has been shown that cutaneous sensory nerve terminals release neuropeptides, including calcitonin gene-related peptide and substance P, both of which have different effects on the local inflammatory response.10,11
Psychological stress is well known to trigger many dermatologic conditions, but it also may lead to abnormal skin barrier function.12 The mechanism in which skin barrier function is affected appears to involve a stress-induced increase of endogenous glucocorticoids, which may consequently disrupt skin barrier function and recovery rates, stratum corneum cohesion, and epidermal antimicrobial function.13,14
Atopic dermatitis, for example, is classified as a psychophysiological disorder. Although it is not caused by stress, atopic dermatitis has been described to be precipitated or exacerbated by stress in patients.15 In fact, it was found that stressful life events preceded the onset of itching in more than 70% of patients with atopic dermatitis,16 which is especially relevant, as there is no cure and patients often experience a lifelong struggle with the condition. Additionally, stress mediates the degranulation of mast cells via corticotropin-releasing hormone and neuropeptides, and the upregulation of mast cell corticotropin-releasing hormone receptors supporting its putative role in the pathogenesis of urticaria.9,17 Furthermore, the increase in cortisol also has been described in the exacerbation of acne during times of stress.18
Psychological factors affect the management of skin conditions in more than one-third of reported dermatology patients; therefore, it is important to consider these factors in the treatment of chronic dermatological conditions, especially when they are inquired by the patient.19,20
Yoga Benefits in the Literature
The therapeutic potential of yoga has been explored in a growing number of randomized controlled trials to date.21 A recently published bibliometric analysis provided a comprehensive review of the characteristics of the randomized yoga trials available in the literature.22 The review included 366 full-text articles, with the 2 earliest studies published in 1975 and nearly 90% published within the last decade. In addition to healthy patients, it was found these randomized controlled yoga trials most commonly enrolled patients with breast cancer, depression, asthma, and type 2 diabetes mellitus.22 Another study examined psychological (eg, self-rated stress and stress behavior, anger, exhaustion, quality of life) and physiological (eg, blood pressure, heart rate, urinary catecholamines, salivary cortisol) measurements obtained before and after a 10-session yoga program that participants completed over a 4-month period, with results showing significant improvements (P<.05) on almost all stress-related subjective and physiological variables. Results were comparable with cognitive behavioral therapy.23
Not only has it been shown that yoga helps patients on a psychological level, but a recent study reported that 90-minute sessions of mindfulness meditation and gentle Hatha yoga over an 8-week period led to observable benefits on a cellular level, as telomere length was maintained in distressed breast cancer survivors compared to decreases in telomere length in the control group with patients who solely participated in a stress management seminar.24 To date, there are no known studies examining the effects of yoga on patients with skin cancer. However, a few studies have specifically examined the effect of yoga in managing non–cancer-related dermatologic issues. Specifically, one small study of psoriasis patients found that those who listened to mindfulness meditation tapes while undergoing standard phototherapy (psoralen plus UVA) healed faster than those who underwent phototherapy treatment alone.25
Because some dermatologic problems have comorbidities and increased risk factors of other medical problems, such as psoriasis with psoriatic arthritis and metabolic diseases (eg, abdominal obesity, diabetes, nonalcoholic fatty liver disease, dyslipidemia, metabolic syndrome, chronic kidney disease), it is even more pertinent to recommend approaches for healthy mind and body well-being as a supplement to medical care.26
Final Thoughts
With accurate diagnosis by a dermatologist, appropriate conventional treatments can improve dermatologic problems. These treatments alone can reduce patients’ stress and improve skin, hair, and nail conditions; however, if it is clear that stress is interfering with a patient’s overall well-being and ability to cope with his/her dermatologic condition, concurrent stress management interventions may be warranted. In some instances, recommending yoga sessions, mindful meditation, or breathing exercises may help, while in others referral to a mental health professional may be necessary.
Beyond the direct physiological effects of stress, it also is worth mentioning that patients who deal with stress also tend to scratch, pick, or irritate their skin more and often lack the motivation to adhere to skin care regimens or treatments, again supporting the idea that our approach in managing these patients must be multifaceted. As dermatologists in training, residents should be cognizant of the potential psychological sequelae of some dermatologic problems and be aware of the possible use of supplemental interventions by our patients.
1. Dangerfield A. Yoga wars. BBC News. http://news.bbc.co.uk/1/hi/7844691.stm. Published January 23, 2009. Accessed March 25, 2015.
2. Yoga Journal releases 2012 yoga in America market study [press release]. San Francisco, CA: Yoga Journal; December 6, 2012.
3. De Michaelis E. A History of Modern Yoga: Patanjali and Western Esotericism. London, United Kingdom: A&C Black; 2005.
4. Telles S, Singh N, Yadav A, et al. Effect of yoga on different aspects of mental health. Indian J Physiol Pharmacol. 2012;56:245-254.
5. Rodriguez-Vallecillo E, Woodbury-Fariña MA. Dermatological manifestations of stress in normal and psychiatric populations. Psychiatr Clin North Am. 2014;37:625-651.
6. Stander S, Raap U, Weisshaar E, et al. Pathogenesis of pruritus. J Dtsch Dermatol Ges. 2011;9:456-463.
7. Arck PC, Slominski A, Theoharides TC, et al. Neuroimmunology of stress: skin takes center stage. J Invest Dermatol. 2006;126:1697-1704.
8. Recognizing the mind-skin connection. Harvard Health Publications Web site. http://www.health.harvard.edu/newsletter_article/Recognizing_the_mind-skin_connection. Published November 1, 2006. Accessed March 31, 2015.
9. Tausk F, Elenkov I, Moynihan J. Psychoneuroimmunology. Dermatol Ther. 2008;21:22-31.
10. Pavlovic S, Liezmann C, Blois SM, et al. Substance P is a key mediator of stress-induced protection from allergic sensitization via modified antigen presentation. J Immunol. 2011;186:848-855.
11. Toyoda M, Nakamura M, Makino T, et al. Nerve growth factor and substance P are useful plasma markers of disease activity in atopic dermatitis. Br J Dermatol. 2002;147:71-79.
12. Koo JYM, Lee CS. General approach to evaluating psychodermatological disorders. In: Koo JYM, Lee CS, eds. Psychocutaneous Medicine. New York, NY: Marcel Dekker; 2003:1-29.
13. Garg A, Chren MM, Sands LP, et al. Psychological stress perturbs epidermal permeability barrier homeostasis: implications for the pathogenesis of stress-associated skin disorders. Arch Dermatol. 2001;137:53-59.
14. Elias PM, Sun R, Eder AR, et al. Treating atopic dermatitis at the source: corrective barrier repair therapy based upon new pathogenic insights. Expert Rev Dermatol. 2013;8:27-36.
15. Morren MA, Przybilla B, Bamelis M, et al. Atopic dermatitis: triggering factors. J Am Acad Dermatol. 1994;31:467-473.
16. Faulstich ME, Williamson DA. An overview of atopic dermatitis: toward a bio-behavioural integration. J Psychosom Res. 1985;29:647-654.
17. Theoharides TC, Donelan JM, Papadopoulou N, et al. Mast cells as targets of corticotropin-releasing factor and related peptides. Trends Pharmacol Sci. 2004;25:563-568.
18. Suh DH, Kwon HH. What’s new in the physiopathology of acne [published online ahead of print Jan 24, 2015]? Br J Dermatol. doi:10.1111/bjd.13634.
19. Picardi A, Mazzotti E, Pasquini P. Prevalence and correlates of suicidal ideation among patients with skin disease. J Am Acad Dermatol. 2006;54:420-426.
20. Ponarovsky B, Amital D, Lazarov A, et al. Anxiety and depression in patients with allergic and non-allergic cutaneous disorders. Int J Dermatol. 2011;50:1217-1222.
21. Khalsa SB. Yoga as a therapeutic intervention: a bibliometric analysis of published research studies. Indian J Physiol Pharmacol. 2004;48:269-285.
22. Cramer H, Lauche R, Dobos G. Characteristics of randomized controlled trials of yoga: a bibliometric analysis. BMC Complement Altern Med. 2014;14:328.
23. Granath J, Ingvarsson S, von Thiele U, et al. Stress management: a randomized study of cognitive behavioural therapy and yoga. Cogn Behav Ther. 2006;35:3-10.
24. Carlson LE, Beattie TL, Giese-Davis J, et al. Mindfulness-based cancer recovery and supportive-expressive therapy maintain telomere length relative to controls in distressed breast cancer survivors. Cancer. 2015;121:476-484.
25. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med. 1998;60:625-632.
26. Gisondi P, Galvan A, Idolazzi L, et al. Management of moderate to severe psoriasis in patients with metabolic comorbidities. Front Med (Lausanne). 2015;2:1.
Regardless of its spiritual origins, yoga has become a popular way of reaching mind and body well-being with nearly 30 million people practicing regularly worldwide.1 Yoga, which is the combination of physical postures, controlled breathing, and meditation or mindfulness, has long been used in complementary and alternative medicine around the world and recently has gained popularity as a therapeutic practice, with nearly 14 million Americans reporting that yoga was recommended to them by a physician or therapist.2,3 Studies suggest that people who participate in even brief yoga programs may see improvements in anxiety, somatic stress and discomfort, health-related quality of life, and self-rated sleep quality, all benefits that can help medical conditions, especially those that are dermatologic in nature.4,5
Stress and Dermatologic Conditions
The interaction between the mind, skin, and body is well known. Research in psychoneuroimmunology, the interaction between psychological processes and the nervous and immune systems, has examined the role of neuropeptides, hormones, and neurotransmitters in psychodermatological disorders. The correlation between neuroimmunological pathways and skin inflammation is now well recognized, specifically the interactions between the brain and skin underlying many dermatological diseases (eg, acne, alopecia areata, various types of eczema and dermatitis, oral and genital herpes, hyperhidrosis, pruritus, psoriasis, rosacea, urticaria, warts, breaking or ridging of the nails).6-9
Two biological systems are known to be affected by the systemic stress response: (1) the hypothalamic-pituitary-adrenal axis, which regulates the release of adrenocorticotropin, ß-endorphin, and cortisol, and (2) the sympathoadrenal medullary system, which regulates the release of catecholamines (eg, epinephrine, norepinephrine).7 Cortisol and catecholamines have been shown to have potent effects on the immune system as well as the inflammatory response.9 Additionally, it has been shown that cutaneous sensory nerve terminals release neuropeptides, including calcitonin gene-related peptide and substance P, both of which have different effects on the local inflammatory response.10,11
Psychological stress is well known to trigger many dermatologic conditions, but it also may lead to abnormal skin barrier function.12 The mechanism in which skin barrier function is affected appears to involve a stress-induced increase of endogenous glucocorticoids, which may consequently disrupt skin barrier function and recovery rates, stratum corneum cohesion, and epidermal antimicrobial function.13,14
Atopic dermatitis, for example, is classified as a psychophysiological disorder. Although it is not caused by stress, atopic dermatitis has been described to be precipitated or exacerbated by stress in patients.15 In fact, it was found that stressful life events preceded the onset of itching in more than 70% of patients with atopic dermatitis,16 which is especially relevant, as there is no cure and patients often experience a lifelong struggle with the condition. Additionally, stress mediates the degranulation of mast cells via corticotropin-releasing hormone and neuropeptides, and the upregulation of mast cell corticotropin-releasing hormone receptors supporting its putative role in the pathogenesis of urticaria.9,17 Furthermore, the increase in cortisol also has been described in the exacerbation of acne during times of stress.18
Psychological factors affect the management of skin conditions in more than one-third of reported dermatology patients; therefore, it is important to consider these factors in the treatment of chronic dermatological conditions, especially when they are inquired by the patient.19,20
Yoga Benefits in the Literature
The therapeutic potential of yoga has been explored in a growing number of randomized controlled trials to date.21 A recently published bibliometric analysis provided a comprehensive review of the characteristics of the randomized yoga trials available in the literature.22 The review included 366 full-text articles, with the 2 earliest studies published in 1975 and nearly 90% published within the last decade. In addition to healthy patients, it was found these randomized controlled yoga trials most commonly enrolled patients with breast cancer, depression, asthma, and type 2 diabetes mellitus.22 Another study examined psychological (eg, self-rated stress and stress behavior, anger, exhaustion, quality of life) and physiological (eg, blood pressure, heart rate, urinary catecholamines, salivary cortisol) measurements obtained before and after a 10-session yoga program that participants completed over a 4-month period, with results showing significant improvements (P<.05) on almost all stress-related subjective and physiological variables. Results were comparable with cognitive behavioral therapy.23
Not only has it been shown that yoga helps patients on a psychological level, but a recent study reported that 90-minute sessions of mindfulness meditation and gentle Hatha yoga over an 8-week period led to observable benefits on a cellular level, as telomere length was maintained in distressed breast cancer survivors compared to decreases in telomere length in the control group with patients who solely participated in a stress management seminar.24 To date, there are no known studies examining the effects of yoga on patients with skin cancer. However, a few studies have specifically examined the effect of yoga in managing non–cancer-related dermatologic issues. Specifically, one small study of psoriasis patients found that those who listened to mindfulness meditation tapes while undergoing standard phototherapy (psoralen plus UVA) healed faster than those who underwent phototherapy treatment alone.25
Because some dermatologic problems have comorbidities and increased risk factors of other medical problems, such as psoriasis with psoriatic arthritis and metabolic diseases (eg, abdominal obesity, diabetes, nonalcoholic fatty liver disease, dyslipidemia, metabolic syndrome, chronic kidney disease), it is even more pertinent to recommend approaches for healthy mind and body well-being as a supplement to medical care.26
Final Thoughts
With accurate diagnosis by a dermatologist, appropriate conventional treatments can improve dermatologic problems. These treatments alone can reduce patients’ stress and improve skin, hair, and nail conditions; however, if it is clear that stress is interfering with a patient’s overall well-being and ability to cope with his/her dermatologic condition, concurrent stress management interventions may be warranted. In some instances, recommending yoga sessions, mindful meditation, or breathing exercises may help, while in others referral to a mental health professional may be necessary.
Beyond the direct physiological effects of stress, it also is worth mentioning that patients who deal with stress also tend to scratch, pick, or irritate their skin more and often lack the motivation to adhere to skin care regimens or treatments, again supporting the idea that our approach in managing these patients must be multifaceted. As dermatologists in training, residents should be cognizant of the potential psychological sequelae of some dermatologic problems and be aware of the possible use of supplemental interventions by our patients.
Regardless of its spiritual origins, yoga has become a popular way of reaching mind and body well-being with nearly 30 million people practicing regularly worldwide.1 Yoga, which is the combination of physical postures, controlled breathing, and meditation or mindfulness, has long been used in complementary and alternative medicine around the world and recently has gained popularity as a therapeutic practice, with nearly 14 million Americans reporting that yoga was recommended to them by a physician or therapist.2,3 Studies suggest that people who participate in even brief yoga programs may see improvements in anxiety, somatic stress and discomfort, health-related quality of life, and self-rated sleep quality, all benefits that can help medical conditions, especially those that are dermatologic in nature.4,5
Stress and Dermatologic Conditions
The interaction between the mind, skin, and body is well known. Research in psychoneuroimmunology, the interaction between psychological processes and the nervous and immune systems, has examined the role of neuropeptides, hormones, and neurotransmitters in psychodermatological disorders. The correlation between neuroimmunological pathways and skin inflammation is now well recognized, specifically the interactions between the brain and skin underlying many dermatological diseases (eg, acne, alopecia areata, various types of eczema and dermatitis, oral and genital herpes, hyperhidrosis, pruritus, psoriasis, rosacea, urticaria, warts, breaking or ridging of the nails).6-9
Two biological systems are known to be affected by the systemic stress response: (1) the hypothalamic-pituitary-adrenal axis, which regulates the release of adrenocorticotropin, ß-endorphin, and cortisol, and (2) the sympathoadrenal medullary system, which regulates the release of catecholamines (eg, epinephrine, norepinephrine).7 Cortisol and catecholamines have been shown to have potent effects on the immune system as well as the inflammatory response.9 Additionally, it has been shown that cutaneous sensory nerve terminals release neuropeptides, including calcitonin gene-related peptide and substance P, both of which have different effects on the local inflammatory response.10,11
Psychological stress is well known to trigger many dermatologic conditions, but it also may lead to abnormal skin barrier function.12 The mechanism in which skin barrier function is affected appears to involve a stress-induced increase of endogenous glucocorticoids, which may consequently disrupt skin barrier function and recovery rates, stratum corneum cohesion, and epidermal antimicrobial function.13,14
Atopic dermatitis, for example, is classified as a psychophysiological disorder. Although it is not caused by stress, atopic dermatitis has been described to be precipitated or exacerbated by stress in patients.15 In fact, it was found that stressful life events preceded the onset of itching in more than 70% of patients with atopic dermatitis,16 which is especially relevant, as there is no cure and patients often experience a lifelong struggle with the condition. Additionally, stress mediates the degranulation of mast cells via corticotropin-releasing hormone and neuropeptides, and the upregulation of mast cell corticotropin-releasing hormone receptors supporting its putative role in the pathogenesis of urticaria.9,17 Furthermore, the increase in cortisol also has been described in the exacerbation of acne during times of stress.18
Psychological factors affect the management of skin conditions in more than one-third of reported dermatology patients; therefore, it is important to consider these factors in the treatment of chronic dermatological conditions, especially when they are inquired by the patient.19,20
Yoga Benefits in the Literature
The therapeutic potential of yoga has been explored in a growing number of randomized controlled trials to date.21 A recently published bibliometric analysis provided a comprehensive review of the characteristics of the randomized yoga trials available in the literature.22 The review included 366 full-text articles, with the 2 earliest studies published in 1975 and nearly 90% published within the last decade. In addition to healthy patients, it was found these randomized controlled yoga trials most commonly enrolled patients with breast cancer, depression, asthma, and type 2 diabetes mellitus.22 Another study examined psychological (eg, self-rated stress and stress behavior, anger, exhaustion, quality of life) and physiological (eg, blood pressure, heart rate, urinary catecholamines, salivary cortisol) measurements obtained before and after a 10-session yoga program that participants completed over a 4-month period, with results showing significant improvements (P<.05) on almost all stress-related subjective and physiological variables. Results were comparable with cognitive behavioral therapy.23
Not only has it been shown that yoga helps patients on a psychological level, but a recent study reported that 90-minute sessions of mindfulness meditation and gentle Hatha yoga over an 8-week period led to observable benefits on a cellular level, as telomere length was maintained in distressed breast cancer survivors compared to decreases in telomere length in the control group with patients who solely participated in a stress management seminar.24 To date, there are no known studies examining the effects of yoga on patients with skin cancer. However, a few studies have specifically examined the effect of yoga in managing non–cancer-related dermatologic issues. Specifically, one small study of psoriasis patients found that those who listened to mindfulness meditation tapes while undergoing standard phototherapy (psoralen plus UVA) healed faster than those who underwent phototherapy treatment alone.25
Because some dermatologic problems have comorbidities and increased risk factors of other medical problems, such as psoriasis with psoriatic arthritis and metabolic diseases (eg, abdominal obesity, diabetes, nonalcoholic fatty liver disease, dyslipidemia, metabolic syndrome, chronic kidney disease), it is even more pertinent to recommend approaches for healthy mind and body well-being as a supplement to medical care.26
Final Thoughts
With accurate diagnosis by a dermatologist, appropriate conventional treatments can improve dermatologic problems. These treatments alone can reduce patients’ stress and improve skin, hair, and nail conditions; however, if it is clear that stress is interfering with a patient’s overall well-being and ability to cope with his/her dermatologic condition, concurrent stress management interventions may be warranted. In some instances, recommending yoga sessions, mindful meditation, or breathing exercises may help, while in others referral to a mental health professional may be necessary.
Beyond the direct physiological effects of stress, it also is worth mentioning that patients who deal with stress also tend to scratch, pick, or irritate their skin more and often lack the motivation to adhere to skin care regimens or treatments, again supporting the idea that our approach in managing these patients must be multifaceted. As dermatologists in training, residents should be cognizant of the potential psychological sequelae of some dermatologic problems and be aware of the possible use of supplemental interventions by our patients.
1. Dangerfield A. Yoga wars. BBC News. http://news.bbc.co.uk/1/hi/7844691.stm. Published January 23, 2009. Accessed March 25, 2015.
2. Yoga Journal releases 2012 yoga in America market study [press release]. San Francisco, CA: Yoga Journal; December 6, 2012.
3. De Michaelis E. A History of Modern Yoga: Patanjali and Western Esotericism. London, United Kingdom: A&C Black; 2005.
4. Telles S, Singh N, Yadav A, et al. Effect of yoga on different aspects of mental health. Indian J Physiol Pharmacol. 2012;56:245-254.
5. Rodriguez-Vallecillo E, Woodbury-Fariña MA. Dermatological manifestations of stress in normal and psychiatric populations. Psychiatr Clin North Am. 2014;37:625-651.
6. Stander S, Raap U, Weisshaar E, et al. Pathogenesis of pruritus. J Dtsch Dermatol Ges. 2011;9:456-463.
7. Arck PC, Slominski A, Theoharides TC, et al. Neuroimmunology of stress: skin takes center stage. J Invest Dermatol. 2006;126:1697-1704.
8. Recognizing the mind-skin connection. Harvard Health Publications Web site. http://www.health.harvard.edu/newsletter_article/Recognizing_the_mind-skin_connection. Published November 1, 2006. Accessed March 31, 2015.
9. Tausk F, Elenkov I, Moynihan J. Psychoneuroimmunology. Dermatol Ther. 2008;21:22-31.
10. Pavlovic S, Liezmann C, Blois SM, et al. Substance P is a key mediator of stress-induced protection from allergic sensitization via modified antigen presentation. J Immunol. 2011;186:848-855.
11. Toyoda M, Nakamura M, Makino T, et al. Nerve growth factor and substance P are useful plasma markers of disease activity in atopic dermatitis. Br J Dermatol. 2002;147:71-79.
12. Koo JYM, Lee CS. General approach to evaluating psychodermatological disorders. In: Koo JYM, Lee CS, eds. Psychocutaneous Medicine. New York, NY: Marcel Dekker; 2003:1-29.
13. Garg A, Chren MM, Sands LP, et al. Psychological stress perturbs epidermal permeability barrier homeostasis: implications for the pathogenesis of stress-associated skin disorders. Arch Dermatol. 2001;137:53-59.
14. Elias PM, Sun R, Eder AR, et al. Treating atopic dermatitis at the source: corrective barrier repair therapy based upon new pathogenic insights. Expert Rev Dermatol. 2013;8:27-36.
15. Morren MA, Przybilla B, Bamelis M, et al. Atopic dermatitis: triggering factors. J Am Acad Dermatol. 1994;31:467-473.
16. Faulstich ME, Williamson DA. An overview of atopic dermatitis: toward a bio-behavioural integration. J Psychosom Res. 1985;29:647-654.
17. Theoharides TC, Donelan JM, Papadopoulou N, et al. Mast cells as targets of corticotropin-releasing factor and related peptides. Trends Pharmacol Sci. 2004;25:563-568.
18. Suh DH, Kwon HH. What’s new in the physiopathology of acne [published online ahead of print Jan 24, 2015]? Br J Dermatol. doi:10.1111/bjd.13634.
19. Picardi A, Mazzotti E, Pasquini P. Prevalence and correlates of suicidal ideation among patients with skin disease. J Am Acad Dermatol. 2006;54:420-426.
20. Ponarovsky B, Amital D, Lazarov A, et al. Anxiety and depression in patients with allergic and non-allergic cutaneous disorders. Int J Dermatol. 2011;50:1217-1222.
21. Khalsa SB. Yoga as a therapeutic intervention: a bibliometric analysis of published research studies. Indian J Physiol Pharmacol. 2004;48:269-285.
22. Cramer H, Lauche R, Dobos G. Characteristics of randomized controlled trials of yoga: a bibliometric analysis. BMC Complement Altern Med. 2014;14:328.
23. Granath J, Ingvarsson S, von Thiele U, et al. Stress management: a randomized study of cognitive behavioural therapy and yoga. Cogn Behav Ther. 2006;35:3-10.
24. Carlson LE, Beattie TL, Giese-Davis J, et al. Mindfulness-based cancer recovery and supportive-expressive therapy maintain telomere length relative to controls in distressed breast cancer survivors. Cancer. 2015;121:476-484.
25. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med. 1998;60:625-632.
26. Gisondi P, Galvan A, Idolazzi L, et al. Management of moderate to severe psoriasis in patients with metabolic comorbidities. Front Med (Lausanne). 2015;2:1.
1. Dangerfield A. Yoga wars. BBC News. http://news.bbc.co.uk/1/hi/7844691.stm. Published January 23, 2009. Accessed March 25, 2015.
2. Yoga Journal releases 2012 yoga in America market study [press release]. San Francisco, CA: Yoga Journal; December 6, 2012.
3. De Michaelis E. A History of Modern Yoga: Patanjali and Western Esotericism. London, United Kingdom: A&C Black; 2005.
4. Telles S, Singh N, Yadav A, et al. Effect of yoga on different aspects of mental health. Indian J Physiol Pharmacol. 2012;56:245-254.
5. Rodriguez-Vallecillo E, Woodbury-Fariña MA. Dermatological manifestations of stress in normal and psychiatric populations. Psychiatr Clin North Am. 2014;37:625-651.
6. Stander S, Raap U, Weisshaar E, et al. Pathogenesis of pruritus. J Dtsch Dermatol Ges. 2011;9:456-463.
7. Arck PC, Slominski A, Theoharides TC, et al. Neuroimmunology of stress: skin takes center stage. J Invest Dermatol. 2006;126:1697-1704.
8. Recognizing the mind-skin connection. Harvard Health Publications Web site. http://www.health.harvard.edu/newsletter_article/Recognizing_the_mind-skin_connection. Published November 1, 2006. Accessed March 31, 2015.
9. Tausk F, Elenkov I, Moynihan J. Psychoneuroimmunology. Dermatol Ther. 2008;21:22-31.
10. Pavlovic S, Liezmann C, Blois SM, et al. Substance P is a key mediator of stress-induced protection from allergic sensitization via modified antigen presentation. J Immunol. 2011;186:848-855.
11. Toyoda M, Nakamura M, Makino T, et al. Nerve growth factor and substance P are useful plasma markers of disease activity in atopic dermatitis. Br J Dermatol. 2002;147:71-79.
12. Koo JYM, Lee CS. General approach to evaluating psychodermatological disorders. In: Koo JYM, Lee CS, eds. Psychocutaneous Medicine. New York, NY: Marcel Dekker; 2003:1-29.
13. Garg A, Chren MM, Sands LP, et al. Psychological stress perturbs epidermal permeability barrier homeostasis: implications for the pathogenesis of stress-associated skin disorders. Arch Dermatol. 2001;137:53-59.
14. Elias PM, Sun R, Eder AR, et al. Treating atopic dermatitis at the source: corrective barrier repair therapy based upon new pathogenic insights. Expert Rev Dermatol. 2013;8:27-36.
15. Morren MA, Przybilla B, Bamelis M, et al. Atopic dermatitis: triggering factors. J Am Acad Dermatol. 1994;31:467-473.
16. Faulstich ME, Williamson DA. An overview of atopic dermatitis: toward a bio-behavioural integration. J Psychosom Res. 1985;29:647-654.
17. Theoharides TC, Donelan JM, Papadopoulou N, et al. Mast cells as targets of corticotropin-releasing factor and related peptides. Trends Pharmacol Sci. 2004;25:563-568.
18. Suh DH, Kwon HH. What’s new in the physiopathology of acne [published online ahead of print Jan 24, 2015]? Br J Dermatol. doi:10.1111/bjd.13634.
19. Picardi A, Mazzotti E, Pasquini P. Prevalence and correlates of suicidal ideation among patients with skin disease. J Am Acad Dermatol. 2006;54:420-426.
20. Ponarovsky B, Amital D, Lazarov A, et al. Anxiety and depression in patients with allergic and non-allergic cutaneous disorders. Int J Dermatol. 2011;50:1217-1222.
21. Khalsa SB. Yoga as a therapeutic intervention: a bibliometric analysis of published research studies. Indian J Physiol Pharmacol. 2004;48:269-285.
22. Cramer H, Lauche R, Dobos G. Characteristics of randomized controlled trials of yoga: a bibliometric analysis. BMC Complement Altern Med. 2014;14:328.
23. Granath J, Ingvarsson S, von Thiele U, et al. Stress management: a randomized study of cognitive behavioural therapy and yoga. Cogn Behav Ther. 2006;35:3-10.
24. Carlson LE, Beattie TL, Giese-Davis J, et al. Mindfulness-based cancer recovery and supportive-expressive therapy maintain telomere length relative to controls in distressed breast cancer survivors. Cancer. 2015;121:476-484.
25. Kabat-Zinn J, Wheeler E, Light T, et al. Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA). Psychosom Med. 1998;60:625-632.
26. Gisondi P, Galvan A, Idolazzi L, et al. Management of moderate to severe psoriasis in patients with metabolic comorbidities. Front Med (Lausanne). 2015;2:1.
Sunscreens Causing Cancer? The Facts
Skin cancer is the most common form of cancer in the United States and continues to rise in incidence and mortality each year.1 It is common knowledge that UV light plays a major role in the development of skin cancer.2,3 Studies have long demonstrated that using sunscreen on a daily basis can help prevent the development of skin cancer, premature aging, and exacerbation of photodermatoses.4-7 Although there are several photoprotective measures available, sunscreen remains the most popular and widely used among patients.8 Sunscreens that are on the market today contain either organic or inorganic UV filters or a combination of both based on their chemical composition and photoprotection mechanisms.9 Concerns about these ingredients causing cancer have created confusion among consumers. I will attempt to clarify these concerns by critically analyzing available evidence-based data on sunscreen use so that as dermatology residents we will be more knowledgeable about sunscreen safety topics and will be able to provide accurate and up-to-date information to our patients.
Organic UV Filters
Organic UV filters are classified as aromatic compounds that provide photoprotection by absorbing UV light.10 Aside from the photoallergic potential of organic UV filters, controversy has arisen in response to studies reporting their possible hormone disruptive effects.11-18 Although there are several US Food and Drug Administration (FDA)–approved organic UV filters in use today, one of the most commonly manufactured and controversial agents is oxybenzone.10 Claims regarding the estrogenic and antiandrogenic effects of oxybenzone have been investigated with results refuting the claims or concluding that more sensitive studies are needed to determine if these organic ingredients pose such risks.10,19,20 One study demonstrated that nearly 300 years of daily sunscreen application would be needed to reach similar exposure levels of oxybenzone used and described in prior animal studies.21 Additionally, most of the studied adverse effects of UV filters have been evaluated based on oral exposure rather than actual dermal application.11 Although these compounds are absorbed systemically, studies have reported that the amounts are insignificant and noncumulative in the body.10,22-24 Furthermore, the binding affinity of oxybenzone for estrogen receptors has been shown to be much weaker and near insignificant compared to estrogen and estradiol.24,25 Although numerous important studies examining systemic absorption have not shown a clinically significant disruption of hormonal homeostasis or acute toxicity in humans by organic UV filters, further studies are needed.
Inorganic UV Filters
Used as the main active ingredients in sunscreen for decades, titanium dioxide (TiO2) and zinc oxide (ZnO) compounds generally are more photostable and less photoallergic than their organic counterparts.10 In recent years, the safety of these long-used photoprotectors has been questioned because of the development of nanoparticle (<100 nm) formulas that are less opaque on application. Although this formula provides a thin, transparent, and cosmetically appealing medium, there is concern that the metal oxides penetrate the skin and cause local and systemic toxicities.26-28 Several recent scientific studies have shown no percutaneous permeation of these particles in normal adult human skin and reported no causal damage to mammalian cells.10,29-31 Although skin penetration of TiO2 and ZnO has been described as insignificant, focus has shifted to health risks associated with inhaling TiO2 through the use of spray or powder products following statements made by the International Agency for Research on Cancer in 2006.32 Several studies investigating increased health risks, specifically lung cancer, in factory workers who were subjected to TiO2 and ZnO inhalation concluded that exposure was unlikely to pose substantial health risks or subchronic toxicity.33,34 Despite a relatively strong safety profile, a major concern of using these metal oxides as UV filters has been potential free radical formation.35-39 For this reason, the Scientific Committee on Emerging and Newly Identified Health Risks extensively researched and delivered opinions on the use of TiO2 and ZnO in cosmetics, concluding that topical application of either compound does not result in toxicity or other adverse effects.30,40-42 Additionally, an effort has been made by manufacturers to encapsulate nanoparticles with magnesium and other materials to quench the reactive oxygen species along with the human body’s own antioxidant defense system.10 In summary, it appears that the current weight of scientific evidence suggests that percutaneous absorption and toxicity by UV filters in humans may be overestimated and that the use of nanoparticles in sunscreens poses no or negligible potential risks to human health.43,44
Concerns Beyond Organic and Inorganic UV Filters
Beyond these concerns with organic and inorganic UV filters, there are several other claims regarding sunscreen safety that have stirred up controversy, including the side-effect profile of retinyl palmitate, vitamin D deficiency, phototoxicity, environmental effects, futility of sun protection factor levels greater than 50, and increased health risks in children. Although some studies report mixed results, the majority of scientific investigations have addressed and refuted several of these claims, again confirming the relative safety of sunscreen use. It is beyond the scope of this article to further discuss these topics specifically. However, it is worth mentioning that consumer studies report that the actual use of sunscreens is 0.5 mg/cm2 or less compared to the ideal application of 2 mg/cm2, thereby confounding many of the claims made about sunscreen use, such as vitamin D deficiency.45 Sunscreens often contain a combination of several UV filters. To date, only a few existing studies have shown that mixtures of the photoprotective agents discussed might interact and exhibit toxic activity when combined, even when there is no observed adverse toxic effect when used individually in products.46-48
The current FDA ruling on sunscreen labeling does not require manufacturers to state if inorganic UV filters have been formulated into nanoparticles; however, manufacturers are now required to include a statement on all sunscreen labels warning consumers to avoid using sunscreen on damaged or broken skin49 in an effort to prevent the active ingredients from getting under the skin, potentially causing inflammation and/or health risks, because available data do not provide conclusive evidence on increased penetration of open skin.50 Additional information regarding the 2011 FDA sunscreen ruling can be found in a prior Cutis Resident Corner column.51
Final Thoughts
As health care providers, we should take advantage of opportunities to educate our patients about other sun safety practices, such as avoiding excessive sun exposure during peak hours (10 am to 2 pm), seeking shade, and wearing photoprotective clothing (eg, wide-brimmed hats, sunglasses).
The research is quite clear: Using broadband sunscreens that absorb and/or block UV radiation results in reduced damage to the skin’s DNA, a fact that should be considered when taking into account the risks and benefits of sunscreen use.2,3 Although sunscreen use is highly recommended in addition to the other sun protection methods, it is ultimately the patient’s choice. If a patient is still concerned about the active ingredients of UV filters, even given the high probability of safety, there are products available on the market that do not include organic filters or nanoparticles. Given the established benefits of UV protection, the use of sunscreens remain one of the most important photoprotective methods, and with increased usage by the public, continuous monitoring of the overall safety and benefit profile of future products is prudent.
1. Skin cancer statistics. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/cancer/skin/statistics/index.htm. Updated September 2, 2014. Accessed December 30, 2014.
2. World Health Organization, International Agency for Research on Cancer. Solar and ultraviolet radiation. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 55. Lyon, France: International Agency for Research on Cancer; 1992.
3. Green AC, Williams GM, Logan V, et al. Reduced melanoma after regular sunscreen use: randomized trial follow-up. J Clin Oncol. 2011;29:257-263.
4. Darlington S, Williams G, Neale R, et al. A randomized controlled trial to assess sunscreen application and beta carotene supplementation in the prevention of solar keratoses. Arch Dermatol. 2003;139:451-455.
5. Van der Pols JC, Williams GM, Pandeya N, et al. Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer Epidemiol Biomarkers Prev. 2006;15:2546-2548.
6. Hughes MC, Williams GM, Baker P, et al. Sunscreen and prevention of skin aging: a randomized trial. Ann Intern Med. 2013;158:781-790.
7. Bissonnette R, Nigen S, Bolduc C. Influence of the quantity of sunscreen applied on the ability to protect against ultraviolet-induced polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2012;28:240-243.
8. Cancer trends progress report 2011/2012 update: sun protection. National Cancer Institute Web site. http://progressreport.cancer.gov/doc_detail.asp?pid¡1&did¡2009&chid¡91&coid¡911. Accessed December 30, 2014.
9. Sunscreen Drug Products for Over-the-counter Human Use, 21 CFR §352.10. http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?fr=352.10. Updated September 1, 2014. Accessed December 30, 2014.
10. Burnett ME, Wang SQ. Current sunscreen controversies: a critical review. Photodermatol Photoimmunol Photomed. 2011;27:58-67.
11. Krause M, Klit A, Blomberg Jensen M, et al. Sunscreens: are they beneficial for health? an overview of endocrine disrupting properties of UV-filters. Int J Androl. 2012;35:424-436.
12. Schlumpf M, Cotton B, Conscience M, et al. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect. 2001;109:239-244.
13. Schlumpf M, Schmid P, Durrer S, et al. Endocrine activity and developmental toxicity of cosmetic UV filters–an update. Toxicol. 2004;205:113-122.
14. Schlumpf M, Kypke K, Vökt C, et al. Endocrine active UV filters: developmental toxicity and exposure through breast milk. Chimia. 2008;62:345-351.
15. Nakagawa Y, Suzuki T. Metabolism of 2-hydroxy-4-methoxybenzophenone in isolated rat hepatocytes and xenoestrogenic effects of its metabolites on MCF-7 human breast cancer cells. Chem Biol Interact. 2002;139:115-128.
16. Ma R, Cotton B, Lichtensteiger W, et al. UV filters with antagonistic action at androgen receptors in the MDA-kb2 cell transcriptional-activation assay. Toxicol Sci. 2003;74:43-50.
17. Heneweer M, Muusse M, van den Berg M, et al. Additive estrogenic effects of mixtures of frequently used UV filters on pS2-gene transcription in MCF-7 cells. Toxicol Appl Pharmacol. 2005;208:170-177.
18. Knobler E, Almeida L, Ruzkowski AM, et al. Photoallergy to benzophenone. Arch Dermatol. 1989;125:801-804.
19. Draelos ZD. Are sunscreens safe? J Cosmet Dermatol. 2010;9:1-2.
20. Gilbert E, Pirot F, Bertholle V. Commonly used UV filter toxicity on biological functions: review of last decade studies. Int J of Cosmet Sci. 2013;35:208-219.
21. Wang SQ, Burnett ME, Lim HW. Safety of oxybenzone: putting numbers into perspective. Arch Dermatol. 2011;147:865-866.
22. Mancebo SE, Hu JY, Wang SQ. Sunscreens: a review of health benefits, regulations, and controversies. Dermatol Clin. 2014;32:427-438.
23. Jansen R, Osterwalder U, Wang SQ, et al. Photoprotection: part II. sunscreen: development, efficacy, and controversies. J Am Acad Dermatol. 2013;69:867.e1-867.e14.
24. Janjua NR, Mogensen B, Andersson AM, et al. Systemic absorption of the sunscreens benzo- phenone-3, octyl-methoxycinnamate, and 3-(4-methyl-benzy-lidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol. 2004;123:57-61.
25. Kadry AM, Chukwuemeka SO, Mohamed S, et al. Pharmacokinetics of benzophenone-3 after oral exposure in male rats. J Appl Toxicol. 1995;15:97-102.
26. Gulson B, McCall M, Korsch M, et al. Small amounts of zinc from zinc oxide particles in sunscreens applied outdoors are absorbed through human skin. Toxicol Sci. 2010;118:140-149.
27. Gulson B, Wong H, Korsch M, et al. Comparison of dermal absorption of zinc from different sunscreen formulations and differing UV exposure based on stable isotope tracing. Sci Total Environ. 2012:420:313-318.
28. Benech-Kieffer F, Meuling WJ, Leclerc C, et al. Percutaneous absorption of Mexoryl SX in human volunteers: comparison with in vitro data. Skin Pharmacol Appl Skin Physiol. 2003;16:343-355.
29. Nash JF. Human safety and efficacy of ultraviolet filters and sunscreen products. Dermatol Clin. 2006;24:35-51.
30. Nohynek GJ, Lademann J, Ribaud C, et al. Grey goo on the skin? nanotechnology, cosmetic and sunscreen safety. Crit Rev Toxicol. 2007;37:251-277.
31. Sadrieh N, Wokovich AM, Gopee NV, et al. Lack of significant dermal penetration of titanium dioxide from sunscreen formulations containing nano- and submicron-size TiO2 particles. Toxicol Sci. 2010;115:156-166.
32. International Agency for Research on Cancer. Carbon black, titanium dioxide, and talc. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 93. Lyon, France: International Agency for Research on Cancer; 2006.
33. Liao CM, Chiang YH, Chio CP. Model-based assessment for human inhalation exposure risk to airborne nano/fine titanium dioxide particles. Sci Total Environ. 2008:15;407:165-177.
34. Adamcakova-Dodd A, Stebounova LV, Kim JS, et al. Toxicity assessment of zinc oxide nanoparticles using sub-acute and sub-chronic murine inhalation models. Part Fibre Toxicol. 2014;11:15.
35. Wamer WG, Yin JJ, Wei RR. Oxidative damage to nucleic acids photosensitized by titanium dioxide. Free Radic Biol Med. 1997;23:851-858.
36. Nakagawa Y, Wakuri S, Sakamoto K, et al. The photogenotoxicity of titanium dioxide particles. Mutat Res. 1997;394:125-132.
37. Dunford R, Salinaro A, Cai L, et al. Chemical oxidation and DNA damage catalysed by inorganic sunscreen ingredients. FEBS Lett. 1997;418:87-90, 99.
38. Hidaka H, Kobayashi H, Koike T, et al. DNA damage photoinduced by cosmetic pigments and sunscreen agents under solar exposure and artificial UV illumination. J Oleo Sci. 2006;55:249-261.
39. Dufour EK, Kumaravel T, Nohynek GJ, et al. Clastogenicity, photo-clastogenicity or pseudo-photo-clastogenicity: genotoxic effects of zinc oxide in the dark, in pre-irradiated or simultaneously irradiated Chinese hamster ovary cells [published online ahead of print June 21, 2006]. Mutat Res. 2006;607:215-224.
40. Opinion of the Scientific Committee on Cosmetic Products and Non-Food Products intended for Consumers concerning titanium dioxide. http://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out135_en.pdf. Published October 24, 2000. Accessed December 30, 2014.
41. The Scientific Committee on Cosmetic Products and Non-Food Products intended for Consumers opinion concerning zinc oxide. http://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out222_en.pdf. Published June 24-25, 2003. Accessed December 30, 2014.
42. Hackenberg S, Friehs G, Kessler M, et al. Nanosized titanium dioxide particles do not induce DNA damage in human peripheral blood lymphocytes. Environ Mol Mutagen. 2010;52:264-268.
43. Bach-Thomsen M, Wulf HC. Sunbather’s application of sunscreen is probably inadequate to obtain the sun protection factor assigned to the preparation. Photodermatol Photoimmunol Photomed. 1993:9;242-244.
44. Nohynek GJ, Antignac E, Re T, et al. Safety assessment of personal care products/cosmetics and their ingredients. Toxicol Appl Pharmacol. 2010:1;243:239-259.
45. Diffey BL. Sunscreens: use and misuse. In: Giacomoni PU, ed. Sun Protection in Man. Vol 3. Amsterdam, the Netherlands: Elsevier Science BV; 2001:521-534.
46. Heneweer M, Muusse M, Van den BM, et al. Additive estrogenic effects of mixtures of frequently used UV-filters on pS2-gene transcription in MCF-7 cells. Toxicol Appl Pharmacol. 2005;208:170-177.
47. Kunz PY, Galicia HF, Fent K. Comparison of in vitro and in vivo estrogenic activity of UV-filters in fish. Toxicol Sci. 2006;90:349-361.
48. Kortenkamp A, Faust M, Scholze M, et al. Low-level exposure to multiple chemicals: reason for human health concerns? Environ Health Perspect. 2007;115(suppl 1):106-114.
49. Labeling and effectiveness testing: sunscreen drug products for over-the-counter human use—small entity compliance guide. US Food and Drug Administration Web site. http://www.fda.gov/drugs/guidancecomplianceregulatoryinformation/guidances/ucm330694.htm. Published December 2012. Updated May 13, 2014. Accessed December 30, 2014.
50. Schafer-Korting M, Korting HC, Ponce-Poschl E. Liposomal tretinoin for uncomplicated acne vulgaris. Clin Investig. 1994;72:1086-1091.
51. Bronfenbrener R. Simplifying sun safety: a guide to the new FDA sunscreen monograph. Cutis. 2014;93:e17-e19.
Skin cancer is the most common form of cancer in the United States and continues to rise in incidence and mortality each year.1 It is common knowledge that UV light plays a major role in the development of skin cancer.2,3 Studies have long demonstrated that using sunscreen on a daily basis can help prevent the development of skin cancer, premature aging, and exacerbation of photodermatoses.4-7 Although there are several photoprotective measures available, sunscreen remains the most popular and widely used among patients.8 Sunscreens that are on the market today contain either organic or inorganic UV filters or a combination of both based on their chemical composition and photoprotection mechanisms.9 Concerns about these ingredients causing cancer have created confusion among consumers. I will attempt to clarify these concerns by critically analyzing available evidence-based data on sunscreen use so that as dermatology residents we will be more knowledgeable about sunscreen safety topics and will be able to provide accurate and up-to-date information to our patients.
Organic UV Filters
Organic UV filters are classified as aromatic compounds that provide photoprotection by absorbing UV light.10 Aside from the photoallergic potential of organic UV filters, controversy has arisen in response to studies reporting their possible hormone disruptive effects.11-18 Although there are several US Food and Drug Administration (FDA)–approved organic UV filters in use today, one of the most commonly manufactured and controversial agents is oxybenzone.10 Claims regarding the estrogenic and antiandrogenic effects of oxybenzone have been investigated with results refuting the claims or concluding that more sensitive studies are needed to determine if these organic ingredients pose such risks.10,19,20 One study demonstrated that nearly 300 years of daily sunscreen application would be needed to reach similar exposure levels of oxybenzone used and described in prior animal studies.21 Additionally, most of the studied adverse effects of UV filters have been evaluated based on oral exposure rather than actual dermal application.11 Although these compounds are absorbed systemically, studies have reported that the amounts are insignificant and noncumulative in the body.10,22-24 Furthermore, the binding affinity of oxybenzone for estrogen receptors has been shown to be much weaker and near insignificant compared to estrogen and estradiol.24,25 Although numerous important studies examining systemic absorption have not shown a clinically significant disruption of hormonal homeostasis or acute toxicity in humans by organic UV filters, further studies are needed.
Inorganic UV Filters
Used as the main active ingredients in sunscreen for decades, titanium dioxide (TiO2) and zinc oxide (ZnO) compounds generally are more photostable and less photoallergic than their organic counterparts.10 In recent years, the safety of these long-used photoprotectors has been questioned because of the development of nanoparticle (<100 nm) formulas that are less opaque on application. Although this formula provides a thin, transparent, and cosmetically appealing medium, there is concern that the metal oxides penetrate the skin and cause local and systemic toxicities.26-28 Several recent scientific studies have shown no percutaneous permeation of these particles in normal adult human skin and reported no causal damage to mammalian cells.10,29-31 Although skin penetration of TiO2 and ZnO has been described as insignificant, focus has shifted to health risks associated with inhaling TiO2 through the use of spray or powder products following statements made by the International Agency for Research on Cancer in 2006.32 Several studies investigating increased health risks, specifically lung cancer, in factory workers who were subjected to TiO2 and ZnO inhalation concluded that exposure was unlikely to pose substantial health risks or subchronic toxicity.33,34 Despite a relatively strong safety profile, a major concern of using these metal oxides as UV filters has been potential free radical formation.35-39 For this reason, the Scientific Committee on Emerging and Newly Identified Health Risks extensively researched and delivered opinions on the use of TiO2 and ZnO in cosmetics, concluding that topical application of either compound does not result in toxicity or other adverse effects.30,40-42 Additionally, an effort has been made by manufacturers to encapsulate nanoparticles with magnesium and other materials to quench the reactive oxygen species along with the human body’s own antioxidant defense system.10 In summary, it appears that the current weight of scientific evidence suggests that percutaneous absorption and toxicity by UV filters in humans may be overestimated and that the use of nanoparticles in sunscreens poses no or negligible potential risks to human health.43,44
Concerns Beyond Organic and Inorganic UV Filters
Beyond these concerns with organic and inorganic UV filters, there are several other claims regarding sunscreen safety that have stirred up controversy, including the side-effect profile of retinyl palmitate, vitamin D deficiency, phototoxicity, environmental effects, futility of sun protection factor levels greater than 50, and increased health risks in children. Although some studies report mixed results, the majority of scientific investigations have addressed and refuted several of these claims, again confirming the relative safety of sunscreen use. It is beyond the scope of this article to further discuss these topics specifically. However, it is worth mentioning that consumer studies report that the actual use of sunscreens is 0.5 mg/cm2 or less compared to the ideal application of 2 mg/cm2, thereby confounding many of the claims made about sunscreen use, such as vitamin D deficiency.45 Sunscreens often contain a combination of several UV filters. To date, only a few existing studies have shown that mixtures of the photoprotective agents discussed might interact and exhibit toxic activity when combined, even when there is no observed adverse toxic effect when used individually in products.46-48
The current FDA ruling on sunscreen labeling does not require manufacturers to state if inorganic UV filters have been formulated into nanoparticles; however, manufacturers are now required to include a statement on all sunscreen labels warning consumers to avoid using sunscreen on damaged or broken skin49 in an effort to prevent the active ingredients from getting under the skin, potentially causing inflammation and/or health risks, because available data do not provide conclusive evidence on increased penetration of open skin.50 Additional information regarding the 2011 FDA sunscreen ruling can be found in a prior Cutis Resident Corner column.51
Final Thoughts
As health care providers, we should take advantage of opportunities to educate our patients about other sun safety practices, such as avoiding excessive sun exposure during peak hours (10 am to 2 pm), seeking shade, and wearing photoprotective clothing (eg, wide-brimmed hats, sunglasses).
The research is quite clear: Using broadband sunscreens that absorb and/or block UV radiation results in reduced damage to the skin’s DNA, a fact that should be considered when taking into account the risks and benefits of sunscreen use.2,3 Although sunscreen use is highly recommended in addition to the other sun protection methods, it is ultimately the patient’s choice. If a patient is still concerned about the active ingredients of UV filters, even given the high probability of safety, there are products available on the market that do not include organic filters or nanoparticles. Given the established benefits of UV protection, the use of sunscreens remain one of the most important photoprotective methods, and with increased usage by the public, continuous monitoring of the overall safety and benefit profile of future products is prudent.
Skin cancer is the most common form of cancer in the United States and continues to rise in incidence and mortality each year.1 It is common knowledge that UV light plays a major role in the development of skin cancer.2,3 Studies have long demonstrated that using sunscreen on a daily basis can help prevent the development of skin cancer, premature aging, and exacerbation of photodermatoses.4-7 Although there are several photoprotective measures available, sunscreen remains the most popular and widely used among patients.8 Sunscreens that are on the market today contain either organic or inorganic UV filters or a combination of both based on their chemical composition and photoprotection mechanisms.9 Concerns about these ingredients causing cancer have created confusion among consumers. I will attempt to clarify these concerns by critically analyzing available evidence-based data on sunscreen use so that as dermatology residents we will be more knowledgeable about sunscreen safety topics and will be able to provide accurate and up-to-date information to our patients.
Organic UV Filters
Organic UV filters are classified as aromatic compounds that provide photoprotection by absorbing UV light.10 Aside from the photoallergic potential of organic UV filters, controversy has arisen in response to studies reporting their possible hormone disruptive effects.11-18 Although there are several US Food and Drug Administration (FDA)–approved organic UV filters in use today, one of the most commonly manufactured and controversial agents is oxybenzone.10 Claims regarding the estrogenic and antiandrogenic effects of oxybenzone have been investigated with results refuting the claims or concluding that more sensitive studies are needed to determine if these organic ingredients pose such risks.10,19,20 One study demonstrated that nearly 300 years of daily sunscreen application would be needed to reach similar exposure levels of oxybenzone used and described in prior animal studies.21 Additionally, most of the studied adverse effects of UV filters have been evaluated based on oral exposure rather than actual dermal application.11 Although these compounds are absorbed systemically, studies have reported that the amounts are insignificant and noncumulative in the body.10,22-24 Furthermore, the binding affinity of oxybenzone for estrogen receptors has been shown to be much weaker and near insignificant compared to estrogen and estradiol.24,25 Although numerous important studies examining systemic absorption have not shown a clinically significant disruption of hormonal homeostasis or acute toxicity in humans by organic UV filters, further studies are needed.
Inorganic UV Filters
Used as the main active ingredients in sunscreen for decades, titanium dioxide (TiO2) and zinc oxide (ZnO) compounds generally are more photostable and less photoallergic than their organic counterparts.10 In recent years, the safety of these long-used photoprotectors has been questioned because of the development of nanoparticle (<100 nm) formulas that are less opaque on application. Although this formula provides a thin, transparent, and cosmetically appealing medium, there is concern that the metal oxides penetrate the skin and cause local and systemic toxicities.26-28 Several recent scientific studies have shown no percutaneous permeation of these particles in normal adult human skin and reported no causal damage to mammalian cells.10,29-31 Although skin penetration of TiO2 and ZnO has been described as insignificant, focus has shifted to health risks associated with inhaling TiO2 through the use of spray or powder products following statements made by the International Agency for Research on Cancer in 2006.32 Several studies investigating increased health risks, specifically lung cancer, in factory workers who were subjected to TiO2 and ZnO inhalation concluded that exposure was unlikely to pose substantial health risks or subchronic toxicity.33,34 Despite a relatively strong safety profile, a major concern of using these metal oxides as UV filters has been potential free radical formation.35-39 For this reason, the Scientific Committee on Emerging and Newly Identified Health Risks extensively researched and delivered opinions on the use of TiO2 and ZnO in cosmetics, concluding that topical application of either compound does not result in toxicity or other adverse effects.30,40-42 Additionally, an effort has been made by manufacturers to encapsulate nanoparticles with magnesium and other materials to quench the reactive oxygen species along with the human body’s own antioxidant defense system.10 In summary, it appears that the current weight of scientific evidence suggests that percutaneous absorption and toxicity by UV filters in humans may be overestimated and that the use of nanoparticles in sunscreens poses no or negligible potential risks to human health.43,44
Concerns Beyond Organic and Inorganic UV Filters
Beyond these concerns with organic and inorganic UV filters, there are several other claims regarding sunscreen safety that have stirred up controversy, including the side-effect profile of retinyl palmitate, vitamin D deficiency, phototoxicity, environmental effects, futility of sun protection factor levels greater than 50, and increased health risks in children. Although some studies report mixed results, the majority of scientific investigations have addressed and refuted several of these claims, again confirming the relative safety of sunscreen use. It is beyond the scope of this article to further discuss these topics specifically. However, it is worth mentioning that consumer studies report that the actual use of sunscreens is 0.5 mg/cm2 or less compared to the ideal application of 2 mg/cm2, thereby confounding many of the claims made about sunscreen use, such as vitamin D deficiency.45 Sunscreens often contain a combination of several UV filters. To date, only a few existing studies have shown that mixtures of the photoprotective agents discussed might interact and exhibit toxic activity when combined, even when there is no observed adverse toxic effect when used individually in products.46-48
The current FDA ruling on sunscreen labeling does not require manufacturers to state if inorganic UV filters have been formulated into nanoparticles; however, manufacturers are now required to include a statement on all sunscreen labels warning consumers to avoid using sunscreen on damaged or broken skin49 in an effort to prevent the active ingredients from getting under the skin, potentially causing inflammation and/or health risks, because available data do not provide conclusive evidence on increased penetration of open skin.50 Additional information regarding the 2011 FDA sunscreen ruling can be found in a prior Cutis Resident Corner column.51
Final Thoughts
As health care providers, we should take advantage of opportunities to educate our patients about other sun safety practices, such as avoiding excessive sun exposure during peak hours (10 am to 2 pm), seeking shade, and wearing photoprotective clothing (eg, wide-brimmed hats, sunglasses).
The research is quite clear: Using broadband sunscreens that absorb and/or block UV radiation results in reduced damage to the skin’s DNA, a fact that should be considered when taking into account the risks and benefits of sunscreen use.2,3 Although sunscreen use is highly recommended in addition to the other sun protection methods, it is ultimately the patient’s choice. If a patient is still concerned about the active ingredients of UV filters, even given the high probability of safety, there are products available on the market that do not include organic filters or nanoparticles. Given the established benefits of UV protection, the use of sunscreens remain one of the most important photoprotective methods, and with increased usage by the public, continuous monitoring of the overall safety and benefit profile of future products is prudent.
1. Skin cancer statistics. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/cancer/skin/statistics/index.htm. Updated September 2, 2014. Accessed December 30, 2014.
2. World Health Organization, International Agency for Research on Cancer. Solar and ultraviolet radiation. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 55. Lyon, France: International Agency for Research on Cancer; 1992.
3. Green AC, Williams GM, Logan V, et al. Reduced melanoma after regular sunscreen use: randomized trial follow-up. J Clin Oncol. 2011;29:257-263.
4. Darlington S, Williams G, Neale R, et al. A randomized controlled trial to assess sunscreen application and beta carotene supplementation in the prevention of solar keratoses. Arch Dermatol. 2003;139:451-455.
5. Van der Pols JC, Williams GM, Pandeya N, et al. Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer Epidemiol Biomarkers Prev. 2006;15:2546-2548.
6. Hughes MC, Williams GM, Baker P, et al. Sunscreen and prevention of skin aging: a randomized trial. Ann Intern Med. 2013;158:781-790.
7. Bissonnette R, Nigen S, Bolduc C. Influence of the quantity of sunscreen applied on the ability to protect against ultraviolet-induced polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2012;28:240-243.
8. Cancer trends progress report 2011/2012 update: sun protection. National Cancer Institute Web site. http://progressreport.cancer.gov/doc_detail.asp?pid¡1&did¡2009&chid¡91&coid¡911. Accessed December 30, 2014.
9. Sunscreen Drug Products for Over-the-counter Human Use, 21 CFR §352.10. http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?fr=352.10. Updated September 1, 2014. Accessed December 30, 2014.
10. Burnett ME, Wang SQ. Current sunscreen controversies: a critical review. Photodermatol Photoimmunol Photomed. 2011;27:58-67.
11. Krause M, Klit A, Blomberg Jensen M, et al. Sunscreens: are they beneficial for health? an overview of endocrine disrupting properties of UV-filters. Int J Androl. 2012;35:424-436.
12. Schlumpf M, Cotton B, Conscience M, et al. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect. 2001;109:239-244.
13. Schlumpf M, Schmid P, Durrer S, et al. Endocrine activity and developmental toxicity of cosmetic UV filters–an update. Toxicol. 2004;205:113-122.
14. Schlumpf M, Kypke K, Vökt C, et al. Endocrine active UV filters: developmental toxicity and exposure through breast milk. Chimia. 2008;62:345-351.
15. Nakagawa Y, Suzuki T. Metabolism of 2-hydroxy-4-methoxybenzophenone in isolated rat hepatocytes and xenoestrogenic effects of its metabolites on MCF-7 human breast cancer cells. Chem Biol Interact. 2002;139:115-128.
16. Ma R, Cotton B, Lichtensteiger W, et al. UV filters with antagonistic action at androgen receptors in the MDA-kb2 cell transcriptional-activation assay. Toxicol Sci. 2003;74:43-50.
17. Heneweer M, Muusse M, van den Berg M, et al. Additive estrogenic effects of mixtures of frequently used UV filters on pS2-gene transcription in MCF-7 cells. Toxicol Appl Pharmacol. 2005;208:170-177.
18. Knobler E, Almeida L, Ruzkowski AM, et al. Photoallergy to benzophenone. Arch Dermatol. 1989;125:801-804.
19. Draelos ZD. Are sunscreens safe? J Cosmet Dermatol. 2010;9:1-2.
20. Gilbert E, Pirot F, Bertholle V. Commonly used UV filter toxicity on biological functions: review of last decade studies. Int J of Cosmet Sci. 2013;35:208-219.
21. Wang SQ, Burnett ME, Lim HW. Safety of oxybenzone: putting numbers into perspective. Arch Dermatol. 2011;147:865-866.
22. Mancebo SE, Hu JY, Wang SQ. Sunscreens: a review of health benefits, regulations, and controversies. Dermatol Clin. 2014;32:427-438.
23. Jansen R, Osterwalder U, Wang SQ, et al. Photoprotection: part II. sunscreen: development, efficacy, and controversies. J Am Acad Dermatol. 2013;69:867.e1-867.e14.
24. Janjua NR, Mogensen B, Andersson AM, et al. Systemic absorption of the sunscreens benzo- phenone-3, octyl-methoxycinnamate, and 3-(4-methyl-benzy-lidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol. 2004;123:57-61.
25. Kadry AM, Chukwuemeka SO, Mohamed S, et al. Pharmacokinetics of benzophenone-3 after oral exposure in male rats. J Appl Toxicol. 1995;15:97-102.
26. Gulson B, McCall M, Korsch M, et al. Small amounts of zinc from zinc oxide particles in sunscreens applied outdoors are absorbed through human skin. Toxicol Sci. 2010;118:140-149.
27. Gulson B, Wong H, Korsch M, et al. Comparison of dermal absorption of zinc from different sunscreen formulations and differing UV exposure based on stable isotope tracing. Sci Total Environ. 2012:420:313-318.
28. Benech-Kieffer F, Meuling WJ, Leclerc C, et al. Percutaneous absorption of Mexoryl SX in human volunteers: comparison with in vitro data. Skin Pharmacol Appl Skin Physiol. 2003;16:343-355.
29. Nash JF. Human safety and efficacy of ultraviolet filters and sunscreen products. Dermatol Clin. 2006;24:35-51.
30. Nohynek GJ, Lademann J, Ribaud C, et al. Grey goo on the skin? nanotechnology, cosmetic and sunscreen safety. Crit Rev Toxicol. 2007;37:251-277.
31. Sadrieh N, Wokovich AM, Gopee NV, et al. Lack of significant dermal penetration of titanium dioxide from sunscreen formulations containing nano- and submicron-size TiO2 particles. Toxicol Sci. 2010;115:156-166.
32. International Agency for Research on Cancer. Carbon black, titanium dioxide, and talc. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 93. Lyon, France: International Agency for Research on Cancer; 2006.
33. Liao CM, Chiang YH, Chio CP. Model-based assessment for human inhalation exposure risk to airborne nano/fine titanium dioxide particles. Sci Total Environ. 2008:15;407:165-177.
34. Adamcakova-Dodd A, Stebounova LV, Kim JS, et al. Toxicity assessment of zinc oxide nanoparticles using sub-acute and sub-chronic murine inhalation models. Part Fibre Toxicol. 2014;11:15.
35. Wamer WG, Yin JJ, Wei RR. Oxidative damage to nucleic acids photosensitized by titanium dioxide. Free Radic Biol Med. 1997;23:851-858.
36. Nakagawa Y, Wakuri S, Sakamoto K, et al. The photogenotoxicity of titanium dioxide particles. Mutat Res. 1997;394:125-132.
37. Dunford R, Salinaro A, Cai L, et al. Chemical oxidation and DNA damage catalysed by inorganic sunscreen ingredients. FEBS Lett. 1997;418:87-90, 99.
38. Hidaka H, Kobayashi H, Koike T, et al. DNA damage photoinduced by cosmetic pigments and sunscreen agents under solar exposure and artificial UV illumination. J Oleo Sci. 2006;55:249-261.
39. Dufour EK, Kumaravel T, Nohynek GJ, et al. Clastogenicity, photo-clastogenicity or pseudo-photo-clastogenicity: genotoxic effects of zinc oxide in the dark, in pre-irradiated or simultaneously irradiated Chinese hamster ovary cells [published online ahead of print June 21, 2006]. Mutat Res. 2006;607:215-224.
40. Opinion of the Scientific Committee on Cosmetic Products and Non-Food Products intended for Consumers concerning titanium dioxide. http://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out135_en.pdf. Published October 24, 2000. Accessed December 30, 2014.
41. The Scientific Committee on Cosmetic Products and Non-Food Products intended for Consumers opinion concerning zinc oxide. http://ec.europa.eu/health/archive/ph_risk/committees/sccp/documents/out222_en.pdf. Published June 24-25, 2003. Accessed December 30, 2014.
42. Hackenberg S, Friehs G, Kessler M, et al. Nanosized titanium dioxide particles do not induce DNA damage in human peripheral blood lymphocytes. Environ Mol Mutagen. 2010;52:264-268.
43. Bach-Thomsen M, Wulf HC. Sunbather’s application of sunscreen is probably inadequate to obtain the sun protection factor assigned to the preparation. Photodermatol Photoimmunol Photomed. 1993:9;242-244.
44. Nohynek GJ, Antignac E, Re T, et al. Safety assessment of personal care products/cosmetics and their ingredients. Toxicol Appl Pharmacol. 2010:1;243:239-259.
45. Diffey BL. Sunscreens: use and misuse. In: Giacomoni PU, ed. Sun Protection in Man. Vol 3. Amsterdam, the Netherlands: Elsevier Science BV; 2001:521-534.
46. Heneweer M, Muusse M, Van den BM, et al. Additive estrogenic effects of mixtures of frequently used UV-filters on pS2-gene transcription in MCF-7 cells. Toxicol Appl Pharmacol. 2005;208:170-177.
47. Kunz PY, Galicia HF, Fent K. Comparison of in vitro and in vivo estrogenic activity of UV-filters in fish. Toxicol Sci. 2006;90:349-361.
48. Kortenkamp A, Faust M, Scholze M, et al. Low-level exposure to multiple chemicals: reason for human health concerns? Environ Health Perspect. 2007;115(suppl 1):106-114.
49. Labeling and effectiveness testing: sunscreen drug products for over-the-counter human use—small entity compliance guide. US Food and Drug Administration Web site. http://www.fda.gov/drugs/guidancecomplianceregulatoryinformation/guidances/ucm330694.htm. Published December 2012. Updated May 13, 2014. Accessed December 30, 2014.
50. Schafer-Korting M, Korting HC, Ponce-Poschl E. Liposomal tretinoin for uncomplicated acne vulgaris. Clin Investig. 1994;72:1086-1091.
51. Bronfenbrener R. Simplifying sun safety: a guide to the new FDA sunscreen monograph. Cutis. 2014;93:e17-e19.
1. Skin cancer statistics. Centers for Disease Control and Prevention Web site. http://www.cdc.gov/cancer/skin/statistics/index.htm. Updated September 2, 2014. Accessed December 30, 2014.
2. World Health Organization, International Agency for Research on Cancer. Solar and ultraviolet radiation. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 55. Lyon, France: International Agency for Research on Cancer; 1992.
3. Green AC, Williams GM, Logan V, et al. Reduced melanoma after regular sunscreen use: randomized trial follow-up. J Clin Oncol. 2011;29:257-263.
4. Darlington S, Williams G, Neale R, et al. A randomized controlled trial to assess sunscreen application and beta carotene supplementation in the prevention of solar keratoses. Arch Dermatol. 2003;139:451-455.
5. Van der Pols JC, Williams GM, Pandeya N, et al. Prolonged prevention of squamous cell carcinoma of the skin by regular sunscreen use. Cancer Epidemiol Biomarkers Prev. 2006;15:2546-2548.
6. Hughes MC, Williams GM, Baker P, et al. Sunscreen and prevention of skin aging: a randomized trial. Ann Intern Med. 2013;158:781-790.
7. Bissonnette R, Nigen S, Bolduc C. Influence of the quantity of sunscreen applied on the ability to protect against ultraviolet-induced polymorphous light eruption. Photodermatol Photoimmunol Photomed. 2012;28:240-243.
8. Cancer trends progress report 2011/2012 update: sun protection. National Cancer Institute Web site. http://progressreport.cancer.gov/doc_detail.asp?pid¡1&did¡2009&chid¡91&coid¡911. Accessed December 30, 2014.
9. Sunscreen Drug Products for Over-the-counter Human Use, 21 CFR §352.10. http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfcfr/cfrsearch.cfm?fr=352.10. Updated September 1, 2014. Accessed December 30, 2014.
10. Burnett ME, Wang SQ. Current sunscreen controversies: a critical review. Photodermatol Photoimmunol Photomed. 2011;27:58-67.
11. Krause M, Klit A, Blomberg Jensen M, et al. Sunscreens: are they beneficial for health? an overview of endocrine disrupting properties of UV-filters. Int J Androl. 2012;35:424-436.
12. Schlumpf M, Cotton B, Conscience M, et al. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect. 2001;109:239-244.
13. Schlumpf M, Schmid P, Durrer S, et al. Endocrine activity and developmental toxicity of cosmetic UV filters–an update. Toxicol. 2004;205:113-122.
14. Schlumpf M, Kypke K, Vökt C, et al. Endocrine active UV filters: developmental toxicity and exposure through breast milk. Chimia. 2008;62:345-351.
15. Nakagawa Y, Suzuki T. Metabolism of 2-hydroxy-4-methoxybenzophenone in isolated rat hepatocytes and xenoestrogenic effects of its metabolites on MCF-7 human breast cancer cells. Chem Biol Interact. 2002;139:115-128.
16. Ma R, Cotton B, Lichtensteiger W, et al. UV filters with antagonistic action at androgen receptors in the MDA-kb2 cell transcriptional-activation assay. Toxicol Sci. 2003;74:43-50.
17. Heneweer M, Muusse M, van den Berg M, et al. Additive estrogenic effects of mixtures of frequently used UV filters on pS2-gene transcription in MCF-7 cells. Toxicol Appl Pharmacol. 2005;208:170-177.
18. Knobler E, Almeida L, Ruzkowski AM, et al. Photoallergy to benzophenone. Arch Dermatol. 1989;125:801-804.
19. Draelos ZD. Are sunscreens safe? J Cosmet Dermatol. 2010;9:1-2.
20. Gilbert E, Pirot F, Bertholle V. Commonly used UV filter toxicity on biological functions: review of last decade studies. Int J of Cosmet Sci. 2013;35:208-219.
21. Wang SQ, Burnett ME, Lim HW. Safety of oxybenzone: putting numbers into perspective. Arch Dermatol. 2011;147:865-866.
22. Mancebo SE, Hu JY, Wang SQ. Sunscreens: a review of health benefits, regulations, and controversies. Dermatol Clin. 2014;32:427-438.
23. Jansen R, Osterwalder U, Wang SQ, et al. Photoprotection: part II. sunscreen: development, efficacy, and controversies. J Am Acad Dermatol. 2013;69:867.e1-867.e14.
24. Janjua NR, Mogensen B, Andersson AM, et al. Systemic absorption of the sunscreens benzo- phenone-3, octyl-methoxycinnamate, and 3-(4-methyl-benzy-lidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol. 2004;123:57-61.
25. Kadry AM, Chukwuemeka SO, Mohamed S, et al. Pharmacokinetics of benzophenone-3 after oral exposure in male rats. J Appl Toxicol. 1995;15:97-102.
26. Gulson B, McCall M, Korsch M, et al. Small amounts of zinc from zinc oxide particles in sunscreens applied outdoors are absorbed through human skin. Toxicol Sci. 2010;118:140-149.
27. Gulson B, Wong H, Korsch M, et al. Comparison of dermal absorption of zinc from different sunscreen formulations and differing UV exposure based on stable isotope tracing. Sci Total Environ. 2012:420:313-318.
28. Benech-Kieffer F, Meuling WJ, Leclerc C, et al. Percutaneous absorption of Mexoryl SX in human volunteers: comparison with in vitro data. Skin Pharmacol Appl Skin Physiol. 2003;16:343-355.
29. Nash JF. Human safety and efficacy of ultraviolet filters and sunscreen products. Dermatol Clin. 2006;24:35-51.
30. Nohynek GJ, Lademann J, Ribaud C, et al. Grey goo on the skin? nanotechnology, cosmetic and sunscreen safety. Crit Rev Toxicol. 2007;37:251-277.
31. Sadrieh N, Wokovich AM, Gopee NV, et al. Lack of significant dermal penetration of titanium dioxide from sunscreen formulations containing nano- and submicron-size TiO2 particles. Toxicol Sci. 2010;115:156-166.
32. International Agency for Research on Cancer. Carbon black, titanium dioxide, and talc. In: IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Vol 93. Lyon, France: International Agency for Research on Cancer; 2006.
33. Liao CM, Chiang YH, Chio CP. Model-based assessment for human inhalation exposure risk to airborne nano/fine titanium dioxide particles. Sci Total Environ. 2008:15;407:165-177.
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