178
Letters / Ann Allergy Asthma Immunol 112 (2014) 175e183
was noticed in the following 3 days when methylprednisolone (400 mg) was administered daily. In drug-induced angioedema, the close temporal relationship between drug administration and appearance of angioedema is usually the key element that makes obvious the identification and subsequent withdrawal of the offending medication.2 Usually, angioedema would be relieved within 24 hours after withdrawal of the offending medication. However, in our patient, angioedema remained after discontinuation of rt-PA therapy for 3 days, indicating that other than rt-PA, olmesartan may also be associated with angioedema. Therefore, amlodipine (5 mg/d) was used instead of olmesartan, and angioedema was attenuated and resolved completely on day 10 of hospitalization. Although the first case report on angioneurotic edema associated with thrombolysis in acute ischemic stroke was published in 1997,3 only a few case reports and a small case series have focused on this rare adverse effect of rt-PA administration in acute ischemic stroke. Angioedema have been reported to occur in 9 (5.1%; 95% CI, 2.3%-9.5%) of the 176 consecutive patients given alteplase for acute ischemic stroke.1 Plasminogen activator is a serine protease that cleaves plasminogen to plasmin, which further cleaves thrombus-bound fibrin, resulting in the fibrinolytic effect that can also activate the complement cascade and kinin pathway. Bradykinin is metabolized by aminopeptidase P, ACE, and kinase I, whereas ACE and aminopeptidase P are its first and second main inactivating pathways, respectively. Kinase I represents a minor pathway unless ACE is inhibited.4 When ACE inhibitors couple with the rt-PAeinduced kinin pathway, they may increase bradykinin significantly and induce anaphylactoid response or angioneurotic edema. Some evidence suggests that for patients who develop angioedema when taking an ACE inhibitor, the risk of development of any subsequent angioedema when taking an ARB is between 2% and 17%. This information will aid clinicians in counseling patients regarding therapy options after development of angioedema due to ACE inhibitors.4 There are 2 types of angiotensin receptors: AT1 and AT2. Olmesartan is a highly potent antagonist of the AT1 receptor. The vasodilatory effect of ARBs is exerted by competitive blockade of the AT1 receptor. The functional role of AT2 receptor is not clear because of its low expression. AT1 and AT2 receptors generally oppose each other physiologically.5,6 Increased pressure in the thoracic aorta can activate angiotensin IIeAT2 receptor binding, which stimulates endothelial nitric oxide synthase phosphorylation via a bradykinin B2 receptor and protein kinase Aedependent pathway, which is not opposed by an ARB.5,7 Another study reported that both losartan and eprosartan increased the serum bradykinin level in hypertensive patients
because of reduced metabolism induced by ACE and neutral endopeptidase.8 Olmesartan may increase the serum bradykinin level and mediate angioneurotic edema via a similar pathway. In our patient, angioedema seems to be the result of the synergistic effect of ARBs, rt-PA, and hypertension. To our knowledge, this is the first report about angioedema associated with olmesartan during rt-PA administration. In addition, it is the third published case and the first case in an Asian patient of olmesartaninduced angioedema.9,10 Shi Wang, MD, PhD* Xiaoying Bi, PhDy Lianbiao Shan, MD* Yingqi Zhou, PhD* *Department of Neurology Navy 411 Hospital Shanghai, People’s Republic of China y Department of Neurology Changhai Hospital Second Military Medical University Shanghai, People’s Republic of China [email protected]
References [1] Hill MD, Lye T, Moss H, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology. 2003;60:1525e1527. [2] Cicardi M, Zingale LC, Bergamaschini L, et al. Angioedema associated with angiotensin-converting enzyme inhibitor use: outcome after switching to a different treatment. Arch Intern Med. 2004;164:910e913. [3] Pancioli A, Brott T, Robertson V, et al. Asymmetric angioneurotic edema associated with thrombolysis for acute stroke. Ann Emerg Med. 1998;30: 227e229. [4] Haymore BR, Yoon J, Mikita CP, et al. Risk of angioedema with angiotensin receptor blockers in patients with prior angioedema associated with angiotensin-converting enzyme inhibitors: a meta-analysis. Ann Allergy Asthma Immunol. 2008;101:495e499. [5] Carey RM, Park J. Role of angiotensin type 2 receptors in vasodilation of resistance and capacitance vessels. Hypertension. 2006;48:824e825. [6] Carey RM. Cardiovascular and renal regulation by the angiotensin type 2 receptor: the AT2 receptor comes of age. Hypertension. 2005;45: 840e844. [7] Hiyoshi H, Yayama K, Takano M, et al. Angiotensin type 2 receptor-mediated phosphorylation of eNOS in the aortas of mice with 2-kidney, 1-clip hypertension. Hypertension. 2005;45:967e973. [8] Campbell DJ, Krum H, Esler MD, et al. Losartan increases bradykinin levels in hypertensive humans. Circulation. 2005;111:315e320. [9] Vasquez JL, Jaramillo JC, Fernandez C, et al. Severe angioedema associated with olmesartan. Ann Allergy Asthma Immunol. 2011;107:285. [10] Nykamp D, Winter EE. Olmesartan medoxomil-induced angioedema. Ann Pharmacother. 2007;41:518e520.
Evaluating for seasonal variation in angiotensin-converting enzyme inhibitoreand angiotensin receptor blocker-induced angioedema Angioedema that occurs as an episodic, adverse effect of angiotensinconverting enzyme inhibitors (ACEIs) presents the emergency physician with some of the most challenging and distressing airway emergencies encountered in common clinical practice.1,2 It is characterized by a bland, nonpainful, nonurticarial swelling of the lips, face, tongue, and the soft tissues of the pharynx and larynx. It may result in airway compromise and rapid progression to respiratory failure and death.3 The benefits of the use of ACEIs are remarkable and include the control of hypertension and positive effects on the progression of coronary artery disease, kidney injury, peripheral Disclosures: Authors have nothing to disclose.
vascular disease, diabetes, and stroke. These effects appear to be mediated by the antagonism of angiotensin II.4 Angioedema has also been shown to occur, although at a lower frequency, in patients using angiotensin receptor blockers (ARBs).5 The extensive benefits of ACEIs and ARBs have resulted in high rates of prescription and use. In 2007 an estimated 40 million people in the United States were using these agents. Angioedema occurs in a small fraction of users (0.1%0.8%)2,6; however, the widespread use of these medicines guarantees a significant number of occurrences. Although the overwhelming benefits of these agents are believed to greatly outweigh the adverse effects, considering the rarity, the consequences for the individual who experiences them can be life altering or ending.3
Letters / Ann Allergy Asthma Immunol 112 (2014) 175e183
Interestingly, little is known about the timing and triggers of ACEI angioedema. It may occur within days to years of the initiation of therapy and is sometimes known to occur in the setting of a surgical intervention or other stressors.2 Epidemiologically, ACEIinduced angioedema most commonly occurs in African American women between the ages of 32 and 92 years.7 In one series, ACEI angioedema accounted for 64% of all patients with angioedema presenting for acute care.2 The angioedema associated with ACEIs is widely believed to result from an excess of bradykinin, which some studies have suggested may interact with histamine.8,9 Despite this potential link to an allergic type response, no published data support an association of ACEI angioedema with seasonal variation and common allergy triggers. We sought to determine whether there is a seasonal variation in the incidence of ACEI and ARB angioedema and if a correlation exists with temperature, dew point, or pollen counts, hypothesizing from clinical observation that this may be so. We performed a retrospective medical record review using a single institution’s electronic health records to identify all cases of angioedema (International Classification of Diseases, Ninth Revision, code 995.1) from all emergency department patient visits from 2009 to 2011. Cases that had an ACEI or ARB recorded as an active patient medication were included for analysis. Patients with discharge diagnoses of angioedema who were not taking ACEIs or ARBs were excluded, and there were also no patients at our institution younger than 18 years. Daily mean temperature and dew point were obtained for the region from the National Oceanic and Atmospheric Administration website. Local pollen counts were obtained from the US Army Centralized Allergen Extract Lab, the local American Academy of Allergy, Asthma, and Immunologyecertified counting station. Data were analyzed using Poisson regression to evaluate for variation in seasonal incidence and multivariate logistic regression to evaluate for temperature and dew point correlation (Stata statistical software, version 12.1; StataCorp, College Station, Texas). A separate analysis was performed for pollen count correlations because counts are only recorded a mean of 3.8 days per week, yielding 605 observations in the 1,095-day study period. The study site is a 901-bed urban teaching hospital in Washington, DC, with an emergency department with approximately 90,000 patient encounters per year. The study was approved by the MedStar Washington Hospital Center Institutional Review Board. A total of 217 cases were included for analysis. Multivariate logistic regression of temperature and dew point revealed a nonstatistically significant model with (P ¼ .63) and individual odds ratios of 0.99 (P ¼ .64) and 1.00 (P ¼ .47), respectively. Poisson regression analysis for seasonal variation also produced a nonsignificant model with P values for spring, summer, and fall (winter was used for reference) of .07, .47, and .12, respectively.
179
A separate multivariate logistic regression of temperature, dew point, and pollen counts restricted to the 605 days with pollen count observations also produced a nonstatistically significant model with a P ¼ .67. The above analyses were also repeated excluding cases where an ARB but not an ACEI was documented on the patient’s medication list (n ¼ 210), and the models were again not statistically significant, yielding P values for temperature, dew point, and pollen count of .21, .42, and .64, respectively. During a 3-year period at a single institution in the midAtlantic region, no seasonal variation was identified in cases of ACEI- and ARB-induced angioedema. Furthermore, no association was identified with mean daily temperature, dew point, or pollen counts for the region. Limitations to this study include a lack of information on patient’s baseline atopic status, the retrospective nature of the study, and the fact that the study was limited to a single institution. Acknowledgments Thanks to Susan E Kosisky, chief microbiologist at the US Army Centralized Allergen Extract Lab, for providing pollen count data for analysis. Matthew Wilson, MD William Frohna, MD Graham Trent, BS Diane Sauter, MD Washington Hospital Center Washington, DC [email protected] References [1] Cicardi M, Zingale LC, Bergamaschini L, Agostoni A. Angioedema associated with angiotensin-converting enzyme inhibitor use: outcome after switching to a different treatment. Arch Intern Med. 2004;164:910e913. [2] Malde B, Regalado J, Greenberger PA. Investigation of angioedema associated with the use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers. Ann Allergy Asthma Immunol. 2007;98:57e63. [3] Peltekis G, Palaskas D, Samanidou M, et al. Severe migratory angioedema due to ACE inhibitors use. Hippokratia. 2009;13:122e124. [4] Dandona P, Dhindsa S, Ghanim H, et al. Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. J Hum Hypertens. 2007;21:20e27. [5] Bas M, Adams V, Suvorava T, et al. Nonallergic angioedema: role of bradykinin. Allergy. 2007;62:842e856. [6] Agostoni A, Cicardi M, Cugno LC, et al. Angioedema due to angiotensinconverting enzyme inhibitors. Immunopharmacology. 1999;44:21e25. [7] Seidman MD, Lewandowski CA, Sarpa JR, et al. Angioedema related to angiotensinconverting enzyme inhibitors. Otolaryngol Head Neck Surg. 1990;102:727e731. [8] Austin CE, Dear JW, Neighbour H, et al. The contribution of histamine to the action of bradykinin in the human nasal airway. Immunopharmacology. 1996; 34:181e189. [9] Ishizaka T, Iwata M, Ishizaka K. Release of histamine and arachidonate from mouse mast cells induced by glycosylation-enhancing factor and bradykinin. J Immumol. 1985;134:1880e1887.
Urinary triclosan levels and recent asthma exacerbations Triclosan is a broad-spectrum antimicrobial chemical with endocrine and immune effects.1,2 The primary source of exposure is considered personal care products (eg, toothpaste and hand soap), but multiple potential sources and routes of exposure exist.2 Because the airway microbiome may be important in the development or maintenance of asthma,3,4 we hypothesized that levels Disclosures: Authors have nothing to disclose. Funding: This work was supported by a grant from the American Academy of Allergy, Asthma and Immunology and Food Allergy Research and Education (Dr Savage).
of the antimicrobial chemical triclosan may be associated with asthma prevalence and control. We previously demonstrated in a cross-sectional study a significantly increased risk of aeroallergen and food sensitization with increasing urinary triclosan levels in US children. Triclosan levels were positively associated with the risk of atopic asthma, although the association did not reach statistical significance.5 A cross-sectional Norwegian study also found that triclosan was associated with aeroallergen sensitization and rhinitis but not with asthma.6 In a mouse model of asthma, triclosan increased bronchial hyperresponsiveness, total IgE, pulmonary eosinophilia, and interleukin 13.1 Given these
Letters / Ann Allergy Asthma Immunol 112 (2014) 175e183
was noticed in the following 3 days when methylprednisolone (400 mg) was administered daily. In drug-induced angioedema, the close temporal relationship between drug administration and appearance of angioedema is usually the key element that makes obvious the identification and subsequent withdrawal of the offending medication.2 Usually, angioedema would be relieved within 24 hours after withdrawal of the offending medication. However, in our patient, angioedema remained after discontinuation of rt-PA therapy for 3 days, indicating that other than rt-PA, olmesartan may also be associated with angioedema. Therefore, amlodipine (5 mg/d) was used instead of olmesartan, and angioedema was attenuated and resolved completely on day 10 of hospitalization. Although the first case report on angioneurotic edema associated with thrombolysis in acute ischemic stroke was published in 1997,3 only a few case reports and a small case series have focused on this rare adverse effect of rt-PA administration in acute ischemic stroke. Angioedema have been reported to occur in 9 (5.1%; 95% CI, 2.3%-9.5%) of the 176 consecutive patients given alteplase for acute ischemic stroke.1 Plasminogen activator is a serine protease that cleaves plasminogen to plasmin, which further cleaves thrombus-bound fibrin, resulting in the fibrinolytic effect that can also activate the complement cascade and kinin pathway. Bradykinin is metabolized by aminopeptidase P, ACE, and kinase I, whereas ACE and aminopeptidase P are its first and second main inactivating pathways, respectively. Kinase I represents a minor pathway unless ACE is inhibited.4 When ACE inhibitors couple with the rt-PAeinduced kinin pathway, they may increase bradykinin significantly and induce anaphylactoid response or angioneurotic edema. Some evidence suggests that for patients who develop angioedema when taking an ACE inhibitor, the risk of development of any subsequent angioedema when taking an ARB is between 2% and 17%. This information will aid clinicians in counseling patients regarding therapy options after development of angioedema due to ACE inhibitors.4 There are 2 types of angiotensin receptors: AT1 and AT2. Olmesartan is a highly potent antagonist of the AT1 receptor. The vasodilatory effect of ARBs is exerted by competitive blockade of the AT1 receptor. The functional role of AT2 receptor is not clear because of its low expression. AT1 and AT2 receptors generally oppose each other physiologically.5,6 Increased pressure in the thoracic aorta can activate angiotensin IIeAT2 receptor binding, which stimulates endothelial nitric oxide synthase phosphorylation via a bradykinin B2 receptor and protein kinase Aedependent pathway, which is not opposed by an ARB.5,7 Another study reported that both losartan and eprosartan increased the serum bradykinin level in hypertensive patients
because of reduced metabolism induced by ACE and neutral endopeptidase.8 Olmesartan may increase the serum bradykinin level and mediate angioneurotic edema via a similar pathway. In our patient, angioedema seems to be the result of the synergistic effect of ARBs, rt-PA, and hypertension. To our knowledge, this is the first report about angioedema associated with olmesartan during rt-PA administration. In addition, it is the third published case and the first case in an Asian patient of olmesartaninduced angioedema.9,10 Shi Wang, MD, PhD* Xiaoying Bi, PhDy Lianbiao Shan, MD* Yingqi Zhou, PhD* *Department of Neurology Navy 411 Hospital Shanghai, People’s Republic of China y Department of Neurology Changhai Hospital Second Military Medical University Shanghai, People’s Republic of China [email protected]
References [1] Hill MD, Lye T, Moss H, et al. Hemi-orolingual angioedema and ACE inhibition after alteplase treatment of stroke. Neurology. 2003;60:1525e1527. [2] Cicardi M, Zingale LC, Bergamaschini L, et al. Angioedema associated with angiotensin-converting enzyme inhibitor use: outcome after switching to a different treatment. Arch Intern Med. 2004;164:910e913. [3] Pancioli A, Brott T, Robertson V, et al. Asymmetric angioneurotic edema associated with thrombolysis for acute stroke. Ann Emerg Med. 1998;30: 227e229. [4] Haymore BR, Yoon J, Mikita CP, et al. Risk of angioedema with angiotensin receptor blockers in patients with prior angioedema associated with angiotensin-converting enzyme inhibitors: a meta-analysis. Ann Allergy Asthma Immunol. 2008;101:495e499. [5] Carey RM, Park J. Role of angiotensin type 2 receptors in vasodilation of resistance and capacitance vessels. Hypertension. 2006;48:824e825. [6] Carey RM. Cardiovascular and renal regulation by the angiotensin type 2 receptor: the AT2 receptor comes of age. Hypertension. 2005;45: 840e844. [7] Hiyoshi H, Yayama K, Takano M, et al. Angiotensin type 2 receptor-mediated phosphorylation of eNOS in the aortas of mice with 2-kidney, 1-clip hypertension. Hypertension. 2005;45:967e973. [8] Campbell DJ, Krum H, Esler MD, et al. Losartan increases bradykinin levels in hypertensive humans. Circulation. 2005;111:315e320. [9] Vasquez JL, Jaramillo JC, Fernandez C, et al. Severe angioedema associated with olmesartan. Ann Allergy Asthma Immunol. 2011;107:285. [10] Nykamp D, Winter EE. Olmesartan medoxomil-induced angioedema. Ann Pharmacother. 2007;41:518e520.
Evaluating for seasonal variation in angiotensin-converting enzyme inhibitoreand angiotensin receptor blocker-induced angioedema Angioedema that occurs as an episodic, adverse effect of angiotensinconverting enzyme inhibitors (ACEIs) presents the emergency physician with some of the most challenging and distressing airway emergencies encountered in common clinical practice.1,2 It is characterized by a bland, nonpainful, nonurticarial swelling of the lips, face, tongue, and the soft tissues of the pharynx and larynx. It may result in airway compromise and rapid progression to respiratory failure and death.3 The benefits of the use of ACEIs are remarkable and include the control of hypertension and positive effects on the progression of coronary artery disease, kidney injury, peripheral Disclosures: Authors have nothing to disclose.
vascular disease, diabetes, and stroke. These effects appear to be mediated by the antagonism of angiotensin II.4 Angioedema has also been shown to occur, although at a lower frequency, in patients using angiotensin receptor blockers (ARBs).5 The extensive benefits of ACEIs and ARBs have resulted in high rates of prescription and use. In 2007 an estimated 40 million people in the United States were using these agents. Angioedema occurs in a small fraction of users (0.1%0.8%)2,6; however, the widespread use of these medicines guarantees a significant number of occurrences. Although the overwhelming benefits of these agents are believed to greatly outweigh the adverse effects, considering the rarity, the consequences for the individual who experiences them can be life altering or ending.3
Letters / Ann Allergy Asthma Immunol 112 (2014) 175e183
Interestingly, little is known about the timing and triggers of ACEI angioedema. It may occur within days to years of the initiation of therapy and is sometimes known to occur in the setting of a surgical intervention or other stressors.2 Epidemiologically, ACEIinduced angioedema most commonly occurs in African American women between the ages of 32 and 92 years.7 In one series, ACEI angioedema accounted for 64% of all patients with angioedema presenting for acute care.2 The angioedema associated with ACEIs is widely believed to result from an excess of bradykinin, which some studies have suggested may interact with histamine.8,9 Despite this potential link to an allergic type response, no published data support an association of ACEI angioedema with seasonal variation and common allergy triggers. We sought to determine whether there is a seasonal variation in the incidence of ACEI and ARB angioedema and if a correlation exists with temperature, dew point, or pollen counts, hypothesizing from clinical observation that this may be so. We performed a retrospective medical record review using a single institution’s electronic health records to identify all cases of angioedema (International Classification of Diseases, Ninth Revision, code 995.1) from all emergency department patient visits from 2009 to 2011. Cases that had an ACEI or ARB recorded as an active patient medication were included for analysis. Patients with discharge diagnoses of angioedema who were not taking ACEIs or ARBs were excluded, and there were also no patients at our institution younger than 18 years. Daily mean temperature and dew point were obtained for the region from the National Oceanic and Atmospheric Administration website. Local pollen counts were obtained from the US Army Centralized Allergen Extract Lab, the local American Academy of Allergy, Asthma, and Immunologyecertified counting station. Data were analyzed using Poisson regression to evaluate for variation in seasonal incidence and multivariate logistic regression to evaluate for temperature and dew point correlation (Stata statistical software, version 12.1; StataCorp, College Station, Texas). A separate analysis was performed for pollen count correlations because counts are only recorded a mean of 3.8 days per week, yielding 605 observations in the 1,095-day study period. The study site is a 901-bed urban teaching hospital in Washington, DC, with an emergency department with approximately 90,000 patient encounters per year. The study was approved by the MedStar Washington Hospital Center Institutional Review Board. A total of 217 cases were included for analysis. Multivariate logistic regression of temperature and dew point revealed a nonstatistically significant model with (P ¼ .63) and individual odds ratios of 0.99 (P ¼ .64) and 1.00 (P ¼ .47), respectively. Poisson regression analysis for seasonal variation also produced a nonsignificant model with P values for spring, summer, and fall (winter was used for reference) of .07, .47, and .12, respectively.
179
A separate multivariate logistic regression of temperature, dew point, and pollen counts restricted to the 605 days with pollen count observations also produced a nonstatistically significant model with a P ¼ .67. The above analyses were also repeated excluding cases where an ARB but not an ACEI was documented on the patient’s medication list (n ¼ 210), and the models were again not statistically significant, yielding P values for temperature, dew point, and pollen count of .21, .42, and .64, respectively. During a 3-year period at a single institution in the midAtlantic region, no seasonal variation was identified in cases of ACEI- and ARB-induced angioedema. Furthermore, no association was identified with mean daily temperature, dew point, or pollen counts for the region. Limitations to this study include a lack of information on patient’s baseline atopic status, the retrospective nature of the study, and the fact that the study was limited to a single institution. Acknowledgments Thanks to Susan E Kosisky, chief microbiologist at the US Army Centralized Allergen Extract Lab, for providing pollen count data for analysis. Matthew Wilson, MD William Frohna, MD Graham Trent, BS Diane Sauter, MD Washington Hospital Center Washington, DC [email protected] References [1] Cicardi M, Zingale LC, Bergamaschini L, Agostoni A. Angioedema associated with angiotensin-converting enzyme inhibitor use: outcome after switching to a different treatment. Arch Intern Med. 2004;164:910e913. [2] Malde B, Regalado J, Greenberger PA. Investigation of angioedema associated with the use of angiotensin converting enzyme inhibitors and angiotensin receptor blockers. Ann Allergy Asthma Immunol. 2007;98:57e63. [3] Peltekis G, Palaskas D, Samanidou M, et al. Severe migratory angioedema due to ACE inhibitors use. Hippokratia. 2009;13:122e124. [4] Dandona P, Dhindsa S, Ghanim H, et al. Angiotensin II and inflammation: the effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockade. J Hum Hypertens. 2007;21:20e27. [5] Bas M, Adams V, Suvorava T, et al. Nonallergic angioedema: role of bradykinin. Allergy. 2007;62:842e856. [6] Agostoni A, Cicardi M, Cugno LC, et al. Angioedema due to angiotensinconverting enzyme inhibitors. Immunopharmacology. 1999;44:21e25. [7] Seidman MD, Lewandowski CA, Sarpa JR, et al. Angioedema related to angiotensinconverting enzyme inhibitors. Otolaryngol Head Neck Surg. 1990;102:727e731. [8] Austin CE, Dear JW, Neighbour H, et al. The contribution of histamine to the action of bradykinin in the human nasal airway. Immunopharmacology. 1996; 34:181e189. [9] Ishizaka T, Iwata M, Ishizaka K. Release of histamine and arachidonate from mouse mast cells induced by glycosylation-enhancing factor and bradykinin. J Immumol. 1985;134:1880e1887.
Urinary triclosan levels and recent asthma exacerbations Triclosan is a broad-spectrum antimicrobial chemical with endocrine and immune effects.1,2 The primary source of exposure is considered personal care products (eg, toothpaste and hand soap), but multiple potential sources and routes of exposure exist.2 Because the airway microbiome may be important in the development or maintenance of asthma,3,4 we hypothesized that levels Disclosures: Authors have nothing to disclose. Funding: This work was supported by a grant from the American Academy of Allergy, Asthma and Immunology and Food Allergy Research and Education (Dr Savage).
of the antimicrobial chemical triclosan may be associated with asthma prevalence and control. We previously demonstrated in a cross-sectional study a significantly increased risk of aeroallergen and food sensitization with increasing urinary triclosan levels in US children. Triclosan levels were positively associated with the risk of atopic asthma, although the association did not reach statistical significance.5 A cross-sectional Norwegian study also found that triclosan was associated with aeroallergen sensitization and rhinitis but not with asthma.6 In a mouse model of asthma, triclosan increased bronchial hyperresponsiveness, total IgE, pulmonary eosinophilia, and interleukin 13.1 Given these
