Allergic rhinitis is a symptomatic disorder of the nose induced after allergen exposure by an IgE-mediated inflammation of the membranes lining the nose. It is a global health problem that causes major illness and disability worldwide. Over 600 million patients from all countries, all ethnic groups and of all ages suffer from allergic rhinitis. It affects social life, sleep, school and work and its economic impact is substantial. Risk factors for allergic rhinitis are well identified. Indoor and outdoor allergens as well as occupational agents cause rhinitis and other allergic diseases. The role of indoor and outdoor pollution is probably very important, but has yet to be fully understood both for the occurrence of the disease and its manifestations.

In 1999, during the Allergic Rhinitis and its Impact on Asthma (ARIA) WHO workshop, the expert panel proposed a new classification for allergic rhinitis which was subdivided into 'intermittent' or 'persistent' disease.

This classification is now validated. The diagnosis of allergic rhinitis is often quite easy, but in some cases it may cause problems and many patients are still under-diagnosed, often because they do not perceive the symptoms of rhinitis as a disease impairing their social life, school and work.

The management of allergic rhinitis is well established and the ARIA expert panel based its recommendations on evidence using an extensive review of the literature available up to December 1999. The statements of evidence for the development of these guidelines followed WHO rules and were based on those of Shekelle et al. A large number of papers have been published since 2000 and are extensively reviewed in the 2008 Update using the same evidence-based system. Recommendations for the management of allergic rhinitis are similar in both the ARIA workshop report and the 2008 Update. In the future, the GRADE approach will be used, but is not yet available.

Another important aspect of the ARIA guidelines was to consider co-morbidities. Both allergic rhinitis and asthma are systemic inflammatory conditions and often co-exist in the same patients. In the 2008 Update, these links have been confirmed.

The ARIA document is not intended to be a standard-of-care document for individual countries. It is provided as a basis for physicians, health care professionals and organizations involved in the treatment of allergic rhinitis and asthma in various countries to facilitate the development of relevant local standard-of-care documents for patients.

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Allergic rhinitis and its impact on asthma (ARIA) 2008 update (in collaboration with the World Health Organization, GA(2)LEN and AllerGen)

Background: Allergic rhinitis represents a global health problem affecting 10% to 20% of the population. The Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines have been widely used to treat the approximately 500 million affected patients globally. Objective: To develop explicit, unambiguous, and transparent clinical recommendations systematically for treatment of allergic rhinitis on the basis of current best evidence. Methods: The authors updated ARIA clinical recommendations in collaboration with Global Allergy and Asthma European Network following the approach suggested by the Grading of Recommendations Assessment, Development and Evaluation working group. Results: This article presents recommendations about the prevention of allergic diseases, the use of oral and topical medications, allergen specific immunotherapy, and complementary treatments in patients with allergic rhinitis as well as patients with both allergic rhinitis and asthma. The guideline panel developed evidence profiles for each recommendation and considered health benefits and harms, burden, patient preferences, and resource use, when appropriate, to formulate recommendations for patients, clinicians, and other health care professionals. Conclusion: These are the most recent and currently the most systematically and transparently developed recommendations about the treatment of allergic rhinitis in adults and children. Patients, clinicians, and policy makers are encouraged to use these recommendations in their daily practice and to support their decisions.

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Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines: 2010 Revision

These parameters were developed by the Joint Task Force on Practice Parameters, representing the American Academy of Allergy, Asthma & Immunology; the American College of Allergy, Asthma and Immunology; and the Joint Council of Allergy, Asthma and Immunology. The American Academy of Allergy, Asthma & Immunology (AAAAI) and the American College of Allergy, Asthma and Immunology (ACAAI) have jointly accepted responsibility for establishing "The diagnosis and Management of Rhinitis: An Updated Practice Parameter." This is a complete and comprehensive document at the current time. The medical environment is a changing environment, and not all recommendations will be appropriate for all patients. Because this document incorporated the efforts of many participants, no single individual, including those who served on the Joint Task Force, is authorized to provide an official AAAAI or ACAAI interpretation of these practice parameters. Any request for information about or an interpretation of these practice parameters by the AAAAI or ACAAI should be directed to the Executive Offices of the AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and Immunology. These parameters are not designed for use by pharmaceutical companies in drug promotion.

The diagnosis and management of rhinitis: An updated practice parameter

Note: This article was originally published with an incorrect version of the Acknowledgments, which appeared on p. 218 of the print version. The correct version of the Acknowledgments appeared on pp. 1–2. The corrected article is available below.

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Human Health Risk Assessment for Aluminium, Aluminium Oxide, and Aluminium Hydroxide

The diesters of 1,2-benzenedicarboxylic acid (phthalic acid), commonly known as phthalates, are a group of man-made chemicals with a wide spectrum of industrial applications (fig 1, table 1). High molecular weight phthalates (for example, di(2-ethylhexyl) phthalate [DEHP], di-isononyl phthalate [DiNP], di-n-octyl phthalate [DnOP]), are primarily used as plasticizers in the manufacture of flexible vinyl which, in turn, is used in consumer products, flooring and wall coverings, food contact applications, and medical devices.1–3 Manufacturers use low molecular weight phthalates (for example, diethyl phthalate [DEP] and dibutyl phthalate [DBP]) in personal-care products (for example, perfumes, lotions, cosmetics), as solvents and plasticizers for cellulose acetate, and in making lacquers, varnishes, and coatings, including those used to provide timed releases in some pharmaceuticals.3–5

View this table:

 Table 1 
 Potential sources of exposure and health effects of selected phthalates





 Figure 1 
 Generic chemical structure of phthalates diesters and phthalate monoester metabolites. R is an alkyl and/or aryl group: CH3 (dimethyl phthalate), CH2CH3 (diethyl phthalate), CH2CH2CH2CH3 (dibutyl phthalate), CH2CH(CH2CH3)CH2CH2CH2CH3 (di[2-ethylhexyl) phthalate), CH2CH2CH2CH3 and CH2C6H5 (butylbenzyl phthalate).



In this paper, we review the uses and metabolism of phthalates, and the studies on health effects of phthalates in human populations published between 1973 and June 2005. The references included in this review were searched using the Web of Science database which provides interactive citation and literature searching of the Institute for Scientific Information’s Science Citation Index Expanded. The database contains data from more than 5000 scientific journals and covers the period from 1980 to present. We also searched the bibliography cited in the selected references for additional relevant citations.

Because phthalates are widely used in …

https://oem.bmj.com/content/oemed/62/11/806.full.pdf

Phthalates and human health

Objective: To estimate the occurrence of hand eczema in hairdressers in Sweden. Methods: The occurrence of hand eczema was estimated in a Swedish longitudinal retrospective cohort study including all female graduates from vocational schools for hairdressers from 1970 to 1995. A stratified sample from the general population acted as controls. A self-administered questionnaire including questions on the occurrence of hand eczema, skin atopy, working periods and number of hair treatments performed per week was sent to the participants. Incidence rate ratios (IRRs) of hand eczema were estimated. Results: The incidence rate of hand eczema in hairdressers was 23.8 cases/1000 person-years, whereas in hairdressers who were aged Conclusion: Hairdressers are highly exposed to skin-damaging substances. The self-reported incidence of hand eczema was substantially higher in female hairdressers than in controls from the general population and than that found previously in register-based studies. For many individuals, onset of hand eczema occurs early in life. Only about 10% of the hand eczema cases among hairdressers would be prevented if no one with skin atopy entered the trade.

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Incidence of hand eczema in female Swedish hairdressers

Background: Exposure to diesel exhaust causes inflammatory responses. Previous controlled exposure studies at a concentration of 300 μg/m 3 of diesel exhaust particles mainly lasted for 1 h. We prolonged the exposure period and investigated how quickly diesel exhaust can induce respiratory and systemic effects. Methods: Eighteen healthy volunteers were exposed twice to diluted diesel exhaust (PM1 ~300 μg/m 3 ) and twice to filtered air (PM1 ~2 μg/m 3 ) for 3 h, seated, in a chamber with a double-blind set-up. Immediately before and after exposure, we performed a medical examination, spirometry, rhinometry, nasal lavage and blood sampling. Nasal lavage and blood samples were collected again 20 h post-exposure. Symptom scores and peak expiratory flow (PEF) were assessed before exposure, and at 15, 75, and 135 min of exposure. Results: Self-rated throat irritation was higher during diesel exhaust than filtered air exposure. Clinical signs of irritation in the upper airways were also significantly more common after diesel exhaust exposure (odds ratio=3.2, p<0.01). PEF increased during filtered air, but decreased during diesel exhaust exposure, with a statistically significant difference at 75 min (+4 L/min vs. -10 L/min, p=0.005). Monocyte and total leukocyte counts in peripheral blood were higher after exposure to diesel exhaust than filtered air 20 h post-exposure, and a trend (p=0.07) towards increased serum IL-6 concentrations was also observed 20 h post-exposure. Conclusions: Diesel exhaust induced acute adverse effects such as symptoms and signs of irritation, decreased PEF, inflammatory markers in healthy volunteers. The effects were first seen at 75 min of exposure.

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Effects of diesel exposure on lung function and inflammation biomarkers from airway and peripheral blood of healthy volunteers in a chamber study

￻￻ Objective: To investigate the risk of asthma in hairdressers. Methods: The incidence of asthma was retrospectively estimated in a Swedish nationwide study including all female hairdressers certified from vocational schools from 1970 to 1995, and a stratified sample of women from the general population were referents. A postal questionnaire included questions on respiratory tract symptoms, atopy, smoking, working periods as a hairdresser, and number of specific hair treatments performed/week. Reported exposures were validated by occupational hygienists. Rate ratios of incidence (IRRs) of asthma were estimated by Poisson regression, adjusted for calendar year of observation, hay fever, smoking, and region of domicile. Results: The crude incidences of asthma/1000 person-years were: 3.9 during active years as a hairdresser, 2.8 among the hairdressers when not working in the profession, and 3.1 among the referents. The corresponding IRR for being an active hairdresser compared with the referents was 1.3 (95% confidence interval (95% CI) 1.0 to 1.6). Moderate effects on risk of asthma were found both from hairdressing work (IRR=1.6 (1.1 to 2.2) among never-smokers) and from smoking (IRR=1.6 (1.2 to 2.2) among referents). However, the combined effect from hairdressing work and smoking (IRR=1.5 (1.0 to 2.1)) was less than expected (p=0.02). No effect modification by respiratory atopy was found. The hairdressers most often performing hair bleaching treatments (IRR=1.5 (0.7 to 3.0)) or using hair spray (IRR=1.4 (0.8 to 2.4)) had, compared with the most infrequent users, a slightly, but not significantly higher incidence of asthma. Exposure to persulphates in hair bleach was estimated to be 0.04‐0.15 3 during mixing of the powder. Reported average number of bleaching treatments agreed well with those performed according to a diary. Conclusions: Active hairdressing work was associated with a moderately increased incidence of asthma among lifelong non-smokers. The results are moderately supportive, but not conclusive, of associations between asthma and exposure to hair bleach or hair spray.

https://oem.bmj.com/content/oemed/59/2/119.full.pdf

Incidence of asthma in female Swedish hairdressers

Out of 118 workers exposed to phthalic anhydride (PA) dust for 2 months or more in four plants producing alkyd and/or polyunsaturated polyester resins, 28 (24%) suffered from work-related rhinitis, 13 (11 %) from chronic productive bronchitis, and 21 (28%) from work-associated asthma. Asthma was generally preceded by rhinitis and was mostly of late type. 3 out of 11 asthmatics had a PA-positive skin test. In 2 subjects the presence of antibodies was demonstrated by the Prausnitz-Kustner test. 4 out of 25 heavily exposed subjects without asthma had a nonspecific bronchial hyperreactivity. The results did not indicate any significant ‘healthy worker selection’ as regarding rhinits and asthma. Chronic productive bronchitis was common and was more prevalent among former workers than among present employees, indicating a selection of nonreacting subjects in the plant. The time-weighted average breathing zone PA levels in two plants were between 3 and 13 mg/m3 during different direct PA handling operations and less than 0.3 mg/m3 at other kinds of work. In 2 subjects, positive bronchial provocation was obtained by short-term exposure to 0.5 and 6 mg PA/m3, respectively.

Phthalic anhydride-induced occupational asthma.

Assessment of environmental tobacco smoke exposure in children with asthmatic symptoms by questionnaire and cotinine concentrations in plasma, saliva, and urine

Jörn Nielsen

Papers

Incidence of hand eczema in female Swedish hairdressers

Effects of diesel exposure on lung function and inflammation biomarkers from airway and peripheral blood of healthy volunteers in a chamber study

Incidence of asthma in female Swedish hairdressers

Phthalic anhydride-induced occupational asthma.

Assessment of environmental tobacco smoke exposure in children with asthmatic symptoms by questionnaire and cotinine concentrations in plasma, saliva, and urine