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Objectives: We tested the hypothesis of high comorbidity between asthma/allergy and chemical intolerance (CI) and between asthma/allergy and building intolerance (BI), and high multimorbidity between asthma/allergy, CI, and BI.

Methods: Population-based questionnaire data were used from 530 participants with asthma/allergy (allergic asthma, nonallergic asthma, allergic rhinitis, and/or atopic dermatitis), 414 with self-reported and 112 with physician-diagnosed CI, and 165 with self-reported and 47 with physician-diagnosed BI. Separate reference groups were formed for each of the five case groups.

Results: Adjusted odds ratios varied from 4.6 to 13.1 for comorbidity, and from 6.6 to 46.4 for multimorbidity.

Conclusion: The large comorbidity and multimorbidity between asthma/allergy, CI, and BI evokes the question as to whether there are similarities in underlying mechanisms between these conditions.

Based on the concept of central sensitisation, the present study tested the hypothesis of comorbidity in allergic asthma and allergic rhinitis with diagnoses of functional somatic syndromes (FSSs), including fibromyalgia, irritable bowel syndrome and migraine. Data were used from the population-based Västerbotten Environmental Health Study (n = 3406). The participants consisted of 164 individuals with allergic asthma and 298 individuals with allergic rhinitis as well as 2876 individuals without allergic or non-allergic asthma, allergic rhinitis or atopic dermatitis. Diagnoses were based on self-reports of having been diagnosed by a physician. Odds ratios (ORs) were calculated from binary logistic regression analysis, both crude and adjusted for age and education. The adjusted ORs (1.87–4.00) for all FSSs differed significantly from unity for both allergic asthma and rhinitis. The results provide support for the hypothesis of comorbidity in allergic asthma and rhinitis with FSSs. Since central sensitisation is likely to underlie FSSs, the present findings raises the question as to whether central sensitisation may also be involved in allergic asthma and rhinitis.

Objectives: To investigate the pathophysiological pathways leading to symptoms elicitation in multiple chemical sensitivity (MCS) by comparing gene expression in MCS participants and healthy controls before and after a chemical exposure optimised to cause symptoms among MCS participants. The first hypothesis was that unexposed and symptom=-free MCS participants have similar gene expression patterns to controls and a second hypothesis that MCS participants can be separated from controls based on differential gene expression upon a controlled n=-butanol exposure.

Design: Participants were exposed to 3.7 ppm n-butanol while seated in a windowed exposure chamber for 60 min. A total of 26 genes involved in biochemical pathways found in the literature have been proposed to play a role in the pathogenesis of MCS and other functional somatic syndromes were selected. Expression levels were compared between MCS and controls before, within 15 min after being exposed to and 4 hours after the exposure.

Settings: Participants suffering from MCS and healthy controls were recruited through advertisement at public places and in a local newspaper.

Participants: 36 participants who considered themselves sensitive were prescreened for eligibility. 18 sensitive persons fulfilling the criteria for MCS were enrolled together with 18 healthy controls.

Outcome measures: 17 genes showed sufficient transcriptional level for analysis. Group comparisons were conducted for each gene at the 3 times points and for the computed area under the curve (AUC) expression levels.

Results: MCS participants and controls displayed similar gene expression levels both at baseline and after the exposure and the computed AUC values were likewise comparable between the 2 groups. The intragroup variation in expression levels among MCS participants was noticeably greater than the controls.

Conclusions: MCS participants and controls have similar gene expression levels at baseline and it was not possible to separate MCS participants from controls based on gene expression measured after the exposure.

Associations between long-term exposure to ambient air pollution and cognitive function have been observed in a few longitudinal studies. Our aim was to investigate the association between long-term exposure to air pollution and episodic memory, a marker of early cognitive decline. We used data from the Betula study in Northern Sweden, and included participants 60 to 85 of age at inclusion, 1,469 persons in total. The participants were followed for up to 22 years, five years apart between 1988 and 2010. A composite of five tasks was used as a measure of episodic memory measure (EMM), and the five-year change in EMM score (ΔEMM) was calculated such that a participant could contribute with up to four measurement pairs. A Land Use Regression Model was used to estimate cumulative annual mean of NOx at the residential address of the participants (a marker for long-term exposure to traffic-related air pollution). There did not seem to be any association between exposure to traffic air pollution and episodic memory change, with a ΔEMM estimate of per 1 µg/m3 increase in NOx of 0.01 (95% Confidence Interval: -0.02,0.03). This is in contrast to a growing body of evidence suggesting associations between air pollution and cognitive function.

Purpose: Multiple chemical sensitivity (MCS) is a prevalent medically unexplained symptom characterized by symptom reactions to everyday chemical exposure below hygienic thresholds. The aim of this study was to investigate the expressions of hyper-reactivity in MCS during whole-body exposure to low concentrations of the odorant n-butanol.

Methods: We exposed 18 participants with MCS and 18 non-ill controls to a low concentration of the odorantn-butanol using an exposure chamber. The first 10 min constituted blank exposure, after which then-butanol concentration increased and reached a plateau at 11.5 mg/m3.

Results: MCS participants, compared with controls, reported greater perceived odor intensities, more unpleasantness to the exposure and increasing symptoms over time. MCS participants also expressed higher pulse rate and lower pulse rate variability than controls did. No group differences were found for breathing rate or tonic electrodermal activity responses.

Conclusions: We conclude that MCS sufferers differ from healthy controls in terms of autonomic responses, symptoms and chemosensory perception during chemical exposure.

Several environmental exposures of particular relevance for indoor air quality, such as exposure to odorants, may be associated with asthma and allergy. The aim of this study was to investigate attribution of symptoms and behavioral disruptions to various chemical and physical environmental sources in persons with self-reported asthma and allergy. Data from a population-based study, the Västerbotten Environmental Health Study, were used to compare persons with asthma, allergic rhinitis, allergic dermatitis, multiple diagnoses of asthma/allergy and no asthma or allergy. Persons with asthma and multiple diagnoses reported odorous/pungent and buildingrelated environmental factors to trigger symptoms to a larger extent than did the reference group, mainly due to perfume and odors from flowers. They also reported behavioral disruptions and affective reactions to odorous/ pungent environments. These findings increase the understanding of the role of odorants in symptom development and thereby the prevention of health problems in asthma and allergy in indoor air.

Asthma and allergies are some of the most common illnesses worldwide that almost everybody will come in contact with. This thesis studied persons with allergic asthma, non-allergic asthma, allergic rhinitis and atopic dermatitis in a population-based sample. At an early stage, these illnesses were regarded as psychosomatic. Over time, as knowledge about asthma/allergy has increased more of a biomedical perspective was taken by the research field. In considering early documentations well as contemporary research, a psychobiosocial perspective was taken in this thesis when conducting the three studies. Thus, as psychological factors may affect the illness and be a result of the illness, it is important to incorporate these factors to better understand asthma and allergy. Study I examined the co- and multimorbidity in asthma/allergy with the environmental intolerances in the form of chemical and building-related intolerance. Study II investigated psychological distress in the four forms of asthma and allergy. Psychological distress was in this study defined as stress, burnout, anxiety, depression and environmental health worries. Study III examined usage of problem and emotion focused coping strategies and perceived social support from the surrounding in high and low asthma/allergy severity. All studies were performed using data from the Västerbotten Environmental Health Study, a questionnaire-based survey with focus on various environmental hypersensitivities and asthma and allergy. The result showed that the co- and multimorbidity with the environmental intolerances in asthma/allergy was larger than what was statistically excepted. Those with allergic asthma and atopic dermatitis experienced more stress, burnout and anxiety than those with non-allergic asthma, allergic rhinitis and non-asthma/allergy. Moreover, the most common way of coping with asthma and allergy was found to be strategies such as avoiding environments that are believed to affect health, and trying to accept the situation, independent of asthma/allergy severity. Finally, in general, those with asthma and allergy reported receiving most support from their partner, other family members and health care, and least support was perceived by those with low asthma/allergy severity.The findings suggest that co- and multimorbidity with environmental intolerances is relatively common in asthma and allergy, and should therefore be included in the clinical anamnesis for this patient group. The elevated level of distress in allergic asthma and atopic dermatitis evokes the question of use of therapies such as mindfulness maybe beneficial in certain afflicted persons. The results on coping and social support provide a foundation for further research regarding informing the asthma/allergy patient and family members about effective coping strategies and the importance of adequate social support. A metaperspective is taken in which interrelations between important variables in the thesis are discussed.

Objectives: Asthma and allergy are stressful conditions that require coping strategies and social support to reduce stress and enhance health-promoting behavior. However, research is limited regarding coping and social support in asthma and allergy. The aim was to better understand use of different coping strategies and perceived social support in low and high severity (exacerbation frequency) of asthma and allergy. Methods: Population-based data were used to provide ratings of coping strategies (Study I) and social support (Study II) from 124 and 94 participants, respectively, with asthma and/or allergy, categorized as low or high in severity. Problem- and emotion-focused coping strategies were assessed as well as emotional, instrumental and informative social support from seven sources. Results: Study I showed that avoiding certain environments (problem-based coping) and trying to accept one’s situation (emotion-based) were the most commonly used coping strategies. These behaviors did not differ due to severity. Study II showed that more emotional than instrumental and informative support was perceived. The highest rated support sources were the partner, family members, and the healthcare system. More social support was reported in low compared to high asthma/allergy severity. Conclusion: The most commonly used coping strategies in the population of persons with these four types of asthma and allergy are avoiding certain environments and trying to accept one’s situation. More emotional support than instrumental and informative is perceived to be received, and most of the support is received from one’s partner and other family members, and least from authorities and patient associations/support groups.

Background Multiple Chemical Sensitivity (MCS) is a chronic condition characterized by reports of recurrent symptoms in response to low level exposure to various chemical substances. Recent findings suggests that dysregulation of the immune system may play a role in MCS pathophysiology. Objectives The aim of this study was to examine baseline and low dose n-butanol-induced upper airway inflammatory response profiles in MCS subjects versus healthy controls. Method Eighteen participants with MCS and 18 age- and sex-matched healthy controls were enrolled in the study. Epithelial lining fluid was collected from the nasal cavity at three time points: baseline, within 15 minutes after being exposed to 3.7 ppm n-butanol in an exposure chamber and four hours after exposure termination. A total of 19 cytokines and chemokines were quantified. Furthermore, at baseline and during the exposure session, participants rated the perceived intensity, valence and levels of symptoms and autonomic recordings were obtained. Results The physiological and psychophysical measurements during the n-butanol exposure session verified a specific response in MCS individuals only. However, MCS subjects and healthy controls displayed similar upper airway inflammatory mediator profiles (P>0.05) at baseline. Likewise, direct comparison of mediator levels in the MCS group and controls after n-butanol exposure revealed no significant group differences. Conclusion We demonstrate no abnormal upper airway inflammatory mediator levels in MCS subjects before or after a symptom-eliciting exposure to low dose n-butanol, implying that upper airways of MCS subjects are functionally intact at the level of cytokine and chemokine production and secretory capacity. This suggests that previous findings of increased cytokine plasma levels in MCS are unlikely to be caused by systemic priming via excessive upper airway inflammatory processes.