Nina Lind

Traffic-Related Air Pollution and Dementia Incidence in Northern Sweden: A Longitudinal Study

Background Exposure to ambient air pollution is suspected to cause cognitive effects, but a prospective cohort is needed to study exposure to air pollution at the home address and the incidence of dementia. Objectives We aimed to assess the association between long-term exposure to traffic-related air pollution and dementia incidence in a major city in northern Sweden. Methods Data on dementia incidence over a 15-year period were obtained from the longitudinal Betula study. Traffic air pollution exposure was assessed using a land-use regression model with a spatial resolution of 50 m × 50 m. Annual mean nitrogen oxide levels at the residential address of the participants at baseline (the start of follow-up) were used as markers for long-term exposure to air pollution. Results Out of 1,806 participants at baseline, 191 were diagnosed with Alzheimer’s disease during follow-up, and 111 were diagnosed with vascular dementia. Participants in the group with the highest exposure were more likely than those in the group with the lowest exposure to be diagnosed with dementia (Alzheimer’s disease or vascular dementia), with a hazard ratio (HR) of 1.43 (95% CI: 0.998, 2.05 for the highest vs. the lowest quartile). The estimates were similar for Alzheimer’s disease (HR 1.38) and vascular dementia (HR 1.47). The HR for dementia associated with the third quartile versus the lowest quartile was 1.48 (95% CI: 1.03, 2.11). A subanalysis that excluded a younger sample that had been retested after only 5 years of follow-up suggested stronger associations with exposure than were present in the full cohort (HR = 1.71; 95% CI: 1.08, 2.73 for the highest vs. the lowest quartile). Conclusions If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer’s disease. Citation Oudin A, Forsberg B, Nordin Adolfsson A, Lind N, Modig L, Nordin M, Nordin S, Adolfsson R, Nilsson LG. 2016. Traffic-related air pollution and dementia incidence in northern Sweden: a longitudinal study. Environ Health Perspect 124:306–312; http://dx.doi.org/10.1289/ehp.1408322

Psychological distress in asthma and allergy: the Västerbotten Environmental Health Study

With the aim to better understand the association between asthma/allergy and psychological distress, it was hypothesized that levels of stress, exhaustion, anxiety, depression, and health worries for environmental pollution would be higher in allergic asthma, allergic rhinitis, and atopic dermatitis than in non-allergic asthma and in referents without asthma or allergy. Taking part in the population-based Västerbotten Environmental Health Study (aged 18–79 years), 76 respondents reported a physician-based diagnosis of allergic asthma, 86 reported non-allergic asthma, 190 reported allergic rhinitis, and 46 reported atopic dermatitis as the only form of asthma/allergy. A group of 2876 respondents without an asthma/allergy diagnosis constituted as referents. The participants responded to the Perceived Stress Scale, the Shirom-Melamed Burnout Questionnaire, the Hospital Anxiety and Depression Scale, and the Environmental Pollution subscale of the Modern Health Worries Scale. Levels of stress, exhaustion, and anxiety were higher in allergic asthma and atopic dermatitis than in non-allergic asthma, allergic rhinitis, and among referents, and there was a strong tendency of such group differences for depression and health worries. The results imply that stress reduction and treatment of negative affect may in certain cases be fruitful interventions in patients with atopy.

Inflammatory Mediator Profiling of n-butanol Exposed Upper Airways in Individuals with Multiple Chemical Sensitivity

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.

Symptom-trigger factors other than allergens in asthma and allergy

Abstract 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 building-related 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.

Human exposure to acrolein: Time-dependence and individual variation in eye irritation

The aim of the study was to examine the time dependence on sensory irritation detection following exposure to threshold levels of acrolein, in humans. The exposures occurred in an exposure chamber and the subjects were breathing fresh air through a mask that covered the nose and mouth. All participants participated in four exposure conditions, of which three consisted of a mixture of acrolein and heptane and one of only heptane. Exposure to acrolein at a concentration half of the TLV-C lead to sensory irritation. The perceived sensory irritation resulted in both increased detectability and sensory irritation after about 6.8min of exposure in 58% of the participants. The study confirm the previously suggested LOAEL of about 0.34mg/m(3) for eye irritation due to acrolein exposure. The sensory irritation was still significant 10min after exposure. These results have implications for risk assessment and limit setting in occupational hygiene.

Coping and Social Support in Asthma and Allergy : The Västerbotten Environmental Health Study

Abstract 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 the 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 asthma/allergy severity 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.

Comorbidity and Multimorbidity of Asthma and Allergy and Intolerance to Chemicals and Certain Buildings

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.

Comorbidity in allergic asthma and allergic rhinitis: functional somatic syndromes.

Abstract 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.

Gene expression profiling in persons with multiple chemical sensitivity before and after a controlled n-butanol exposure session

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.

Is Long-Term Exposure to Air Pollution Associated with Episodic Memory? A Longitudinal Study from Northern Sweden

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.