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BETA
Forsberg, Bertil
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Publications (10 of 257) Show all publications
Accordini, S., Calciano, L., Johannessen, A., Portas, L., Benediktsdóttir, B., Bertelsen, R. J., . . . Svanes, C. (2018). A three-generation study on the association of tobacco smoking with asthma. International Journal of Epidemiology, 47(4), 1106-1117
Open this publication in new window or tab >>A three-generation study on the association of tobacco smoking with asthma
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2018 (English)In: International Journal of Epidemiology, ISSN 0300-5771, E-ISSN 1464-3685, Vol. 47, no 4, p. 1106-1117Article in journal (Refereed) Published
Abstract [en]

Background: Mothers' smoking during pregnancy increases asthma risk in their offspring. There is some evidence that grandmothers' smoking may have a similar effect, and biological plausibility that fathers' smoking during adolescence may influence offspring's health through transmittable epigenetic changes in sperm precursor cells. We evaluated the three-generation associations of tobacco smoking with asthma.

Methods: Between 2010 and 2013, at the European Community Respiratory Health Survey III clinical interview, 2233 mothers and 1964 fathers from 26 centres reported whether their offspring (aged ≤51 years) had ever had asthma and whether it had coexisted with nasal allergies or not. Mothers and fathers also provided information on their parents' (grandparents) and their own asthma, education and smoking history. Multilevel mediation models within a multicentre three-generation framework were fitted separately within the maternal (4666 offspring) and paternal (4192 offspring) lines.

Results: Fathers' smoking before they were 15 [relative risk ratio (RRR) = 1.43, 95% confidence interval (CI): 1.01-2.01] and mothers' smoking during pregnancy (RRR = 1.27, 95% CI: 1.01-1.59) were associated with asthma without nasal allergies in their offspring. Grandmothers' smoking during pregnancy was associated with asthma in their daughters [odds ratio (OR) = 1.55, 95% CI: 1.17-2.06] and with asthma with nasal allergies in their grandchildren within the maternal line (RRR = 1.25, 95% CI: 1.02-1.55).

Conclusions: Fathers' smoking during early adolescence and grandmothers' and mothers' smoking during pregnancy may independently increase asthma risk in offspring. Thus, risk factors for asthma should be sought in both parents and before conception.

Place, publisher, year, edition, pages
Oxford University Press, 2018
Keywords
asthma, mothers’ smoking during pregnancy, grandmothers’ smoking during pregnancy, fathers’ smoking during puberty, multilevel mediation model, Ageing Lungs in European Cohorts (ALEC) Study
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-145740 (URN)10.1093/ije/dyy031 (DOI)000444559900020 ()29534228 (PubMedID)
Funder
EU, Horizon 2020, GA-633212
Available from: 2018-03-16 Created: 2018-03-16 Last updated: 2018-10-05Bibliographically approved
Nagel, G., Stafoggia, M., Pedersen, M., Andersen, Z. J., Galassi, C., Munkenast, J., . . . Weinmayr, G. (2018). Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE). International Journal of Cancer, 143(7), 1632-1643
Open this publication in new window or tab >>Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE)
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2018 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 143, no 7, p. 1632-1643Article in journal (Refereed) Published
Abstract [en]

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancersof the stomach and upper aerodigestive tract (UADT). We investigated the association of long-term exposure to ambient airpollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land-useregression models for particulate matter (PM) below 10mm (PM10), below 2.5mm (PM2.5), between 2.5 and 10mm (PMcoarse),PM2.5absorbance and nitrogen oxides (NO2and NOX) as well as approximated by traffic indicators. Cox regression modelswith adjustment for potential confounders were used for cohort-specific analyses. Combined estimates were determined withrandom effects meta-analyses. During average follow-up of 14.1 years of 305,551 individuals, 744 incident cases of gastriccancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5mg/m3of PM2.5was 1.38 (95% CI 0.99; 1.92)for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures consid-ered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influencemarkedly the effect estimate for PM2.5and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5wasfound in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study showsan association between long-term exposure to PM2.5and gastric cancer, but not UADT cancers, suggesting that air pollutionmay contribute to gastric cancer risk.

Place, publisher, year, edition, pages
John Wiley & Sons, 2018
Keywords
ESCAPE, air pollution, epidemiology, gastric cancer, upper aerodigestive tract cancer
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-147272 (URN)10.1002/ijc.31564 (DOI)000443392100009 ()29696642 (PubMedID)
Available from: 2018-05-02 Created: 2018-05-02 Last updated: 2018-11-05Bibliographically approved
Raza, W., Forsberg, B., Johansson, C. & Nilsson Sommar, J. (2018). Air pollution as a risk factor in health impact assessments of a travel mode shift towards cycling. Global Health Action, 11(1), Article ID 1429081.
Open this publication in new window or tab >>Air pollution as a risk factor in health impact assessments of a travel mode shift towards cycling
2018 (English)In: Global Health Action, ISSN 1654-9716, E-ISSN 1654-9880, Vol. 11, no 1, article id 1429081Article, review/survey (Refereed) Published
Abstract [en]

BACKGROUND: Promotion of active commuting provides substantial health and environmental benefits by influencing air pollution, physical activity, accidents, and noise. However, studies evaluating intervention and policies on a mode shift from motorized transport to cycling have estimated health impacts with varying validity and precision.

OBJECTIVE: To review and discuss the estimation of air pollution exposure and its impacts in health impact assessment studies of a shift in transport from cars to bicycles in order to guide future assessments.

METHODS: A systematic database search of PubMed was done primarily for articles published from January 2000 to May 2016 according to PRISMA guidelines.

RESULTS: We identified 18 studies of health impact assessment of change in transport mode. Most studies investigated future hypothetical scenarios of increased cycling. The impact on the general population was estimated using a comparative risk assessment approach in the majority of these studies, whereas some used previously published cost estimates. Air pollution exposure during cycling was estimated based on the ventilation rate, the pollutant concentration, and the trip duration. Most studies employed exposure-response functions from studies comparing background levels of fine particles between cities to estimate the health impacts of local traffic emissions. The effect of air pollution associated with increased cycling contributed small health benefits for the general population, and also only slightly increased risks associated with fine particle exposure among those who shifted to cycling. However, studies calculating health impacts based on exposure-response functions for ozone, black carbon or nitrogen oxides found larger effects attributed to changes in air pollution exposure.

CONCLUSION: A large discrepancy between studies was observed due to different health impact assessment approaches, different assumptions for calculation of inhaled dose and different selection of dose-response functions. This kind of assessments would improve from more holistic approaches using more specific exposure-response functions.

Place, publisher, year, edition, pages
Taylor & Francis, 2018
Keywords
Active commuting, mode shift, emission factors, population exposure, commuters’ exposure, exposure response function, comparative risk assessment
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-144660 (URN)10.1080/16549716.2018.1429081 (DOI)000424246900001 ()29400262 (PubMedID)
Available from: 2018-02-09 Created: 2018-02-09 Last updated: 2018-06-09Bibliographically approved
Burte, E., Leynaert, B., Bono, R., Brunekreef, B., Bousquet, J., Carsin, A.-E., . . . Jacquemin, B. (2018). Association between air pollution and rhinitis incidence in two European cohorts. Environment International, 115, 257-266
Open this publication in new window or tab >>Association between air pollution and rhinitis incidence in two European cohorts
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2018 (English)In: Environment International, ISSN 0160-4120, E-ISSN 1873-6750, Vol. 115, p. 257-266Article in journal (Refereed) Published
Abstract [en]

The association between air pollution and rhinitis is not well established.

Aim: The aim of this longitudinal analysis was to study the association between modeled air pollution at the subjects' home addresses and self-reported incidence of rhinitis.

Methods: We used data from 1533 adults from two multicentre cohorts' studies (EGEA and ECRHS). Rhinitis incidence was defined as reporting rhinitis at the second follow-up (2011 to 2013) but not at the first follow-up (2000 to 2007). Annual exposure to NO2, PM10 and PM2.5 at the participants' home addresses was estimated using land-use regression models developed by the ESCAPE project for the 2009-2010 period. Incidence rate ratios (IRR) were computed using Poisson regression. Pooled analysis, analyses by city and meta-regression testing for heterogeneity were carried out.

Results: No association between long-term air pollution exposure and incidence of rhinitis was found (adjusted IRR (aIRR) for an increase of 10 mu g center dot m(-3) of NO2: 1.00 [0.91-1.09], for an increase of 5 mu g center dot m(-3) of PM2.5: 0.88 [0.73-1.04]). Similar results were found in the two-pollutant model (aIRR for an increase of 10 mu g center dot m(-3) of NO2: 1.01 [0.87-1.17], for an increase of 5 mu g center dot m(-3) of PM2.5: 0.87 [0.68-1.08]). Results differed depending on the city, but no regional pattern emerged for any of the pollutants.

Conclusions: This study did not find any consistent evidence of an association between long-term air pollution and incident rhinitis.

Place, publisher, year, edition, pages
Elsevier, 2018
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-146297 (URN)10.1016/j.envint.2018.03.021 (DOI)000432523500028 ()29605678 (PubMedID)
Available from: 2018-04-04 Created: 2018-04-04 Last updated: 2018-06-27Bibliographically approved
Oudin, A., Segersson, D., Adolfsson, R. & Forsberg, B. (2018). Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden. PLoS ONE, 13(6), Article ID e0198283.
Open this publication in new window or tab >>Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden
2018 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 6, article id e0198283Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: There is highly suggestive evidence for an effect of air pollution exposure on dementia-related outcomes, but evidence is not yet present to clearly pinpoint which pollutants are the probable causal agents. The aims of this study was to assess the longitudinal association between exposures of fine ambient particulate matter (PM2.5) from residential wood burning, and vehicle exhaust, with dementia.

METHOD: We used data from the Betula study, a longitudinal study of dementia in Umeå, Northern Sweden. The study size was 1 806 and the participants were followed from study entry (1993-1995) to 2010. Modelled levels of source-specific fine particulate matter at the residential address were combined with information on wood stoves or wood boilers, and with validated data on dementia diagnosis and individual-level characteristics from the Betula study. Cox proportional hazards models were used to estimate Hazard Ratios (HRs) and their 95% CIs for dementia incidence (vascular dementia and Alzheimer's disease), adjusted for individual-level characteristics.

RESULTS: The emission of PM2.5 from local residential wood burning was associated with dementia incidence with a hazard ratio of 1.55 for a 1 μg/m3 increase in PM2.5 (95% Confidence Interval (CI): 1.00-2.41, p-value 0.05). Study participants with an address in an area with the highest quartile of PM2.5 from residential wood burning and who also had a wood-burning stove were more likely to develop dementia than those in the lower three quartiles without a wood-burning stove with hazard ratios of 1.74 (CI: 1.10-2.75, p-value 0.018). Particulate matter from traffic exhaust seemed to be associated with dementia incidence with hazard ratios of 1.66, (CI: 1.16-2.39), p-value 0.006, and 1.41 (CI: 0.97-2.23), p-value 0.07, in the third and fourth quartiles, respectively.

CONCLUSIONS: If the associations we observed are causal, then air pollution from residential wood burning, and air pollution from traffic, might be independent important risk factors for dementia.

Place, publisher, year, edition, pages
Public Library of Science, 2018
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-149048 (URN)10.1371/journal.pone.0198283 (DOI)29897947 (PubMedID)
Available from: 2018-06-14 Created: 2018-06-14 Last updated: 2018-10-01Bibliographically approved
Mindus, S., Malinovschi, A., Ekerljung, L., Forsberg, B., Gíslason, T., Jõgi, R., . . . Janson, C. (2018). Asthma and COPD overlap (ACO) is related to a high burden of sleep disturbance and respiratory symptoms: results from the RHINE and Swedish GA2LEN surveys. PLoS ONE, 13(4), Article ID e0195055.
Open this publication in new window or tab >>Asthma and COPD overlap (ACO) is related to a high burden of sleep disturbance and respiratory symptoms: results from the RHINE and Swedish GA2LEN surveys
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2018 (English)In: PLoS ONE, ISSN 1932-6203, E-ISSN 1932-6203, Vol. 13, no 4, article id e0195055Article in journal (Refereed) Published
Abstract [en]

Background: The term Asthma and COPD Overlap (ACO) describes a condition where asthma and COPD overlap. We aimed to investigate associations between ACO and insomnia and respiratory symptoms, and to investigate the prevalence of ACO and the characteristics of subjects with ACO in two Northern European population studies.

Methods: The study comprised 25 429 subjects aged ≥ 40 years who participated in one of two Northern European general population surveys. Both surveys included questions on asthma, COPD, respiratory and sleep-related symptoms, including difficulty initiating sleep, difficulty maintaining sleep, early-morning awakening, and excessive daytime sleepiness. ACO was defined as having both self-reported asthma and COPD.

Results: The prevalence of ACO was 1.0%. The group with ACO had a higher prevalence of both insomnia and respiratory symptoms than subjects with only asthma or COPD. Having ACO was independently associated with a 2-3 times higher probability of having sleep-related symptoms as compared with the group without asthma or COPD, after adjustment for age, sex, BMI, smoking history and educational level (adjusted odds ratio 2.14-3.36, 95% CI).

Conclusion: Subjects with ACO have a high prevalence of insomnia and respiratory symptoms. To our knowledge, this is the first study to assess the association between sleep-related symptoms and ACO.

Place, publisher, year, edition, pages
Public Library of Science, 2018
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-146281 (URN)10.1371/journal.pone.0195055 (DOI)000428988800023 ()29608582 (PubMedID)
Available from: 2018-04-03 Created: 2018-04-03 Last updated: 2018-08-06Bibliographically approved
Bråbäck, L., Lowe, A. J., Lodge, C. J., Dharmage, S. C., Olsson, D. & Forsberg, B. (2018). Childhood asthma and smoking exposures before conception - a three-generational cohort study.. Pediatric Allergy and Immunology, 29(4), 361-368
Open this publication in new window or tab >>Childhood asthma and smoking exposures before conception - a three-generational cohort study.
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2018 (English)In: Pediatric Allergy and Immunology, ISSN 0905-6157, E-ISSN 1399-3038, Vol. 29, no 4, p. 361-368Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Some human and animal studies have recently shown that maternal grandmother's smoking during pregnancy increases the risk of asthma in the grandchildren. We have investigated whether sex of the exposed parent and/or grandchild modifies the association between grandmaternal smoking and grandchild asthma.

METHODS: We formed a cohort study based on linkage of national registries with prospectively collected data over three generations. Smoking habits in early pregnancy were registered since 1982 and purchases of prescribed medication since 2005. In all, 10329 children born since 2005 had information on maternal and grandmaternal smoking on both sides and were followed from birth up to 6 years of age. Ages when medication was purchased were used to classify the cohort into never, early transient (0-3 years), early persistent (0-3 and 4-6 years) and late-onset (4-6 years) phenotypes of childhood asthma.

RESULTS: Maternal grandmother's smoking was associated with an increased odds of early persistent asthma after adjustment for maternal smoking and other confounders (odds ratio 1.29, 95% confidence interval 1.10-1.51). Grandchild sex did not modify the association. Paternal grandmother's smoking was not associated with any of the asthma phenotypes.

CONCLUSION: Maternal but not paternal exposure to nicotine before conception was related to an increased risk of early persistent childhood asthma, but not other asthma phenotypes. Our findings are possibly consistent with a sex specific mode of epigenetic transfer. 

Keywords
childhood asthma, grandmother, multigenerational study, pregnancy, tobacco smoke
National Category
Respiratory Medicine and Allergy
Identifiers
urn:nbn:se:umu:diva-145533 (URN)10.1111/pai.12883 (DOI)000434155900004 ()29512835 (PubMedID)
Available from: 2018-03-09 Created: 2018-03-09 Last updated: 2018-07-16Bibliographically approved
Svanes, Ø., Bertelsen, R. J., Lygre, S. H. L., Carsin, A. E., Antó, J. M., Forsberg, B., . . . Svanes, C. (2018). Cleaning at Home and at Work in Relation to Lung Function Decline and Airway Obstruction. American Journal of Respiratory and Critical Care Medicine, 197(9), 1157-1163
Open this publication in new window or tab >>Cleaning at Home and at Work in Relation to Lung Function Decline and Airway Obstruction
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2018 (English)In: American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, E-ISSN 1535-4970, Vol. 197, no 9, p. 1157-1163Article in journal (Refereed) Published
Abstract [en]

Rationale: Cleaning tasks may imply exposure to chemical agents with potential harmful effects to the respiratory system, and increased risk of asthma and respiratory symptoms among professional cleaners and in persons cleaning at home has been reported. Long-term consequences of cleaning agents on respiratory health are, however, not well described.

Objectives: This study aimed to investigate long-term effects of occupational cleaning and cleaning at home on lung function decline and airway obstruction.

Methods: The European Community Respiratory Health Survey (ECRHS) investigated a multicenter population-based cohort at three time points over 20 years. A total of 6,235 participants with at least one lung function measurement from 22 study centers, who in ECRHS II responded to questionnaire modules concerning cleaning activities between ECRHS I and ECRHS II, were included. The data were analyzed with mixed linear models adjusting for potential confounders.

Measurements and Main Results: As compared with women not engaged in cleaning (ΔFEV1 = −18.5 ml/yr), FEV1 declined more rapidly in women responsible for cleaning at home (−22.1; P = 0.01) and occupational cleaners (−22.4; P = 0.03). The same was found for decline in FVC (ΔFVC = −8.8 ml/yr; −13.1, P = 0.02; and −15.9, P = 0.002; respectively). Both cleaning sprays and other cleaning agents were associated with accelerated FEV1 decline (−22.0, P = 0.04; and −22.9, P = 0.004; respectively). Cleaning was not significantly associated with lung function decline in men or with FEV1/FVC decline or airway obstruction.

Conclusions: Women cleaning at home or working as occupational cleaners had accelerated decline in lung function, suggesting that exposures related to cleaning activities may constitute a risk to long-term respiratory health.

Keywords
cleaning, ECRHS, lung function decline, occupational medicine, spirometry, lung diseases
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-145044 (URN)10.1164/rccm.201706-1311OC (DOI)000431196700015 ()29451393 (PubMedID)
Available from: 2018-02-19 Created: 2018-02-19 Last updated: 2018-06-09Bibliographically approved
Garcia-Larsen, V., Thawer, N., Charles, D., Cassidy, A., van Zele, T., Thilsing, T., . . . Burney, P. G. J. (2018). Dietary intake of flavonoids and ventilatory function in European adults: a GA²LEN study. Nutrients, 10(1), Article ID 95.
Open this publication in new window or tab >>Dietary intake of flavonoids and ventilatory function in European adults: a GA²LEN study
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2018 (English)In: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 10, no 1, article id 95Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Flavonoids exert anti-inflammatory properties and modulate oxidative stress in vitro, suggesting a protective effect on lung function, but epidemiological studies examining this association are scarce.

METHODS: A stratified random sample was drawn from the GA²LEN screening survey, in which 55,000 adults aged 15 to 75 answered a questionnaire on respiratory symptoms. Post-bronchodilator spirometry was obtained from 2850 subjects. Forced vital capacity (FVC), the ratio between the forced exhaled volume in 1 second (FEV₁) and FVC (FEV₁/FVC), FVC below lower limit of normal (FVC < LLN), and FEV₁/FVC < LLN were calculated. Intake of the six main subclasses of flavonoids was estimated using the GA²LEN Food Frequency Questionnaire. Adjusted associations between outcomes and each subclass of flavonoids were examined with multivariate regressions. Simes' procedure was used to test for multiple comparisons.

RESULTS: A total of 2599 subjects had valid lung function and dietary data. A lower prevalence of FVC < LLN (airway restriction) was observed in those with higher total flavonoid (adjusted odds ratio (aOR), higher vs. lowest quintile intake 0.58; 95% Confidence Interval (CI) 0.36, 0.94), and pro-anthocyanidin intakes (aOR 0.47; 95% CI 0.27, 0.81). A higher FEV₁/FVC was associated with higher intakes of total flavonoids and pro-anthocyanidins (adjusted correlation coefficient (a β-coeff 0.33; 0.10, 0.57 and a β-coeff 0.44; 95% CI 0.19, 0.69, respectively). After Simes' procedure, the statistical significance of each of these associations was attenuated but remained below 0.05, with the exception of total flavonoids and airway restriction.

CONCLUSIONS: This population-based study in European adults provides cross-sectional evidence of a positive association of total flavonoid intake and pro-anthocyanidins and ventilatory function, and a negative association with spirometric restriction in European adults.

Place, publisher, year, edition, pages
Basel: MDPI AG, 2018
Keywords
flavonoids, pro-anthocyanidins, lung function, GA2LEN
National Category
Nutrition and Dietetics
Identifiers
urn:nbn:se:umu:diva-144048 (URN)10.3390/nu10010095 (DOI)000424088000095 ()29342980 (PubMedID)
Available from: 2018-01-19 Created: 2018-01-19 Last updated: 2018-06-09Bibliographically approved
Andersson, M., Backman, H., Nordberg, G., Hagenbjörk, A., Hedman, L., Eriksson, K., . . . Rönmark, E. (2018). Early life swimming pool exposure and asthma onset in children: a case-control study. Environmental health, 17, Article ID 34.
Open this publication in new window or tab >>Early life swimming pool exposure and asthma onset in children: a case-control study
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2018 (English)In: Environmental health, ISSN 1476-069X, E-ISSN 1476-069X, Vol. 17, article id 34Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Trichloramine exposure in indoor swimming pools has been suggested to cause asthma in children. We aimed to investigate the risk of asthma onset among children in relation to individual trichloramine exposure.

METHODS: A longitudinal nested case-control study of 337 children with asthma (cases) and 633 controls aged 16-17 years was performed within a population-based cohort from The Obstructive Lung Disease in Northern Sweden studies (OLIN). Year of asthma onset and exposure time at different ages were obtained in telephone interviews. Trichloramine concentrations in the pool buildings were measured. Skin prick test results for inhalant allergens were available from previous examinations of the cohort. The risk for asthma was analyzed in relation to the cumulative trichloramine exposure before onset of asthma.

RESULTS: Swimming pool exposure in early life was associated with a significantly higher risk of pre-school asthma onset. A dose-response relationship between swimming pool exposure and asthma was indicated in children with asthma onset at 1 year of age. Children who were both sensitized and exposed had a particularly high risk.

CONCLUSIONS: Early life exposure to chlorinated swimming pool environments was associated with pre-school asthma onset.

Place, publisher, year, edition, pages
BioMed Central, 2018
Keywords
Asthma, Children, Swimming, Trichloramine
National Category
Occupational Health and Environmental Health
Identifiers
urn:nbn:se:umu:diva-146654 (URN)10.1186/s12940-018-0383-0 (DOI)000429733700001 ()29642932 (PubMedID)
Available from: 2018-04-16 Created: 2018-04-16 Last updated: 2018-06-09Bibliographically approved
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