| 1. |
- Thacher, Jesse D., et al.
(författare)
-
Biomass fuel use and the risk of asthma in Nigerian children
- 2013
-
Ingår i: Respiratory Medicine. - : Elsevier BV. - 1532-3064 .- 0954-6111. ; 107:12, s. 1845-1851
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Biomass fuel smoke exposure contributes to respiratory infections in childhood, but its association with asthma has not been established. We studied the relationship of biomass fuel use with asthma symptoms and lung function in Nigerian children. Methods: A cross-sectional study was performed in 299 village children aged 5-11 years in North Central Nigeria. Data were collected regarding the cooking fuels used and duration of daily smoke exposure in the cooking area. Asthma symptoms were assessed with a modified International Study of Asthma and Allergies in Childhood (ISAAC) questionnaire, and lung function was assessed with spirometry. Results: The prevalence of a lifetime history of wheeze was 9.4% (95% CI: 6.3%-13.2%). Fourteen children (4.7%) had airway obstruction (FEV1/FEV6 <85%). Female subjects had lower FEV1 and FEV6 (110% and 120% percent predicted, respectively) than males (121% and 130%, respectively, P<0.001 for both differences). Advancing age was associated with a relative decline in the predicted value of FEV1 of 7.8% per year (r = -0.61; P < 0.001). Children in families that used firewood daily did not have a significantly increased likelihood of asthma-related symptoms (OR = 2.36, 95% Cl: 0.66-8.44). Similarly, airway obstruction did not differ significantly between children in households that did and did not use firewood daily (mean FEV1/FEV6 of 0.95 and 0.97, respectively; P = 0.41). Conclusion: Reported smoke exposure was not associated with an increased risk of asthma symptoms or airway obstruction. However, lifetime smoke exposure may explain the reduction in spirometric values in female subjects and with advancing age. (C) 2013 Elsevier Ltd. All rights reserved.
|
|
| 2. |
- Thacher, Jesse D., et al.
(författare)
-
Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts
- 2022
-
Ingår i: OCCUPATIONAL AND ENVIRONMENTAL MEDICINE. - : BMJ. - 1351-0711 .- 1470-7926. ; 79:9, s. 594-601
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND). Methods We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (L-Aeq8h): <70, 70-74, 75-79, 80-84, >= 85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders. Results Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and >= 85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (>= 85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63). Conclusions We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.
|
|
| 3. |
- Roswall, Nina, et al.
(författare)
-
Long-term exposure to traffic noise and risk of incident colon cancer : A pooled study of eleven Nordic cohorts
- 2023
-
Ingår i: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 224
-
Tidskriftsartikel (refereegranskat)abstract
- BackgroundColon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this.ObjectivesThe objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons.MethodsWe identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data.ResultsDuring follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99–1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98–1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure.DiscussionA prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.
|
|
| 4. |
- Thacher, Jesse D., et al.
(författare)
-
Exposure to long-term source-specific transportation noise and incident breast cancer : A pooled study of eight Nordic cohorts
- 2023
-
Ingår i: Environment International. - : Elsevier. - 0160-4120 .- 1873-6750. ; 178
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Environmental noise is an important environmental exposure that can affect health. An association between transportation noise and breast cancer incidence has been suggested, although current evidence is limited. We investigated the pooled association between long-term exposure to transportation noise and breast cancer incidence.Methods: Pooled data from eight Nordic cohorts provided a study population of 111,492 women. Road, railway, and aircraft noise were modelled at residential addresses. Breast cancer incidence (all, estrogen receptor (ER) positive, and ER negative) was derived from cancer registries. Hazard ratios (HR) were estimated using Cox Proportional Hazards Models, adjusting main models for sociodemographic and lifestyle variables together with long-term exposure to air pollution.Results: A total of 93,859 women were included in the analyses, of whom 5,875 developed breast cancer. The median (5th–95th percentile) 5-year residential road traffic noise was 54.8 (40.0–67.8) dB Lden, and among those exposed, the median railway noise was 51.0 (41.2–65.8) dB Lden. We observed a pooled HR for breast cancer (95 % confidence interval (CI)) of 1.03 (0.99–1.06) per 10 dB increase in 5-year mean exposure to road traffic noise, and 1.03 (95 % CI: 0.96–1.11) for railway noise, after adjustment for lifestyle and sociodemographic covariates. HRs remained unchanged in analyses with further adjustment for PM2.5 and attenuated when adjusted for NO2 (HRs from 1.02 to 1.01), in analyses using the same sample. For aircraft noise, no association was observed. The associations did not vary by ER status for any noise source. In analyses using <60 dB as a cutoff, we found HRs of 1.08 (0.99–1.18) for road traffic and 1.19 (0.95–1.49) for railway noise.Conclusions: We found weak associations between road and railway noise and breast cancer risk. More high-quality prospective studies are needed, particularly among those exposed to railway and aircraft noise before conclusions regarding noise as a risk factor for breast cancer can be made.
|
|
| 5. |
- Thacher, Jesse D, et al.
(författare)
-
Exposure to Paracetamol in Early Pregnancy and the Risk of Developing Cerebral Palsy : A Case-Control Study Using Serum Samples
- 2024
-
Ingår i: Journal of Pediatrics. - 1097-6833.
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate whether maternal paracetamol use in early pregnancy is associated with cerebral palsy (CP) in offspring.STUDY DESIGN: We conducted a registry and biobank-based case-control study with mother-child pairs. We identified CP cases (n=322) born between 1995-2014 from a nationwide CP-registry. Randomly selected controls (n=343) and extra preterm controls (n=258) were obtained from a birth registry. For each mother, a single serum sample from early pregnancy (gestation weeks 10-14) was retrieved from a biobank and analyzed for serum concentrations of paracetamol, categorized into unexposed (<1 ng/ml), mildly exposed (1-100 ng/ml), and highly exposed (>100 ng/ml), and in quartiles. Analyses were performed using logistic regression and adjusted for potential confounders. Separate analyses were conducted including only those children born preterm and only those born term.RESULTS: Of the 923 participants, 36.8% were unexposed, 53.2% mildly exposed, and 10% highly exposed to paracetamol. Overall, prenatal exposure to paracetamol was not associated with CP. Sensitivity and subgroup analyses showed no clear associations between paracetamol and CP across strata of term/preterm birth as well as subtypes of CP.CONCLUSIONS: The present study does not support an association between intrauterine exposure to paracetamol in early pregnancy and the risk of CP. However, it is important to stress that the exposure estimate is based on a single serum sample.
|
|
| 6. |
- Thacher, Jesse D
(författare)
-
Indoor environment and tobacco smoke exposure in relation to allergic disease and lung function
- 2017
-
Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Asthma and other allergy related diseases are the most common chronic diseases in childhood, and have become a major public health concern. The rapid increase in the occurrence of these diseases, especially in high-income countries, has led to the study of the role ofvarious environmental and lifestyle factors. The overall aim of this thesis was to evaluate the association between indoor environmental factors and the development of allergic diseases in childhood and adolescence, and more specifically, to study the association between tobacco smoke exposure during pre- or postnatal life as well as exposure to indoor mold or dampness and allergic diseases from birth to age 16 years. We used data from the Swedish prospective birth cohort BAMSE (N = 4089) and in study III data from BAMSE combined with four other European birth cohorts (N = 10860). We found that exposure to maternal smoking during pregnancy was associated with asthma up to adolescence, especially early-transient asthma. Additionally, exposure to high doses of maternal smoking during pregnancy (≥10 cigarettes/day) was associated with persistent asthma as well as persistent rhinoconjunctivitis up to age 16 years. Based on spirometry, exposure to maternal smoking during pregnancy was also associated with lower FEV1/FVC ratios at age 16 years. Additionally, indices from impulse oscillometry indicated increased peripheral airway resistance at age 16 years among subjects exposed to maternal smoking during pregnancy. Exposure to secondhand smoke (SHS) during infancy was associated with overall increased risks of asthma, rhinitis, and eczema up to adolescence. However, we found suggestive evidence that the association between SHS during infancy and asthma was likely driven by exposure in utero. Our findings indicate that exposure to SHS during infancy, without prior exposure to maternal smoking during pregnancy, was associated with food allergen sensitization up to age 16 years. Furthermore, exposure to SHS during infancy was associated with increased risks ofrhinitis without concomitant sensitization and eczema with concomitant sensitization. SHS exposure during other periods of childhood was not associated with the onset of asthma or rhinoconjunctivitis in adolescence. Compared with non-smokers, participants who smoked daily or occasionally tended to have reduced FEV1/FVC ratios at age 16 years, even after controlling for maternal smoking during pregnancy. Using indices from impulse oscillometry (IOS) we found increased peripheral airway resistance among adolescent smokers. These findings were corroborated when we used saliva cotinine concentrations to discriminate smokers from non-smokers. Exposure to indicators of mold or dampness during infancy were associated with increased risk of asthma up to age 16 years, as well as an increased risk of persistent asthma. We also found suggestive evidence of an association between reported mold odor or visible mold during infancy and rhinitis up to age 16 years. No association between exposure to indicators of mold or dampness and IgE sensitization was observed. In conclusion, findings from the studies included in this thesis suggest that exposure to maternal smoking during pregnancy is associated with asthma and measures of airway obstruction, such as reduced FEV1/FVC ratios, up to adolescence. Exposure to SHS during infancy seems to be associated with food allergen sensitization and rhinitis up to age 16 years. Adolescent smoking is associated with reduced FEV1/FVC ratios and increased peripheral airway resistance at age 16 years. Exposure to indicators of mold or dampness during infancy may be associated with an increased risk of asthma, and more specifically with persistent asthma up to age 16 years. The results from this thesis can be used to help inform public health policy as well as clinicians to motivate their patients to abstain from smoking. Indoor mold and dampness is a modifiable risk factor related to the onset and persistence of asthma in children and adolescence, and further research should focus on identifying the causal agents.
|
|
| 7. |
- Thacher, Jesse D., et al.
(författare)
-
Influence of the COVID-19 pandemic on births and induced abortions in Southern Sweden : A register-based study
-
Ingår i: BMJ Sexual and Reproductive Health. - 2515-1991. ; , s. 1-9
-
Tidskriftsartikel (refereegranskat)abstract
- Background: Pandemics are linked with declining birth rates, but little is known about how the COVID-19 pandemic has influenced childbearing decisions. We aimed to investigate the associations between the COVID-19 pandemic and reproductive decisions, specifically to identify potential changes in the frequency of deliveries and induced abortions in Skåne, Sweden. Methods: Using the Skåne Healthcare Register, we identified women aged 15-45 years who had at least one pregnancy-related care visit registered between 1 January 2013 and 11 November 11 2021. Deliveries and induced abortions were identified, and changes in weekly delivery and abortion counts were assessed using an interrupted time series design. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated from a Poisson regression model. Results: During the study period we identified 129 131 deliveries and 38 591 abortions. Compared with the counterfactual (exposed interval assuming COVID-19 had not occurred), pandemic exposure was associated with fewer deliveries (RR 0.93; 95% CI 0.89 to 0.98). For abortions, pandemic exposure appeared to be associated with fewer abortions (RR 0.95; 95% CI 0.90 to 1.00); however, age-related differences were found. Among women aged 25 years and over, pandemic exposure was more strongly associated with fewer abortions. Contrastingly, among women aged under 25 years, abortions appeared to increase. Conclusions: The COVID-19 pandemic seemed to have contributed to a decline in births in Southern Sweden. During the same period, abortions declined in women in the older age range, but contrastingly increased among younger women.
|
|
| 8. |
- Thacher, Jesse D, et al.
(författare)
-
Parental smoking and development of allergic sensitization from birth to adolescence
- 2016
-
Ingår i: Allergy. European Journal of Allergy and Clinical Immunology. - : Wiley. - 0105-4538 .- 1398-9995. ; 71:2, s. 239-248
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The relation between secondhand tobacco smoke (SHS) exposure and the development of allergic sensitization in children is unclear. The aim of this study was to determine whether maternal smoking during pregnancy and postnatal SHS exposure contributes to the development of allergic sensitization in children and adolescents up to 16 years of age.METHODS: We included 3316 children from a birth cohort followed for 16 years. SHS exposure and symptoms of allergic disease were assessed using repeated parental questionnaires. Serum immunoglobulin E against eight common inhalant and six food allergens was assessed at ages 4, 8, and 16 years with ImmunoCAP. The association between SHS exposure and sensitization was explored using logistic regression and generalized estimating equations.RESULTS: Exposure to SHS in infancy without prior exposure in utero, was associated with an excess risk of food sensitization at age 4 (OR 1.47, 95% CI 1.08-2.00), with comparable ORs at ages 8 and 16 years. In longitudinal analyses, an overall association was indicated between SHS in infancy and food sensitization up to age 16 years (OR 1.24, 95% CI 0.98-1.56). Maternal smoking during pregnancy was unrelated to sensitization up to 16 years of age. When sensitization was combined with concurrent symptoms of allergic disease, SHS in infancy was associated with an overall elevated risk of eczema with sensitization (OR 1.62, 95% CI 1.20-2.18).CONCLUSIONS: SHS exposure in infancy appears to increase the risk of sensitization to food allergens up to age 16 years as well as eczema in combination with sensitization.
|
|
| 9. |
- Thacher, Jesse D., et al.
(författare)
-
Pre- and Postnatal Exposure to Parental Smoking and Allergic Disease Through Adolescence
- 2014
-
Ingår i: Pediatrics. - : American Academy of Pediatrics (AAP). - 0031-4005 .- 1098-4275. ; 134:3, s. 428-434
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To examine the role of prenatal and postnatal second-hand tobacco smoke (SHS) exposure on asthma, rhinitis, and eczema development up to 16 years of age. METHODS: A birth cohort of 4089 children was followed for 16 years. Information on parental smoking habits, lifestyle factors, and symptoms of allergic disease was gathered using repeated parental questionnaires. Generalized estimating equations assessed the overall and age-specific associations between SHS exposure and allergic disease at ages 1 to 16 years. RESULTS: Exposure to SHS in utero was associated with an overall elevated risk of developing asthma up to 16 years (odds ratio [OR] = 1.45; 95% confidence interval [CI], 1.15-1.83) but not for rhinitis or eczema. After additional adjustment for parental smoking throughout childhood, excess overall risks for asthma remained statistically significant. Moreover, a dose-dependent pattern with SHS was observed. Exposure to SHS during infancy was associated with an overall elevated risk of asthma (OR = 1.23; 95% CI, 1.01-1.51), rhinitis (OR = 1.18; 95% CI, 1.01-1.39), and eczema (OR = 1.26; 95% CI, 1.09-1.45) up to 16 years. When age-specific associations were examined, the elevated risks related to SHS exposure in utero or during infancy were mostly confined to early childhood for asthma and rhinitis, whereas the excess risk of eczema appeared greatest at later ages. CONCLUSIONS: Our findings indicate that early SHS exposure, in utero or during infancy, influences the development of allergic disease up to adolescence. Excess risks for asthma and rhinitis were seen primarily in early childhood, whereas those for eczema occurred at later ages.
|
|
| 10. |
- Vilhelmsson, Andreas, et al.
(författare)
-
Exposure to per- and polyfluoroalkyl substances in early pregnancy and risk of cerebral palsy in children
- 2023
-
Ingår i: Science of the Total Environment. - 1879-1026. ; 899
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Most cerebral palsy (CP) cases have an unexplained etiology, but a role for environmental exposures has been suggested. One purported environmental risk factor is exposure to endocrine-disrupting pollutants specifically per- and polyfluoroalkyl substances (PFAS).OBJECTIVES: We investigated the association between prenatal PFAS exposures and CP in Swedish children.METHODS: In this case-control study, 322 CP cases, 343 population controls, and 258 preterm controls were identified from a birth registry in combination with a CP follow-up program from 1995 to 2014 and linked to a biobank which contains serum samples from week 10-14 of pregnancy. Maternal serum concentrations of four PFAS compounds: perfluorohexane sulfonate (PFHxS), perfluorooctanoic acid (PFOA), perfluorononanoic acid (PFNA), and perfluorooctane sulfonate (PFOS) were analyzed using liquid chromatography-tandem-mass-spectrometry. We estimated odds ratios (ORs) and 95 % confidence intervals (CIs) for CP and each PFAS in quartiles and as continuous variables controlling for various sociodemographic and lifestyle factors.RESULTS: In crude and adjusted analyses, we did not find consistent evidence of associations between serum PFHxS, PFOA, PFNA, PFOS and concentrations in early pregnancy and CP, except in preterm infants. The ORs comparing the highest PFAS quartiles to the lowest were 1.05 (95 % CI: 0.63-1.76), 0.96 (95 % CI: 0.55-1.68), 0.71 (95 % CI: 0.41-1.25), and 1.17 (95 % CI: 0.61-2.26), for PFHxS, PFOA, PFNA, and PFOS, respectively. Some positive associations were observed for preterm infants, but the results were imprecise. Similar patterns were observed in analyses treating PFAS as continuous variables.CONCLUSIONS: In this study, we found little evidence that early pregnancy prenatal exposure to PFHxS, PFOA, PFNA, or PFOS increases the risk of CP. However, some positive associations were observed for preterm cases and warrant further investigation.
|
|
