Background Associations between traffic-related air pollution (TRAP) and allergic rhinitis remain inconsistent, possibly because of unexplored gene-environment interactions. Objective In a pooled ...analysis of 6 birth cohorts (Ntotal = 15,299), we examined whether TRAP and genetic polymorphisms related to inflammation and oxidative stress predict allergic rhinitis and sensitization. Methods Allergic rhinitis was defined with a doctor diagnosis or reported symptoms at age 7 or 8 years. Associations between nitrogen dioxide, particulate matter 2.5 (PM2.5 ) mass, PM2.5 absorbance, and ozone, estimated for each child at the year of birth, and single nucleotide polymorphisms within the GSTP1 , TNF , TLR2 , or TLR4 genes with allergic rhinitis and aeroallergen sensitization were examined with logistic regression. Models were stratified by genotype and interaction terms tested for gene-environment associations. Results Point estimates for associations between nitrogen dioxide, PM2.5 mass, and PM2.5 absorbance with allergic rhinitis were elevated, but only that for PM2.5 mass was statistically significant (1.37 1.01, 1.86 per 5 μg/m3 ). This result was not robust to single-cohort exclusions. Carriers of at least 1 minor rs1800629 ( TNF ) or rs1927911 ( TLR4 ) allele were consistently at an increased risk of developing allergic rhinitis (1.19 1.00, 1.41 and 1.24 1.01, 1.53, respectively), regardless of TRAP exposure. No evidence of gene-environment interactions was observed. Conclusion The generally null effect of TRAP on allergic rhinitis and aeroallergen sensitization was not modified by the studied variants in the GSTP1 , TNF , TLR2 , or TLR4 genes. Children carrying a minor rs1800629 ( TNF ) or rs1927911 ( TLR4 ) allele may be at a higher risk of allergic rhinitis.
Despite the important contribution of traffic sources to urban air quality, relatively few studies have evaluated the effects of traffic-related air pollution on health, such as its influence on the ...development of asthma and other childhood respiratory diseases. We examined the relationship between traffic-related air pollution and the development of asthmatic/allergic symptoms and respiratory infections in a birth cohort (n approximately 4,000) study in The Netherlands. A validated model was used to assign outdoor concentrations of traffic-related air pollutants (nitrogen dioxide, particulate matter less than 2.5 micro m in aerodynamic diameter, and "soot") at the home of each subject of the cohort. Questionnaire-derived data on wheezing, dry nighttime cough, ear, nose, and throat infections, skin rash, and physician-diagnosed asthma, bronchitis, influenza, and eczema at 2 years of age were analyzed in relation to air pollutants. Adjusted odds ratios for wheezing, physician-diagnosed asthma, ear/nose/throat infections, and flu/serious colds indicated positive associations with air pollutants, some of which reached borderline statistical significance. No associations were observed for the other health outcomes analyzed. Sensitivity analyses generally supported these results and suggested somewhat stronger associations with traffic, for asthma that was diagnosed before 1 year of age. These findings are subject to confirmation at older ages, when asthma can be more readily diagnosed.
Epidemiology studies of health effects from air pollution, as well as impact assessments, typically rely on ambient monitoring data or modelled residential levels. The relationship between these and ...personal exposure is not clear. To investigate personal exposure to NO(2) and its relationship with other exposure metrics and time-activity patterns in a randomly selected sample of healthy working adults (20-59 years) living and working in Stockholm. Personal exposure to NO(2) was measured with diffusive samplers in sample of 247 individuals. The 7-day average personal exposure was 14.3 µg/m(3) and 12.5 µg/m(3) for the study population and the inhabitants of Stockholm County, respectively. The personal exposure was significantly lower than the urban background level (20.3 µg/m(3)). In the univariate analyses the most influential determinants of individual exposure were long-term high-resolution dispersion-modelled levels of NO(2) outdoors at home and work, and concurrent NO(2) levels measured at a rural location, difference between those measured at an urban background and rural location and difference between those measured in busy street and at an urban background location, explaining 20, 16, 1, 2 and 4% (R(2)) of the 7-day personal NO(2) variation, respectively. A regression model including these variables explained 38% of the variation in personal NO(2) exposure. We found a small improvement by adding time-activity variables to the latter model (R(2) = 0.44). The results adds credibility primarily to long-term epidemiology studies that utilise long-term indices of NO(2) exposure at home or work, but also indicates that such studies may still suffer from exposure misclassification and dilution of any true effects. In contrast, urban background levels of NO(2) are poorly related to individual exposure.
Long-term exposure to traffic noise has been suggested to increase the risk of cardiovascular diseases (CVD). However, few studies have been performed in the general population and on railway noise. ...This study aimed to investigate the cardiovascular effects of living near noisy roads and railways. This cross-sectional study comprised 25,851 men and women, aged 18-80 years, who had resided in Sweden for at least 5 years. All subjects participated in a National Environmental Health Survey, performed in 2007, in which they reported on health, annoyance reactions and environmental factors. Questionnaire data on self-reported doctor's diagnosis of hypertension and/or CVD were used as outcomes. Exposure was assessed as Traffic Load (millions of vehicle kilometres per year) within 500 m around each participant's residential address. For a sub-population (n = 2498), we also assessed road traffic and railway noise in L(den) at the dwelling façade. Multiple logistic regression models were used to assess Prevalence Odds Ratios (POR) and 95% Confidence Intervals (CI). No statistically significant associations were found between Traffic Load and self-reported hypertension or CVD. In the sub-population, there was no association between road traffic noise and the outcomes; however, an increased risk of CVD was suggested among subjects exposed to railway noise ≥50 dB(A); POR 1.55 (95% CI 1.00-2.40). Neither Traffic Load nor road traffic noise was, in this study, associated with self-reported cardiovascular outcomes. However, there was a borderline-significant association between railway noise and CVD. The lack of association for road traffic may be due to methodological limitations.
Background: Extremely-low-frequency magnetic field (ELF-MF) exposure is suspected to increase the risk of Alzheimer's disease. Such fields are present in the vicinity of electrical motors and other ...electric appliances containing coils. Methods: We investigated lifetime occupational ELF-MF exposure in relation to Alzheimer's disease and dementia among a community dementia-free cohort (n = 931) age 75 years and older in Stockholm, Sweden. This cohort was followed from 1987-1989 until 1994-1996 to detect dementia cases ("Diagnostic and Statistical Manual of Mental Disorders," revised 3rd edition criteria). Information on lifetime job history was obtained by interview, usually of next of kin. ELF-MF exposure was assessed using a job-exposure matrix, measurement on historical equipment, and expert estimation. We analyzed the data with Cox models controlling for potential confounders. Results: Dementia was diagnosed in 265 subjects, including 202 with Alzheimer's disease. Among men, ELF-MF exposure ≥0.2 μT in lifetime principal job was related to multivariate-adjusted relative risks of 2.3 (95% CI = 1.0-5.1) for Alzheimer's disease and 2.0 (1.1-3.7) for dementia. We found no association among women. A similar sex-specific pattern was seen for the associations with average ELF-MF exposure throughout the work life. A dose-response relation was suggested in men, with multivariate-adjusted relative risks of 2.4 (0.8-6.8) for Alzheimer's disease and 2.5 (1.1-5.6) for dementia for the upper tertile of lifetime average exposure. Conclusions: Long-term occupational exposure to a higher ELF-MF level may increase the risk of Alzheimer's disease and dementia in men. Similar patterns were not seen in women, which may in part be the result of a greater exposure misclassification in women than in men.
Emerging yet contrasting evidence associates air pollution with incident dementia, and the potential role of cardiovascular disease (CVD) in this association is unclear.
To investigate the ...association between long-term exposure to air pollution and dementia and to assess the role of CVD in that association.
Data for this cohort study were extracted from the ongoing Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study with baseline assessments from March 21, 2001, through August 30, 2004. Of the 5111 randomly selected residents in the Kungsholmen district of Stockholm 60 years or older and living at home or in institutions, 521 were not eligible (eg, due to death before the start of the study or no contact information). Among the remaining 4590 individuals, 3363 (73.3%) were assessed. For the current analysis, 2927 participants who did not have dementia at baseline were examined, with follow-up to 2013 (mean SD follow-up time, 6.01 2.56 years). Follow-up was completed February 18, 2013, and data were analyzed from June 26, 2018, through June 20, 2019.
Two major air pollutants (particulate matter ≤2.5 μm PM2.5 and nitrogen oxide NOx) were assessed yearly from 1990, using dispersion models for outdoor levels at residential addresses.
The hazard of dementia was estimated using Cox proportional hazards regression models. The potential of CVD (ie, atrial fibrillation, ischemic heart disease, heart failure, and stroke) to modify and mediate the association between long-term exposure to air pollution and dementia was tested using stratified analyses and generalized structural equation modeling.
At baseline, the mean (SD) age of the 2927 participants was 74.1 (10.7) years, and 1845 (63.0%) were female. Three hundred sixty-four participants with incident dementia were identified. The hazard of dementia increased by as much as 50% per interquartile range difference in mean pollutant levels during the previous 5 years at the residential address (hazard ratio HR for difference of 0.88 μg/m3 PM2.5, 1.54 95% CI, 1.33-1.78; HR for difference of 8.35 μg/m3 NOx, 1.14 95% CI, 1.01-1.29). Heart failure (HR for PM2.5, 1.93 95% CI, 1.54-2.43; HR for NOx, 1.43 95% CI, 1.17-1.75) and ischemic heart disease (HR for PM2.5, 1.67 95% CI, 1.32-2.12; HR for NOx, 1.36 95% CI, 1.07-1.71) enhanced the dementia risk, whereas stroke appeared to be the most important intermediate condition, explaining 49.4% of air pollution-related dementia cases.
This study found that long-term exposure to air pollution was associated with a higher risk of dementia. Heart failure and ischemic heart disease appeared to enhance the association between air pollution and dementia, whereas stroke seemed to be an important intermediate condition between the association of air pollution exposure with dementia.
Short-term exposure to air pollutants has been extensively related to daily mortality, however most of the evidence comes from studies conducted in major cities, and little is known on the extent of ...the spatial heterogeneity in the effects within areas including both urban and non-urban settings. We aimed to investigate the short-term association of air pollutants with daily cause-specific mortality in the Stockholm county, and to test whether an association exists also outside the metropolitan area. We used a spatiotemporal random forest model to predict daily concentrations of fine and inhalable particulate matter (PM2.5 and PM10), nitrogen dioxide (NO2) and ozone (O3) at 1-km spatial resolution over Sweden for 2005–2016. We collected data on daily mortality for each small area for market statistics (SAMS) of the Stockholm county, to which we matched daily exposures to air pollutants and air temperature. We applied a case-crossover design to investigate the short-term association between the four pollutants and mortality from non-accidental, cardiovascular and respiratory causes. We compared the associations in and out the Stockholm urban area, by SAMS population density and across the 26 municipalities of the county. We found weak effects of most air pollutants on cause-specific mortality in the full year analysis, with estimates much larger and significant only during the warmer months (April to September): non-accidental mortality increased by 4.58% (95% confidence interval – 95% CI: 0.89%, 8.41%) and by 2.21% (95% CI: 0.71%, 3.73%) per 10 μg/m3 increase in lag 0–1 PM2.5 and O3, respectively. Associations were in general higher in the Stockholm city and in SAMS with high population density. When comparing the 26 municipalities, we didn't detect a significant heterogeneity in the short-term associations with air pollutants. In conclusion, we found a suggestion of a harmful role of air pollution also in non-urban areas, but the study was underpowered to draw firm conclusions. We consider this study as a pilot to investigate the spatial heterogeneity of the association between daily air pollution and mortality at the national level in Sweden.
•Limited evidence on the acute effects of air pollution outside major urban areas.•Estimates of air pollutants at high spatiotemporal resolution in Sweden.•Strong effects of particles and ozone on mortality in the warm season in Stockholm.•Clearer effects compared to those from monitor-based daily mean concentrations.•Health effects comparable between more and less urbanized areas of the county.
Here we compare PM(2.5) (particles with aerodynamic diameter less than 2.5 microm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same ...site as well as collocated PM(2.5) and PM(10) (particles with aerodynamic diameter less than 10 microm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM(2.5) absorbance measurements were at traffic sites on average 43-84% and 26-76% higher, respectively, compared to urban background sites. The contrast for PM(2.5) mass measurements was lower (8-35%). The smaller contrast observed for PM(2.5) mass in comparison with PM(2.5) absorbance and EC documents that PM(2.5) mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM(10) and PM(2.5) was high, documenting that most of the spatial variation of PM(10) was because of PM(2.5). The measurement of PM(2.5) absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM(2.5) and PM(10) mass ranged from 0.54 to 0.68, the ratio of PM(2.5) absorbance and PM(10) absorbance was 0.96-0.97, indicating that PM(2.5) absorbance captures nearly all of the particle absorbance.
Objectives The prevalence of medically unexplained symptoms attributed to exposure to electromagnetic fields is still largely unknown. Previous studies have investigated reported hypersensitivity to ...electricity in selected groups recruited from workplaces or outpatient clinics. The aim of this study was to estimate the prevalence of self-reported hypersensitivity to electric or magnetic fields in the general population and to describe characteristics of the group reporting such hypersensitivity with regard to demographics, other complaints, hypersensitivities, and traditional allergies. Methods A cross-sectional questionnaire survey was conducted in 1997 among 15 000 men and women between 19 and 80 years of age in Stockholm County. The response rate was 73%. Results One and a half percent of the respondents reported hypersensitivity to electric or magnetic fields. Prevalence was highest among women and in the 60-to 69-year age group. The hypersensitive group reported all symptoms, allergies, and other types of hypersensitivities'included in the survey (as well as being disturbed by various factors in the home) to a significantly greater extent than the rest of the respondents. No specific symptom profile set off the hypersensitive group from the rest of the respondents. Conclusions The results should be interpreted with caution. But they suggest that there is widespread concern among the general population about risks to health posed by electric and magnetic fields. More research is warranted to explore ill health among people reporting hypersensitivity to electric or magnetic fields.
Common Genetic Polymorphisms and Haplotypes of Fibrinogen Alpha, Beta, and Gamma Chains Affect Fibrinogen Levels and the Response to Proinflammatory Stimulation in Myocardial Infarction Survivors: ...The AIRGENE Study Bénédicte Jacquemin, Charalambos Antoniades, Fredrik Nyberg, Estel Plana, Martina Müller, Sonja Greven, Veikko Salomaa, Jordi Sunyer, Tom Bellander, Alexandros-Georgios Chalamandaris, Ricardo Pistelli, Wolfgang Koenig, Annette Peters We investigated whether single nucleotide polymorphisms (SNPs) and haplotypes of the fibrinogen gene-cluster (fibrinogen chain alpha FGA, beta FGB, and gamma FGG) could affect plasma levels of fibrinogen in patients with history of myocardial infarction (MI). We analyzed 21 SNPs and the corresponding haplotypes in the 3 genes. We identified several haplotypes and SNPs on the FGA/FGB genes that contributed to explain the interindividual and intraindividual variability of fibrinogen levels, in patients with a history of MI. We have also identified SNPs/haplotypes on FGA/FGB whose effects on fibrinogen expression are modified by the underlying interleukin-6 levels. These findings may be important for risk stratification of patients after MI and may be useful for the design of genetically guided therapeutic approaches in these patients.
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