| 1. |
- Fuks, Kateryna B., et al.
(författare)
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Arterial blood pressure and long-term exposure to traffic-related air pollution : an analysis in the European Study of Cohorts for Air Pollution Effects (ESCAPE)
- 2014
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Ingår i: Journal of Environmental Health Perspectives. - : National Institute of Environmental Health Sciences (NIEHS). - 0091-6765 .- 1552-9924. ; 122:9, s. 896-905
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Forskningsöversikt (refereegranskat)abstract
- BACKGROUND: Long-term exposure to air pollution is hypothesized to elevate arterial blood pressure (BP). The existing evidence is scarce and country-specific. OBJECTIVES: We investigated the cross-sectional association of long-term traffic-related air pollution with BP and prevalent hypertension in European populations. METHODS: Fifteen population-based cohorts, participating in the European Study of Cohorts for Air Pollution Effects (ESCAPE), were analysed. Residential exposure to particulate matter and nitrogen oxides was modelled with land use regression using a uniform protocol. Traffic exposure was assessed with traffic indicator variables. We analysed systolic and diastolic BP in participants medicated and non-medicated with BP lowering medication (BPLM) separately, adjusting for personal and area-level risk factors and environmental noise. Prevalent hypertension was defined as ≥ 140 mmHg systolic, or ≥ 90 mmHg diastolic BP, or intake of BPLM. We combined cohort-specific results using random-effects meta-analysis. RESULTS: In the main meta-analysis of 113,926 participants, traffic load on major roads within 100 m of the residence was associated with increased systolic and diastolic BP in non-medicated participants (0.35 mmHg [95% CI: 0.02-0.68] and 0.22 mmHg [95% CI: 0.04-0.40] per 4,000,000 vehicles × m/day, respectively). The estimated odds ratio for prevalent hypertension was 1.05 [95% CI: 0.99-1.11] per 4,000,000 vehicles × m/day. Modelled air pollutants and BP were not clearly associated. CONCLUSIONS: In this first comprehensive meta-analysis of European population-based cohorts we observed a weak positive association of high residential traffic exposure with BP in non-medicated participants, and an elevated OR for prevalent hypertension. The relationship of modelled air pollutants with BP was inconsistent.
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| 2. |
- Panasevich, Sviatlana
(författare)
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Air pollution, genetic susceptibility and inflammation : focusing on cardiovascular effects in adults and respiratory effects in children
- 2011
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Air pollution exposure can induce low-grade systemic inflammation with consequences for both cardiovascular and respiratory systems. The overall aim of this thesis was to investigate the effects of air pollutants on the development of complex inflammatory diseases (myocardial infarction and respiratory disease), and genetically determined susceptibility for these effects, using epidemiologic methodology. The two study populations were drawn from a case-control study of myocardial infarction (SHEEP) and a birth cohort (BAMSE). From SHEEP, the present study population included 1192 first-time myocardial infarction (MI) cases aged 45-70 years identified in Stockholm County during 1992-1994, and 1536 matched population controls from the study base. Participants completed questionnaires and underwent medical examination as well as blood sampling. Their air pollution exposure was assessed retrospectively both long-term (1-30 years) and short-term (12 h - 5 days). NO2 was used as an indicator of emissions from road traffic and SO2 as an indicator of emissions from residential heating. From the BAMSE cohort, which recruited 4089 new-born children during 1994-1996 in four municipalities in Stockholm County, this study included 497 wheezers and 485 non-wheezing controls at 4 years, and 198 asthma cases and 192 non-asthma controls at 8 years. Questionnaires were completed by the parents when the children were 2 months, 1, 2, 4, and 8 years of age. The children were also invited for medical examination and blood sampling at 4 and 8 years. In adults, long-term exposure to both traffic- NO2 and heating-SO2 emissions showed an association with IL-6 levels. For instance, 30-year traffic-NO2 exposure was associated with a 64.5% (95%CI 6.7-153.8%) increase in serum IL-6 per 28.8 μg/m3 (corresponding to the difference between the 5th and the 95th percentile exposure value). There was also suggested association between short-term exposure to traffic-related air pollutants and inflammatory markers (IL-6, TNF-α). Gene-environment interaction was observed for several IL6 and TNF single nucleotide polymorphisms (SNPs) in relation to inflammation blood marker levels. For example, 1-year traffic-NO2 exposure interacted with IL6 -174G/C in an additive way, where each additional IL6-174C allele was associated with an increased air pollution effect on IL-6 levels, and 1-year heating-SO2 exposure was associated with higher TNF-α levels in TNF-308AA homozygotes but not in -308G carriers. Also short-term air pollution exposure interacted with IL6 and TNF SNPs in relation to marker levels. The risk of MI followed the pattern of effect on blood markers across genotype groups. In children, interaction with early maternal smoking was seen for 3 TNF SNPs with respect to early wheeze. The odds ratio for developing early wheeze related to maternal smoking was 2.4 (95%CI 1.6-3.7) in TNF -857CC homozygote children, while no tobacco-related risk was seen in children with the rare -857T allele. Suggestive interaction with early maternal smoking was also seen for 3 GSTP1 SNPs with respect to transient wheeze. SNPs in TNS1, ADAM19, THSD4 and ADCY2 identified through genome-wide analyses on lung function in adults showed association also with lung function in children; DAAM2 rs2395730 showed suggestive interaction with current tobacco smoke exposure at 8 years. In summary, the results indicate that air pollutants affect levels of inflammatory blood markers, and this effect appears to be modified by genetic variants, affecting both blood marker levels and consequent MI risk. Polymorphisms in genes related to inflammation (TNF) and antioxidant defense (GSTP1) seem to modify the effect of early tobacco smoke exposure on childhood wheezing. Several gene variants of importance for lung function in adults also seem to affect lung function in children.
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| 3. |
- Panasevich, Sviatlana, et al.
(författare)
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Investigation of novel genes for lung function in children and their interaction with tobacco smoke exposure : a preliminary report.
- 2013
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Ingår i: Acta Paediatrica. - : Wiley. - 0803-5253 .- 1651-2227. ; 102:5, s. 498-503
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To replicate newly reported single nucleotide polymorphism (SNP) associations with adult lung function in a cohort of children and to investigate interactions with tobacco smoke exposure on lung function.METHODS: Of 37 reported SNPs in adults, 21 were available in our genome-wide association study data set, either directly genotyped or as proxy SNPs. We tested for association with lung function (FEV1 , FVC, FEV1 /FVC%) in 8-year-old children and analysed interaction with tobacco smoke exposure both prenatally and/or during infancy, as well as at the age of 8 years.RESULTS: SNPs in TNS1, ADAM19, THSD4 and ADCY2 showed significant association with lung function in children, although ADCY2 variants not in the expected direction. For example, variant allele A in THSD4 rs12899618 was associated with 50.2 mL higher FEV1 (p = 0.007) and variant allele C in ADAM19 rs2277027 with 1% unit lower FEV1 /FVC% (p = 0.03) per allele. DAAM2 rs2395730 showed interaction with current tobacco smoke exposure, with variant C allele associated with 1.3% unit decrease in FEV1 /FVC% in exposed children, but not in unexposed (p for interaction 0.04).CONCLUSION: Our data replicate in children an association for TNS1, ADAM19, THSD4 and ADCY2 gene variants with lung function and suggest that interaction with tobacco smoke exposure may be of importance.
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