Jaana Halonen

Dr. Jaana Halonen

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Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 January 2009 in Epidemiology
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Journal Article
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JHJaana Halonen
Jaana Halonen
TLTimo Lanki
Timo Lanki
TYTarja Yli-Tuomi
Tarja Yli-Tuomi
PTPekka Tiittanen
Pekka Tiittanen
MKMarkku Kulmala
Markku Kulmala
JPJuha Pekkanen
Juha Pekkanen
Background: It is known that particulate air pollution affects cardiorespiratory health; however, it is unclear which particle size fractions and sources of particles are responsible for the health effects. Methods: Daily levels of nucleation (<0.03 μm), Aitken (0.03–0.1 μm), accumulation (0.1–0.29 μm), and coarse mode (2.5–10 μm) particles, particles with diameter <2.5 μm (PM2.5), and gaseous pollutants were measured at central outdoor measurement sites in Helsinki, Finland between 1998 and 2004. We determined the associations of particles with daily cardiorespiratory mortality and acute hospital admissions among the elderly (≥65 years). For the analyses we used Poisson generalized additive models and for the source apportionment of PM2.5 we used the EPA positive matrix factorization method. Results: There was a suggestion of an association of hospital admissions for arrhythmia with Aitken mode particles and PM2.5 from traffic. Otherwise few associations were observed between various sizes and types of particles and either cardiovascular admissions or mortality. In contrast, most particle fractions had positive associations with admissions for pneumonia and asthma-chronic obstructive pulmonary disease (COPD). The strongest and most consistent associations were found for accumulation mode particles (3.1%; 95% confidence interval = 0.43–5.8 for pneumonia over the 5-day mean, and 3.8%; 1.3–6.3 for asthma-COPD at lag 0, for an interquartile increase in particles). We also found a positive association of respiratory mortality mainly with accumulation mode particles (5.1%; 1.2–9.0 at lag 0). Conclusions: All particle fractions including Aitken, accumulation, and coarse mode had especially adverse respiratory health effects among the elderly. Overall associations were stronger for respiratory than for cardiovascular outcomes.

23 June 2015 in European Heart Journal
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Journal Article
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JHJaana Halonen
Jaana Halonen
AHAnna L. Hansell
Anna L. Hansell
JGJohn Gulliver
John Gulliver
DMDavid Morley
David Morley
MBMarta Blangiardo
Marta Blangiardo
CTCathryn Tonne
Cathryn Tonne
Road traffic noise has been associated with hypertension but evidence for the long-term effects on hospital admissions and mortality is limited. We examined the effects of long-term exposure to road traffic noise on hospital admissions and mortality in the general population. The study population consisted of 8.6 million inhabitants of London, one of Europe's largest cities. We assessed small-area-level associations of day- (7:00–22:59) and nighttime (23:00–06:59) road traffic noise with cardiovascular hospital admissions and all-cause and cardiovascular mortality in all adults (≥25 years) and elderly (≥75 years) through Poisson regression models. We adjusted models for age, sex, area-level socioeconomic deprivation, ethnicity, smoking, air pollution, and neighbourhood spatial structure. Median daytime exposure to road traffic noise was 55.6 dB. Daytime road traffic noise increased the risk of hospital admission for stroke with relative risk (RR) 1.05 [95% confidence interval (CI): 1.02–1.09] in adults, and 1.09 (95% CI: 1.04–1.14) in the elderly in areas >60 vs. 60 vs. <55 dB]. Positive but non-significant associations were seen with mortality for cardiovascular and ischaemic heart disease, and stroke. Results were similar for the elderly. Long-term exposure to road traffic noise was associated with small increased risks of all-cause mortality and cardiovascular mortality and morbidity in the general population, particularly for stroke in the elderly.

1 July 2008 in Thorax
Verified
Journal Article
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JHJaana Halonen
Jaana Halonen
TLT Lanki
T Lanki
TYTarja Yli-Tuomi
Tarja Yli-Tuomi
MKM Kulmala
M Kulmala
PTP Tiittanen
P Tiittanen
JPJ Pekkanen
J Pekkanen
Background: There is little previous information of the effects of size fractioned particulate air pollution and source specific fine particles (PM2.5; <2.5 μm) on asthma and chronic obstructive pulmonary disease (COPD) among children, adults and the elderly. Objectives: To determine the effects of daily variation in levels of different particle size fractions and gaseous pollutants on asthma and COPD by age group. Methods: Levels of particulate air pollution, NO2 and CO were measured from 1998 to 2004 at central outdoor monitoring sites in Helsinki, Finland. Associations between daily pollution levels and hospital emergency room visits were evaluated for asthma (ICD10: J45+J46) in children <15 years old, and for asthma and COPD (ICD10: J41+J44) in adults (15–64 years) and the elderly (⩾65 years). Results: Three to 5 day lagged increases in asthma visits were found among children in association with nucleation (<0.03 μm), Aitken (0.03–0.1 μm) and accumulation (0.1–0.29 μm) mode particles, gaseous pollutants and traffic related PM2.5 (7.8% (95% CI 3.5 to 12.3) for 1.1 μg/m3 increase in traffic related PM2.5 at lag 4). Pooled asthma–COPD visits among the elderly were associated with lag 0 of PM2.5, coarse particles, gaseous pollutants and long range transported and traffic related PM2.5 (3.9% (95% CI 0.28 to 7.7) at lag 0). Only accumulation mode and coarse particles were associated with asthma and COPD among adults. Conclusions: Among children, traffic related PM2.5 had delayed effects, whereas among the elderly, several types of particles had effects that were more immediate. These findings suggest that the mechanisms of the respiratory effects of air pollution, and responsible pollutants, differ by age group.

23 July 2010 in Environmental Health
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JHJaana Halonen
Jaana Halonen
AZAntonella Zanobetti
Antonella Zanobetti
DSDavid Sparrow
David Sparrow
PVPantel S Vokonas
Pantel S Vokonas
JSJoel Schwartz
Joel Schwartz
Associations between ambient temperature and cardiovascular mortality are well established. This study investigated whether inflammation could be part of the mechanism leading to temperature-related cardiovascular deaths.

23 September 2010 in Occupational and Environmental Medicine
Verified
Journal Article
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JHJaana Halonen
Jaana Halonen
AZAntonella Zanobetti
Antonella Zanobetti
DSDavid Sparrow
David Sparrow
PVPantel S Vokonas
Pantel S Vokonas
JSJoel Schwartz
Joel Schwartz
Objectives Cardiovascular mortality has been linked to changes in outdoor temperature. However, the mechanisms behind these effects are not well established. We aimed to study the effect of outdoor temperature on blood pressure, as increased blood pressure is a risk factor for cardiovascular death. Methods The study population consisted of men aged 53–100 years living in the Boston area. We used a mixed effects model to estimate the effect of three temperature variables: ambient, apparent and dew point temperature (DPT), on repeated measures (every 3–5 years) of diastolic (DBP) and systolic blood pressure (SBP). Random intercepts for subjects and several possible confounders were used in the models, including black carbon and barometric pressure. Results We found modest associations between DBP and ambient and apparent temperature. In the basic models, DBP in association with a 5°C decrease in 7-day moving averages of temperatures increased by 1.01% (95% CI −0.06% to 2.09%) and 1.55% (95% CI 0.61% to 2.49%) for ambient and apparent temperature, respectively. Excluding extreme temperatures strengthened these associations (2.13%, 95% CI 0.66% to 3.63%, and 1.65%, 95% CI 0.41% to 2.90%, for ambient and apparent temperature, respectively). Effect estimates for DPT were close to null. The effect of apparent temperature on SBP was similar (1.30% increase (95% CI 0.32% to 2.29%) for a 5°C decrease in 7-day moving average). Conclusions Cumulative exposure to decreasing ambient and apparent temperature may increase blood pressure. These findings suggest that an increase in blood pressure could be a mechanism behind cold-related, but not heat-related, cardiovascular mortality.

25 August 2022 in PLOS Medicine
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OROtavio T. Ranzani
Otavio T. Ranzani
AKAnjani Kalra
Anjani Kalra
CGChiara Di Girolamo
Chiara Di Girolamo
ATAriadna Curto Tirado
Ariadna Curto Tirado
FVFernanda Valerio
Fernanda Valerio
CTCathryn Tonne
Cathryn Tonne
Background: The influence of urbanicity on hypertension prevalence remains poorly understood. We conducted a systematic review and meta-analysis to assess the difference in hypertension prevalence between urban and rural areas in low-income and middle-income countries (LMICs), where the most pronounced urbanisation is underway.Methods and findings: We searched PubMed, Web of Science, Scopus, and Embase, from 01/01/1990 to 10/03/2022. We included population-based studies with ≥400 participants 15 years and older, selected by using a valid sampling technique, from LMICs that reported the urban-rural difference in hypertension prevalence using similar blood pressure measurements. We excluded abstracts, reviews, non-English studies, and those with exclusively self-reported hypertension prevalence. Study selection, quality assessment, and data extraction were performed by 2 independent reviewers following a standardised protocol. Our primary outcome was the urban minus rural prevalence of hypertension. Hypertension was defined as systolic blood pressure ≥140 mm Hg and/or diastolic blood pressure as ≥90 mm Hg and could include use of antihypertensive medication, self-reported diagnosis, or both. We investigated heterogeneity using study-level and socioeconomic country-level indicators. We conducted meta-analysis and meta-regression using random-effects models. This systematic review and meta-analysis has been registered with PROSPERO (CRD42018091671).We included 299 surveys from 66 LMICs, including 19,770,946 participants (mean age 45.4 ± SD = 9 years, 53.0% females and 63.1% from rural areas). The pooled prevalence of hypertension was 30.5% (95% CI, 28.9, 32.0) in urban areas and 27.9% (95% CI, 26.3, 29.6) in rural areas, resulting in a pooled urban-rural difference of 2.45% (95% CI, 1.57, 3.33, I-square: 99.71%, tau-square: 0.00524, Pheterogeneity< 0.001). Hypertension prevalence increased over time and the rate of change was greater in rural compared to urban areas, resulting in a pooled urban-rural difference of 5.75% (95% CI, 4.02, 7.48) in the period 1990 to 2004 and 1.38% (95% CI, 0.40, 2.37) in the period 2005 to 2020,p< 0.001 for time period. We observed substantial heterogeneity in the urban-rural difference of hypertension, which was partially explained by urban-rural definition, probably high risk of bias in sampling, country income status, region, and socioeconomic indicators. The urban-rural difference was 5.67% (95% CI, 4.22, 7.13) in low, 2.74% (95% CI, 1.41, 4.07) in lower-middle and −1.22% (95% CI, −2.73, 0.28) in upper-middle-income countries in the period 1990 to 2020,p< 0.001 for country income. The urban-rural difference was highest for South Asia (7.50%, 95% CI, 5.73, 9.26), followed by sub-Saharan Africa (4.24%, 95% CI, 2.62, 5.86) and reversed for Europe and Central Asia (−6.04%, 95% CI, −9.06, −3.01), in the period 1990 to 2020,p< 0.001 for region. Finally, the urban-rural difference in hypertension prevalence decreased nonlinearly with improvements in Human Development Index and infant mortality rate. Limitations included lack of data available from all LMICs and variability in urban and rural definitions in the literature.Conclusions: The prevalence of hypertension in LMICs increased between 1990 and 2020 in both urban and rural areas, but with a stronger trend in rural areas. The urban minus rural hypertension difference decreased with time, and with country-level socioeconomic development. Focused action, particularly in rural areas, is needed to tackle the burden of hypertension in LMICs.