Charlotta Eriksson

Development of Land Use Regression Models for Particle Composition in Twenty Study Areas in Europe

Land Use Regression (LUR) models have been used to describe and model spatial variability of annual mean concentrations of traffic related pollutants such as nitrogen dioxide (NO2), nitrogen oxides (NOx) and particulate matter (PM). No models have yet been published of elemental composition. As part of the ESCAPE project, we measured the elemental composition in both the PM10 and PM2.5 fraction sizes at 20 sites in each of 20 study areas across Europe. LUR models for eight a priori selected elements (copper (Cu), iron (Fe), potassium (K), nickel (Ni), sulfur (S), silicon (Si), vanadium (V), and zinc (Zn)) were developed. Good models were developed for Cu, Fe, and Zn in both fractions (PM10 and PM2.5) explaining on average between 67 and 79% of the concentration variance (R(2)) with a large variability between areas. Traffic variables were the dominant predictors, reflecting nontailpipe emissions. Models for V and S in the PM10 and PM2.5 fractions and Si, Ni, and K in the PM10 fraction performed moderately with R(2) ranging from 50 to 61%. Si, NI, and K models for PM2.5 performed poorest with R(2) under 50%. The LUR models are used to estimate exposures to elemental composition in the health studies involved in ESCAPE.

Aircraft noise and incidence of hypertension.

Background: An association between aircraft noise exposure and hypertension prevalence has been suggested but there are no longitudinal studies of this association. Our aim was to investigate the influence of aircraft noise on the incidence of hypertension. Methods: A cohort of 2754 men in 4 municipalities around Stockholm Arlanda airport was followed between 1992–1994 and 2002–2004. The cohort was based on the Stockholm Diabetes Preventive Program; half of the study subjects had a family history of diabetes. Residential aircraft noise exposure (expressed as time-weighted equal energy and maximal noise levels) was assessed by geographical information systems techniques among those living near the airport. Incident cases of hypertension were identified by physical examinations, including blood pressure measurements, and questionnaires in which subjects reported treatment or diagnosis of hypertension and information on cardiovascular risk factors. Analyses were restricted to 2027 subjects who completed the follow-up examination, were not treated for hypertension, and had a blood pressure below 140/90 mm Hg at enrollment. Results: For subjects exposed to energy-averaged levels above 50 dB(A) the adjusted relative risk for hypertension was 1.19 (95% CI = 1.03–1.37). Maximum aircraft noise levels presented similar results, with a relative risk of 1.20 (1.03–1.40) for those exposed above 70 dB(A). Stronger associations were suggested among older subjects, those with a normal glucose tolerance, nonsmokers, and subjects not annoyed by noise from other sources. Conclusion: These findings suggest that long-term aircraft noise exposure may increase the risk for hypertension.

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin-1 system.

The evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro‐ and anti‐inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin‐1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin‐1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. In this review, we have summarized the experimental data available with regard to the involvement of the interleukin‐1 system in kainic acid‐induced changes in the brain and emphasized the modulatory role of interleukin‐1β in this model of epilepsy.

Increased expression of mRNA encoding interleukin-1? and caspase-1, and the secreted isoform of interleukin-1 receptor antagonist in the rat brain following systemic kainic acid administration

Kainic acid, an analogue of glutamate, injected systemically to rats evokes seizures that are accompanied by nerve cell damage primarily in the limbic system. In the present study, we have analyzed the temporal profile of the expression of the cytokines interleukin‐1β (IL‐1β) and IL‐1 receptor antagonist (IL‐1ra), and the related IL‐1β‐converting enzyme (ICE/caspase‐1), in different regions of the rat brain in response to peripheral kainic acid administration (10 mg/kg, i.p.). In situ hybridization histochemistry experiments revealed that IL‐1β mRNA–expressing cells, morphologically identified as microglial cells, were mainly localized to regions showing pronounced neuronal degeneration; hippocampus, thalamus, amygdala, and certain cortical regions. The strongest expression of IL‐1β mRNA was observed after 12 hr in these regions. A weak induction of the IL‐1β mRNA expression was observed already at 2 hr. Similar results were obtained by RT‐PCR analysis, showing a significantly increased expression of IL‐1β mRNA in the hippocampus and amygdala after 12 hr. In addition, RT‐PCR analysis revealed that IL‐1ra mRNA, and specifically mRNA encoding the secreted isoform of IL‐1ra (sIL‐1ra), was strongly induced in the hippocampus and amygdala at 12 and 24 hr post‐injection. RT‐PCR analysis of mRNA encoding caspase‐1 showed a significantly increased expression in the amygdala after 12 hr. In conclusion, in response to systemic kainic acid injection IL‐1β mRNA is rapidly induced and followed by induction of IL‐1ra mRNA and caspase‐1 mRNA, supporting a role of the IL‐1 system in the inflammatory response during excitotoxic damage. J. Neurosci. Res. 60:266–279, 2000

Kainic acid induced expression of interleukin-1 receptor antagonist mRNA in the rat brain

The endogenous interleukin-1 receptor antagonist (IL-1ra), a protein with partial homology with the proinflammatory cytokine interleukin-1beta (IL-1beta), prevents binding of IL-1beta to the signalling receptor. Exogenous IL-1ra has been shown to reduce the neuronal damage occurring after excitotoxic amino acid administration and ischemia. In the present study, in situ hybridization histochemistry was employed to investigate the regulation of endogenous IL-1ra mRNA expression in the rat brain after peripheral administration of kainic acid (10 mg/kg). IL-1ra mRNA expression was markedly induced in the hippocampus, thalamus, amygdala, piriform cortex, perirhinal cortex, entorhinal cortex, and to a lesser extent in the hypothalamus, and parietal and temporal cortex. The expression was first detected at 5 h after the kainic acid administration and it was markedly increased at 24 h. No signal was detected at 4 days after the injection. The majority of the cells expressing IL-1ra mRNA displayed the morphological characteristics of microglia. Expression of IL-1ra mRNA in neurons occurred mainly in the piriform and perirhinal cortex. The distribution pattern of IL-1ra mRNA expressing microglia-like cells was similar to that of cells labelled with ED1, a marker for activated microglia. The induction of IL-1ra mRNA expression may represent an endogenous response to balance IL-1 receptor mediated activity in the brain following kainic acid administration, conceivably to elicit neuroprotective and/or antiinflammatory effects.

Aircraft noise and incidence of hypertension—Gender specific effects

Recent studies show associations between aircraft noise and cardiovascular outcomes such as hypertension. However, these studies were mostly cross-sectional and there are uncertainties regarding potential gender differences as well as sensitive subgroups. In this study, we investigated the cumulative incidence of hypertension in relation to aircraft noise exposure among Swedish men and women living in Stockholm County. A total of 4721 subjects, aged 35-56 at baseline, were followed for 8-10 years. The population was selected according to family history of diabetes, which was present for half of the subjects. The exposure assessment was performed by geographical information systems and based on residential history during the period of follow-up. Blood pressure was measured at baseline and at the end of follow-up. Additional information regarding diagnosis and treatment of hypertension as well as various lifestyle factors was provided by questionnaires. In the overall population, no increased risk for hypertension was found among subjects exposed to aircraft noise ≥ 50 dB(A) L(den); relative risk (RR) 1.02 (95% CI 0.90-1.15). When restricting the cohort to those not using tobacco at the blood pressure measurements, a significant risk increase per 5 dB(A) of aircraft noise exposure was found in men; RR 1.21 (1.05-1.39), but not in women; RR 0.97 (0.83-1.13). In both sexes combined, an increased risk of hypertension related to aircraft noise exposure was indicated primarily among those reporting annoyance to aircraft noise; RR 1.42 (1.11-1.82). No consistent effect modification was detected for any of the cardiovascular risk factors under investigation although a family history of diabetes appeared to modify the risk in women. In conclusion, the results suggest an increased risk of hypertension following long-term aircraft noise exposure in men, and that subjects annoyed by aircraft noise may be particularly sensitive to noise related hypertension.

Long-term aircraft noise exposure and body mass index, waist circumference, and type 2 diabetes: a prospective study.

Background: Long-term aircraft noise exposure may increase the risk of cardiovascular disease, but no study has investigated chronic effects on the metabolic system. Objectives: The aim of this study was to investigate effects of long-term aircraft noise exposure on body mass index (BMI), waist circumference, and type 2 diabetes. Furthermore, we explored the modifying effects of sleep disturbance. Methods: This prospective cohort study of residents of Stockholm County, Sweden, followed 5,156 participants with normal baseline oral glucose tolerance tests (OGTT) for up to 10 years. Exposure to aircraft noise was estimated based on residential history. Information on outcomes and confounders was obtained from baseline and follow-up surveys and examinations, and participants who developed prediabetes or type 2 diabetes were identified by self-reported physician diagnosis or OGTT at follow-up. Adjusted associations were assessed by linear, logistic, and random-effects models. Results: The mean (± SD) increases in BMI and waist circumference during follow-up were 1.09 ± 1.97 kg/m2 and 4.39 ± 6.39 cm, respectively. The cumulative incidence of prediabetes and type 2 diabetes was 8% and 3%, respectively. Based on an ordinal noise variable, a 5-dB(A) increase in aircraft noise was associated with a greater increase in waist circumference of 1.51 cm (95% CI: 1.13, 1.89), fully adjusted. This association appeared particularly strong among those who did not change their home address during the study period, which may be a result of lower exposure misclassification. However, no clear associations were found for BMI or type 2 diabetes. Furthermore, sleep disturbances did not appear to modify the associations with aircraft noise. Conclusions: Long-term aircraft noise exposure may be linked to metabolic outcomes, in particular increased waist circumference. Citation: Eriksson C, Hilding A, Pyko A, Bluhm G, Pershagen G, Östenson CG. 2014. Long-term aircraft noise exposure and body mass index, waist circumference, and type 2 diabetes: a prospective study. Environ Health Perspect 122:687–694; http://dx.doi.org/10.1289/ehp.1307115

Exposure to traffic noise and markers of obesity

Objectives Limited evidence suggests adverse effects of traffic noise exposure on the metabolic system. This study investigates the association between road traffic noise and obesity markers as well as the role of combined exposure to multiple sources of traffic noise. Methods In a cross-sectional study performed in 2002–2006, we assessed exposure to noise from road traffic, railways and aircraft at the residences of 5075 Swedish men and women, primarily from suburban and semirural areas of Stockholm County. A detailed questionnaire and medical examination provided information on markers of obesity and potential confounders. Multiple linear and logistic regression models were used to assess associations between traffic noise and body mass index (BMI), waist circumference and waist–hip ratio using WHO definitions of obesity. Results Road traffic noise was significantly related to waist circumference with a 0.21 cm (95% CI 0.01 to 0.41) increase per 5 dB(A) rise in Lden. The OR for central obesity among those exposed to road traffic noise ≥45 dB(A) was 1.18 (95% CI 1.03 to 1.34) in comparison to those exposed below this level. Similar results were seen for waist–hip ratio (OR 1.29; 95% CI 1.14 to 1.45) but not for BMI (OR 0.89; 95% CI 0.76 to 1.04). Central obesity was also associated with exposure to railway and aircraft noise, and a particularly high risk was seen for combined exposure to all three sources of traffic noise (OR 1.95; 95% CI 1.24 to 3.05). Conclusions Our results suggest that traffic noise exposure can increase the risk of central obesity. Combined exposure to different sources of traffic noise may convey a particularly high risk.

Inhibition of kainic acid induced expression of interleukin-1β and interleukin-1 receptor antagonist mRNA in the rat brain by NMDA receptor antagonists

The cytokines interleukin-1 beta (IL-1 beta) and IL-1 receptor antagonist (IL-1ra) are rapidly induced in response to excitotoxic and ischemic brain damage. The aim of the present study was to investigate the influence of a non-competitive (dizocilpine maleate, MK-801) and a competitive ((R)-CPP) NMDA receptor antagonist on the transient cytokine expression in the rat brain induced by systemic kainic acid administration. Peripheral administration of kainic acid (10 mg/kg, i.p.) results in a transient expression of IL-1 beta and IL-1ra mRNA, mainly in microglia, in regions showing neurodegeneration such as the hippocampus, thalamus, amygdala, and certain cortical regions. In addition, a few neurons expressing IL-1ra mRNA were observed in the piriform cortex and amygdala following kainic acid injection. Administration of MK-801 (i.p.) 1 h prior to kainic acid injection reduced cytokine expression in all of these regions. MK-801 at 3.0 mg/kg decreased the IL-1 beta mRNA expression, blocked or decreased the IL-1ra mRNA expression, depending on the brain region. MK-801 at 5.0 mg/kg abolished IL-1ra mRNA expression in all of the regions, whereas the IL-1 beta mRNA expression was decreased or blocked, depending on the brain region, or the time point investigated. Peripheral administration of (R)-CPP (15 mg/kg, i.p.) 15 min prior to the kainic acid injection abolished the IL-1 beta mRNA expression. The IL-1ra mRNA expression was abolished in all regions except for a few neurons in the piriform cortex. The finding that NMDA receptor antagonists inhibit the IL-1 beta and IL-1ra mRNA synthesis induced by kainic acid suggests that NMDA receptor activation may be involved in triggering cytokine synthesis following excitotoxic brain damage.

Cardiovascular effects of environmental noise: Research in Sweden

In Sweden, as in many other European countries, traffic noise is an important environmental health issue. At present, almost two million people are exposed to average noise levels exceeding the outdoor national guideline value (55 dB(A)). Despite efforts to reduce the noise burden, noise-related health effects, such as annoyance and sleep disturbances, are increasing. The scientific interest regarding more serious health effects related to the cardiovascular system is growing, and several experimental and epidemiological studies have been performed or are ongoing. Most of the studies on cardiovascular outcomes have been related to noise from road or aircraft traffic. Few studies have included railway noise. The outcomes under study include morning saliva cortisol, treatment for hypertension, self-reported hypertension, and myocardial infarction. The Swedish studies on road traffic noise support the hypothesis of an association between long-term noise exposure and cardiovascular disease. However, the magnitude of effect varies between the studies and has been shown to depend on factors such as sex, number of years at residence, and noise annoyance. Two national studies have been performed on the cardiovascular effects of aircraft noise exposure. The first one, a cross-sectional study assessing self-reported hypertension, has shown a 30% risk increase per 5 dB(A) noise increase. The second one, which to our knowledge is the first longitudinal study assessing the cumulative incidence of hypertension, found a relative risk (RR) of 1.10 (95% CI 1.01 - 1.19) per 5 dB(A) noise increase. No associations have been found between railway noise and cardiovascular diseases. The findings regarding noise-related health effects and their economic consequences should be taken into account in future noise abatement policies and community planning.