Controlled exposure to particulate matter from urban street air is associated with decreased vasodilation and heart rate variability in overweight and older adults

BACKGROUND: Exposure to particulate matter (PM) is generally associated with elevated risk of cardiovascular morbidity and mortality. Elderly and obese subjects may be particularly susceptible, although short-term effects are poorly described. METHODS: Sixty healthy subjects (25 males, 35 females, age 55 to 83 years, body mass index > 25 kg/m(2)) were included in a cross-over study with 5 hours of exposure to particle- or sham-filtered air from a busy street using an exposure-chamber. The sham- versus particle-filtered air had average particle number concentrations of ~23.000 versus ~1800/cm(3) and PM(2.5) levels of 24 versus 3μg/m(3), respectively. The PM contained similar fractions of elemental and black carbon (~20-25%) in both exposure scenarios. Reactive hyperemia and nitroglycerin-induced vasodilation in finger arteries and heart rate variability (HRV) measured within 1 h after exposure were primary outcomes. Potential explanatory mechanistic variables included markers of oxidative stress (ascorbate/dehydroascorbate, nitric oxide-production cofactor tetrahydrobiopterin and its oxidation product dihydrobiopterin) and inflammation markers (C-reactive protein and leukocyte differential counts). RESULTS: Nitroglycerin-induced vasodilation was reduced by 12% [95% confidence interval: −22%; −1.0%] following PM exposure, whereas hyperemia-induced vasodilation was reduced by 5% [95% confidence interval: −11.6%; 1.6%]. Moreover, HRV measurements showed that the high and low frequency domains were significantly decreased and increased, respectively. Redox and inflammatory status did not change significantly based on the above measures. CONCLUSIONS: This study indicates that exposure to real-life levels of PM from urban street air impairs the vasomotor function and HRV in overweight middle-aged and elderly adults, although this could not be explained by changes in inflammation, oxidative stress or nitric oxide-cofactors. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12989-015-0081-9) contains supplementary material, which is available to authorized users

Health effects of residential wood smoke particles: the importance of combustion conditions and physicochemical particle properties

Background: Residential wood combustion is now recognized as a major particle source in many developed countries, and the number of studies investigating the negative health effects associated with wood smoke exposure is currently increasing. The combustion appliances in use today provide highly variable combustion conditions resulting in large variations in the physicochemical characteristics of the emitted particles. These differences in physicochemical properties are likely to influence the biological effects induced by the wood smoke particles. Outline: The focus of this review is to discuss the present knowledge on physicochemical properties of wood smoke particles from different combustion conditions in relation to wood smoke-induced health effects. In addition, the human wood smoke exposure in developed countries is explored in order to identify the particle characteristics that are relevant for experimental studies of wood smoke-induced health effects. Finally, recent experimental studies regarding wood smoke exposure are discussed with respect to the applied combustion conditions and particle properties. Conclusion: Overall, the reviewed literature regarding the physicochemical properties of wood smoke particles provides a relatively clear picture of how these properties vary with the combustion conditions, whereas particle emissions from specific classes of combustion appliances are less well characterised. The major gaps in knowledge concern; (i) characterisation of the atmospheric transformations of wood smoke particles, (ii) characterisation of the physicochemical properties of wood smoke particles in ambient and indoor environments, and (iii) identification of the physicochemical properties that influence the biological effects of wood smoke particles

Low-level exposure to lead, blood pressure, and hypertension in a population-based cohort.

Abstract Background Environmental lead exposure is a possible causative factor for increased blood pressure and hypertension, but large studies at low-level exposure are scarce, and results inconsistent. Objective We aimed to examine the effects of environmental exposure to lead in a large population-based sample. Methods We assessed associations between blood lead and systolic/diastolic blood pressure and hypertension in 4452 individuals (46–67 years) living in Malmo, Sweden, in 1991–1994. Blood pressure was measured using a mercury sphygmomanometer after 10 min supine rest. Hypertension was defined as high systolic (≥140 mmHg) or diastolic (≥90 mmHg) blood pressure and/or current use of antihypertensive medication. Blood lead was calculated from lead in erythrocytes and haematocrit. Multivariable associations between blood lead and blood pressure or hypertension were assessed by linear and logistic regression. Two-thirds of the cohort was re-examined 16 years later. Results At baseline, mean blood pressure was 141/87 mmHg, 16% used antihypertensive medication, 63% had hypertension, and mean blood lead was 28 µg/L. Blood lead in the fourth quartile was associated with significantly higher systolic and diastolic blood pressure (point estimates: 1–2 mmHg) and increased prevalence of hypertension (odds ratio: 1.3, 95% confidence interval: 1.1–1.5) versus the other quartiles after adjustment for sex, age, smoking, alcohol, waist circumference, and education. Associations were also significant with blood lead as a continuous variable. Blood lead at baseline, having a half-life of about one month, was not associated with antihypertensive treatment at the 16-year follow-up. Conclusions Low-level lead exposure increases blood pressure and may increase the risk of hypertension

Detailed diesel exhaust characteristics including particle surface area and lung deposited dose for better understanding of health effects in human chamber exposure studies.

Several diesel exhaust (DE) characteristics, comprising both particle and gas phase, recognized as important when linking with health effects, are not reported in human chamber exposure studies. In order to understand effects of DE on humans there is a need for better characterization of DE when performing exposure studies. The aim of this study was to determine and quantify detailed DE characteristics during human chamber exposure. Additionally to compare to reported DE properties in conducted human exposures. A wide battery of particle and gas phase measurement techniques have been used to provide detailed DE characteristics including the DE particles (DEP) surface area, fraction and dose deposited in the lungs, chemical composition of both particle and gas phase such as NO, NO2, CO, CO2, volatile organic compounds (including aldehydes, benzene, toluene) and polycyclic aromatic hydrocarbons (PAHs). Eyes, nose and throat irritation effects were determined. Exposure conditions with PM1 (<1 mm) mass concentration 280 mg m3, number concentration 4 105 cm3 and elemental to total carbon fraction of 82% were generated from a diesel vehicle at idling. When estimating the lung deposited dose it was found that using the size dependent effective density (in contrast to assuming unity density) reduced the estimated respiratory dose by 132% by mass. Accounting for agglomerated structure of DEP prevented underestimation of lung deposited dose by surface area by 37% in comparison to assuming spherical particles. Comparison of DE characteristics reported in conducted chamber exposures showed that DE properties vary to a great extent under the same DEP mass concentration and engine load. This highlights the need for detailed and standardized approach for measuring and reporting of DE properties. Eyes irritation effects, most probably caused by aldehydes in the gas phase, as well as nose irritation were observed at exposure levels below current occupational exposure limit values given for exhaust fumes. Reporting detailed DE characteristics that include DEP properties (such as mass and number concentration, size resolved information, surface area, chemical composition, lung deposited dose by number, mass and surface) and detailed gas phase including components known for their carcinogenic and irritation effect (e.g. aldehydes, benzene, PAHs) can help in determination of key parameters responsible for observed health effects and comparison of chamber exposure studies

The effect of secondary inorganic aerosols, soot and the geographical origin of air mass on acute myocardial infarction hospitalisations in Gothenburg, Sweden during 1985 - 2010 : a case-crossover study

BACKGROUND: The relative importance of different sources of air pollution for cardiovascular disease is unclear. The aims were to compare the associations between acute myocardial infarction (AMI) hospitalisations in Gothenburg, Sweden and 1) the long-range transported (LRT) particle fraction, 2) the remaining particle fraction, 3) geographical air mass origin, and 4) influence of local dispersion during 1985–2010. METHODS : A case-crossover design was applied using lag0 (the exposure the same day as hospitalisation), lag1 (exposure one day prior hospitalisation) and 2-day cumulative average exposure (CA2) (mean of lag0 and lag1). The LRT fractions included PMion (sum of sulphate, nitrate and ammonium) and soot measured at a rural site. The difference between urban PM10 (particulate matter with an aerodynamic diameter smaller than 10 μm) and rural PMion was a proxy for locally generated PM10 (PMrest). The daily geographical origin of air mass was estimated as well as days with limited or effective local dispersion. The entire year was considered, as well as warm and cold periods, and different time periods. RESULTS : In total 28 215 AMI hospitalisations occurred during 26 years. PM10, PMion, PMrest and soot did not influence AMI for the entire year. In the cold period, the association was somewhat stronger for PMrest than for urban PM10; the strongest associations were observed during 1990–2000 between AMI and CA2 of PMrest (6.6% per inter-quartile range (IQR), 95% confidence interval 2.1 to 11.4%) and PM10 (4.1%, 95% CI 0.2% − 8.2%). Regarding the geographical air mass origins there were few associations. Days with limited local dispersion showed an association with AMI in the cold period of 2001–2010 (6.7%, 95% CI 0.0% − 13.0%). CONCLUSIONS : In the cold period, locally generated PM and days with limited local dispersion affected AMI hospitalisations, indicating importance of local emissions from e.g. traffic.The Swedish Research Council Formas funded the study.http://www.ehjournal.netam201

Wood smoke particles from different combustion phases induce similar pro-inflammatory effects in a co-culture of monocyte and pneumocyte cell lines

Background Exposure to particulate matter (PM) has been linked to several adverse cardiopulmonary effects, probably via biological mechanisms involving inflammation. The pro-inflammatory potential of PM depends on the particles’ physical and chemical characteristics, which again depend on the emitting source. Wood combustion is a major source of ambient air pollution in Northern countries during the winter season. The overall aim of this study was therefore to investigate cellular responses to wood smoke particles (WSPs) collected from different phases of the combustion cycle, and from combustion at different temperatures. Results WSPs from different phases of the combustion cycle induced very similar effects on pro-inflammatory mediator release, cytotoxicity and cell number, whereas WSPs from medium-temperature combustion were more cytotoxic than WSPs from high-temperature incomplete combustion. Furthermore, comparisons of effects induced by native WSPs with the corresponding organic extracts and washed particles revealed that the organic fraction was the most important determinant for the WSP-induced effects. However, the responses induced by the organic fraction could generally not be linked to the content of the measured polycyclic aromatic hydrocarbons (PAHs), suggesting that also other organic compounds were involved. Conclusion The toxicity of WSPs seems to a large extent to be determined by stove type and combustion conditions, rather than the phase of the combustion cycle. Notably, this toxicity seems to strongly depend on the organic fraction, and it is probably associated with organic components other than the commonly measured unsubstituted PAHs

Variability of Urinary Creatinine in Healthy Individuals

Many urinary biomarkers are adjusted for dilution using creatinine or specific gravity. The aim was to evaluate the variability of creatinine excretion, in 24 h and spot samples, and to describe an openly available variability biobank. Urine and blood samples were collected from 60 healthy non-smoking adults, 29 men and 31 women. All urine was collected at six time points during two 24 h periods. Blood samples were also collected twice and stored frozen. Analyses of creatinine in urine was performed in fresh urine using an enzymatic method. For creatinine in urine, the intra-class correlation (ICC) was calculated for 24 h urine and spot samples. Diurnal variability was examined, as well as association with urinary flow rate. The creatinine excretion rate was lowest in overnight samples and relatively constant in the other five samples. The creatinine excretion rate in each individual was positively correlated with urinary flow rate. The creatinine concentration was highest in the overnight sample and at 09:30. For 24 h samples the ICC was 0.64, for overnight samples it was 0.5, and for all spot samples, it was much lower. The ICC for urinary creatinine depends on the time of day of sampling. Frozen samples from this variability biobank are open for researchers examining normal variability of their favorite biomarker(s)

Low-level exposure to lead, cadmium and mercury, and histopathological findings in kidney biopsies

Background: Lead (Pb), cadmium (Cd) and mercury (Hg) are all nephrotoxic metals, and a large part of the body burden of Cd and Hg is found in the kidneys. There are, however, few studies on associations between exposure to these toxic metals and renal biopsy findings, and none at low-level exposure. Aim: To examine the hypothesis that low-level concentration of Pb, Cd or Hg in the kidneys is associated with histopathological changes in the kidneys. Methods: We determined concentrations of Pb, Cd and Hg in kidney, blood and urine in 109 healthy kidney donors, aged 24–70 years. The renal biopsies were scored according to the Banff classification regarding tubular atrophy, interstitial fibrosis, glomerulosclerosis, arteriosclerosis, and arteriolohyalinosis. Kidney function was assessed based on glomerular filtration rate (GFR) as well as urinary excretion of albumin, low molecular weight proteins, kidney injury molecule 1 and N-acetylglucose aminidase. Associations between metal concentrations and histopathological changes, were assessed in models also including age, sex and smoking. Results: The median kidney concentrations of Pb, Cd and Hg were 0.08, 13 and 0.21 μg/g, respectively. There were signs of tubular atrophy in 63%, interstitial fibrosis in 21%, glomerulosclerosis in 71%, arteriosclerosis in 47%, and arteriolohyalinosis in 36% of the donors, but, as could be expected, the histopathological findings were limited, mostly Banff grade 1. In models adjusted for age, sex and smoking, kidney Cd was positively associated with tubular atrophy (p = 0.03) and possibly with arteriolohyalinosis (p = 0.06). Kidney Hg was associated with arteriosclerosis (p = 0.004). Discussion and conclusions: The results suggest that even low levels of Cd in the kidney can induce a mild degree of tubular atrophy. This is in line with previous findings at high-level Cd exposure. The association between kidney Hg and renal arteriosclerosis was unexpected, and may be a chance finding