Lars Barregard

Ambient Air Pollution Exposure Estimation for the Global Burden of Disease 2013.

Exposure to ambient air pollution is a major risk factor for global disease. Assessment of the impacts of air pollution on population health and evaluation of trends relative to other major risk factors requires regularly updated, accurate, spatially resolved exposure estimates. We combined satellite-based estimates, chemical transport model simulations, and ground measurements from 79 different countries to produce global estimates of annual average fine particle (PM2.5) and ozone concentrations at 0.1° × 0.1° spatial resolution for five-year intervals from 1990 to 2010 and the year 2013. These estimates were applied to assess population-weighted mean concentrations for 1990-2013 for each of 188 countries. In 2013, 87% of the worlds population lived in areas exceeding the World Health Organization Air Quality Guideline of 10 μg/m(3) PM2.5 (annual average). Between 1990 and 2013, global population-weighted PM2.5 increased by 20.4% driven by trends in South Asia, Southeast Asia, and China. Decreases in population-weighted mean concentrations of PM2.5 were evident in most high income countries. Population-weighted mean concentrations of ozone increased globally by 8.9% from 1990-2013 with increases in most countries-except for modest decreases in North America, parts of Europe, and several countries in Southeast Asia.

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

BackgroundResidential 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.OutlineThe 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.ConclusionOverall, 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.

Experimental exposure to wood-smoke particles in healthy humans : Effects on markers of inflammation, coagulation, and lipid peroxidation

Particulate air pollution is known to increase cardiovascular morbidity and mortality. Proposed mechanisms underlying this increase include effects on inflammation, coagulation factors, and oxidative stress, which could increase the risk of coronary events and atherosclerosis. The aim of this study was to examine whether short-term exposure to wood smoke affects markers of inflammation, blood hemostasis, and lipid peroxidation in healthy humans. Thirteen subjects were exposed to wood smoke and clean air in a chamber during two 4-h sessions, 1 wk apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95,000–180,000/cm3. About half of the particles were ultrafine (< 100 nm). Blood and urine samples were taken before and after the experiment. Exposure to wood smoke increased the levels of serum amyloid A, a cardiovascular risk factor, as well as factor VIII in plasma and the factor VIII/von Willebrand factor ratio, indicating a slight effect on the balance of coagulation factors. Moreover, there was an increased urinary excretion of free 8-iso-prostaglandin2α, a major F2-isoprostane, though this was based on nine subjects only, indicating a temporary increase in free radical-mediated lipid peroxidation. Thus, wood-smoke particles at levels that can be found in smoky indoor environments seem to affect inflammation, coagulation, and possibly lipid peroxidation. These factors may be involved in the mechanisms whereby particulate air pollution affects cardiovascular morbidity and mortality. The exposure setup could be used to establish which particle characteristics are critical for the effects.

Experimental exposure to wood smoke: effects on airway inflammation and oxidative stress

Background: Particulate air pollution affects cardiovascular and pulmonary disease and mortality. A main hypothesis about the mechanisms involved is that particles induce inflammation in lower airways, systemic inflammation and oxidative stress. Objectives: To examine whether short-term exposure to wood smoke in healthy subjects affects markers of pulmonary inflammation and oxidative stress. Methods: 13 subjects were exposed first to clean air and then to wood smoke in a chamber during 4-hour sessions, 1 week apart. The mass concentrations of fine particles at wood smoke exposure were 240–280 μg/m3, and number concentrations were 95 000–180 000/cm3, about half of the particles being ultrafine (<100 nm). Blood and breath samples were taken before and at various intervals after exposure to wood smoke and clean air and examined for exhaled nitric oxide and Clara cell protein in serum and urine, and malondialdehyde in exhaled breath condensate. Results: Exposure to wood smoke increased alveolar nitric oxide 3 hours post-exposure while malondialdehyde levels in breath condensate were higher both immediately after and 20 hours after exposure. Serum Clara cell protein was increased 20 hours after exposure. Conclusions: Wood smoke at levels that can be found in smoky indoor environments caused an inflammatory response and signs of increased oxidative stress in the respiratory tract, especially in the lower airways.

The prevalence of demarcated opacities in permanent first molars in a group of Swedish children

The permanent teeth of 516 7- and 8-year-old Swedish children from a low-fluoride area were examined for developmental enamel defects. Special attention was paid to demarcated opacities in permanent first molars and permanent incisors (MIH). The examination was done in their schools, using a portable light, a mirror, and a probe. The modified DDE index of 1992 was used for recording the enamel defects, supplemented with a further classification into severe, moderate, and mild defects. Demarcated opacities in permanent first molars were present in 18.4% of the children. The mean number of hypomineralized teeth of the affected children was 3.2 (standard deviation, 1.8), of which 2.4 were first molars. Of the children 6.5% had severe defects, 5% had moderate defects, whereas 7% had only mildly hypomineralized teeth. In conclusion, hypomineralized first molars appeared to be common and require considerable treatment in the Swedish child population.

Long-term Use of Nicotine Chewing Gum and Mercury Exposure from Dental Amalgam Fillings

In experimental studies, chewing gum has been shown to increase the release rate of mercury vapor from dental amalgam fillings. The aim of the present study was to investigate the influence of long-term frequent chewing on mercury levels in plasma and urine. Mercury levels in plasma (P-Hg) and urine (U-Hg), and urinary cotinine were examined in 18 subjects who regularly used nicotine chewing gum, and in 19 referents. Age and number of amalgam surfaces were similar in the two groups. Total mercury concentrations in plasma and urine were determined by means of cold vapor atomic absorption spectrometry. Urinary cotinine was determined by gas chromatography-mass spectrometry. The chewers had been using 10 (median) pieces of gum per day for the past 27 (median) months. P-Hg and U-Hg levels were significantly higher in the chewers (27 nmol/L and 6.5 nmol/mmol creatinine) than in the referents (4.9 nmol/L and 1.2 nmol/mmol creatinine). In both groups, significant correlations were found between P-Hg or U-Hg on the one hand and the number of amalgam surfaces on the other. In the chewers, no correlations were found between P-Hg or U-Hg and chewing time per day or cotinine in urine. Cotinine in urine increased with the number of pieces of chewing gum used. The impact of excessive chewing on mercury levels was considerable.

Validity of self-reports of hand eczema.

The validity of questionnaire answers with respect to hand eczema was investigated. Car mechanics, dentists and office workers answered a questionnaire on the occurrence of hand eczema on any occasion during the past 12 months. “Yes”‐responders and a random sample of “no”‐responders were subsequently interviewed and examined by a dermatologist. 10.0% of the car mechanics, 12.0% of the dentists and 12.5% of the office workers were found to have hand eczema despite previous “no”‐answers. In the same populations, 81%, 94% and 80% of the “yes”‐answers were confirmed at the clinical examination. Considering false‐negative and false‐positive answers, the sensitivity was 53–59% and the specificity 96–99% in the 3 groups. The 1‐year prevalence changed from self‐reported 15% to estimated 21% in the car mechanics, from 15% to 24% in the dentists and from 15% to 23% in the office workers. It is concluded that self‐reported 1‐year prevalence of hand eczema considerably underestimates the true prevalence.

Exposure to Mercury Vapor and Impact on Health in the Dental Profession in Sweden

Possible adverse effects of mercury exposure in dentistry have been discussed in several studies. The objective of the present study was to carry out detailed measurements of mercury exposure in the dental profession in Sweden, and to search for adverse health effects from such exposure. We examined 22 dentists and 22 dental nurses, working in teams, at six Swedish dental clinics. Measurements of air mercury, performed with personal, active air samplers, showed a median air Hg of 1.8 μg/m3 for the dentists, and 2.1 μg/m 3 for the dental nurses. Spot measurements with a direct reading instrument displayed temporarily elevated air Hg, especially during the preparation and application of amalgam. The average concentration of mercury in whole blood (B-Hg) was 18 nmol/L, in plasma (P-Hg) 5.1 nmol/L, and in urine (U-Hg) 3.0 nmol/mmol creatinine. Possible effects on the central nervous system (CNS) were registered with three questionnaires: Q16, Eysenck Personality Inventory (EPI), and the Profile of Mood Scales (POMS). In the Q16, the number of symptoms was statistically significantly higher in the dentistry group compared with an age- and gender-matched control group (n = 44). The urinary excretion of albumin and urinary activity of the tubular enzyme N-acetyl-β-glucose-aminidase (NAG) did not differ between the two groups. The results confirm that exposure to mercury in the dental profession in Sweden is low. The air Hg levels were mainly influenced by the method of amalgam preparation and inserting, and by the method of air evacuation during drilling and polishing.

Contact allergy and hand eczema in Swedish dentists

Hand eczema and contact allergy in Swedish dentists were studied in a multidisciplinary project. The aims of the study were to establish diagnoses, to investigate the occurrence of contact allergy, in particular to (meth)acrylates, and to evaluate certain consequences of hand eczema. A postal questionnaire on skin symptoms, atopy and occupational experience was mailed to 3500 dentists aged <65 years, and licensed 1965–1995. The response rate was 88%. Among dentists living in 3 major cities, 14.9% (n=191) reported hand eczema during the previous year. They were invited to a clinical examination, including patch testing with a standard and a dental series. 158/191 (83%) dentists attended, and hand eczema diagnosis was confirmed in 149/158 (94%). Irritant contact dermatitis was diagnosed in 67% and allergic contact dermatitis in 28%. On patch testing, 50% presented at least 1 positive reaction. The most frequent allergens were nickel sulfate, fragrance mix, gold sodium thiosulfate and thiuram mix. 7 (5%) had positive reactions to (meth)acrylates, all to 2‐hydroxyethyl methacrylate and 6 also to ethyleneglycol dimethacrylate. 38% had consulted a physician, 4% had been on sick‐leave and 1% had changed occupational tasks due to hand eczema. No dentist with allergy to acrylates had been on sick‐leave or changed occupation. It is concluded that dentistry is a high‐risk occupation for hand eczema, and that irritant contact dermatitis is most common. The prevalence of contact allergy to acrylates was below 1% in the population of responding dentists, and in most cases did not have serious medical, social or occupational consequences.

Risk of hypertension from exposure to road traffic noise in a population-based sample

Objectives: To assess the association between hypertension and traffic noise. Methods: The prevalence and incidence of hypertension were examined in a Swedish municipality partly affected by noise from a highway (20 000 vehicles/24 h) and a railway (200 trains/24 h). A-weighed 24 h average sound levels (LAeq,24h) from road and railway traffic were calculated at each residential building using a geographical information system and a validated model. Physician-diagnosed hypertension, antihypertensive medication and background factors were evaluated in 1953 individuals using postal questionnaires (71% response rate). Prevalence ratios and odds ratios (ORs) were calculated for different noise categories. Based on year of moving into the residence and year of diagnosis, person-years and incidence rates of hypertension were estimated, as well as relative risks including covariates, using Poisson and Cox regression. Results: When road traffic noise, age, sex, heredity and body mass index were included in logistic regression models, and allowing for >10 years of latency, the OR for hypertension was 1.9 (95% CI 1.1 to 3.5) in the highest noise category (56−70 dBA) and 3.8 (95% CI 1.6 to 9.0) in men. The incidence rate ratio was increased in this group of men, and the relative risk of hypertension in a Poisson regression model was 2.9 (95% CI 1.4 to 6.2). There were no clear associations in women or for railway noise. Conclusions: The study shows a positive association between residential road traffic noise and hypertension among men, and an exposure–response relationship. While prevalence ratios were increased, findings were more pronounced when incidence was assessed.