Lower respiratory disease (LRD) is a common cause of hospitalization in infants, and episodes of obstructive LRD increase the risk for asthma later in life. The purpose of this study was to assess time trends and geographical variation of first time hospitalization for LRD among children in Stockholm County, Sweden. Data on first time admittance for LRD among children aged up to 5 yrs from 1973 through 1992 were obtained from the Stockholm County Council hospital discharge register, and population register data were used for estimation of the population at risk. Municipal data were available for 1982-1992 on outbreaks of respiratory syncytial virus (RSV) infections and socio-economic factors. A total of 12,450 children had been hospitalized for the first time with LRD. For children aged
In Stockholm, Sweden, 17 children with newly diagnosed sensitization to house-dust mites (HDM) and 11 children with previously diagnosed HDM-sensitization were included in a study of HDM-allergen avoidance. Mattress dust was collected on repeated occasions during 18 months and assayed for concentration of major HDM allergens. During the first 12 months, the parents of the intervention group were instructed to intensify cleaning and airing of the child's bedroom. During the last 6 months of the study, the mattresses and pillows of seven children in the intervention group and sibling controls were encased in semipermeable polyurethane covers. The homes exhibited a high absolute indoor humidity throughout the year, and even during the winter the mean levels exceeded 7 g/kg. No mite allergen reduction was seen in the intervention group during the first year. However, among the newly diagnosed HDM-sensitized children, there was a mean reduction of the mattress mite allergen concentration of 83% (P = 0.02), and this was most pronounced in the homes with low humidity. At the end of the mattress encasement period, an average difference of 98% (P
Factors favoring sensitization to house dust mites (HDM) were studied in a cold, temperate climate in northern Sweden. Sixty-five children previously found to react positively to a skin prick test (SPT) to HDM were included. The SPT to HDM was repeated, and serum IgE antibodies to D. pteronyssinus and D. farinae were determined. HDM, Euroglyphus maynei, Tarsonemus, or storage mites occurred in mattress dust samples from 23 of the 65 homes, and in 10 homes more than 100 HDM/g of mattress dust were found. Mites were more prevalent in mattress dust from the basement and ground levels than from the upper floors. Sensitization to HDM was strongly with the presence of domestic mites in mattress and floor dust. Previous longer stays in southern Sweden or Europe were also associated with present sensitization to HDM, and this was independent of occurrence of mites in the residence. The results indicate that HDM growth and potential for sensitization in cold, temperate regions is highly dependent on the microhabitat, and that sensitization to HDM should be possible to prevent in such climatic regions.
Lung cancer risk in relation to indoor radon was examined in three case-control studies in Stockholm (Sweden), New Jersey (United States), and Shenyang (People's Republic of China). Year-long measurements of radon gas were made in current and past homes of 966 women who developed lung cancer and of 1,158 control women, included in the combined analysis. Nearly 14 percent of the participants were estimated to have a time-weighted, mean, radon concentration in their homes of more than 4 pCi/l (150 Bq/m3) during the period from five to 35 years prior to the date of lung cancer diagnosis (or comparable date for controls). There was a tendency for risk to increase with increasing levels of radon in NJ and Stockholm, but the trends for individual studies and overall were not statistically significant. The estimates of the excess relative risk for indoor exposure per pCi/l were 0.18 (95 percent [CI] = -0.04-0.70) in NJ, 0.06 (CI = -0.05-0.34) in Stockholm, and -0.02 (CI = -infinity-0.03) for Shenyang; these estimates did not differ significantly from each other. The overall excess RR per pCi/l was 0.00 (CI = -0.05-0.07); the confidence limits were sufficiently broad, however, that the overall estimate was still compatible with extrapolations of risks from miners. Cigarette smoking was the predominant cause of lung cancer with the RR significantly elevated in all studies. Within smoking categories, the trend in risk with increasing mean radon concentration was inconsistent. Analyses of data from several studies are complicated by the possibility that there may exist important differences in study bases which might affect results, and which may be controlled only partially through adjustment procedures. Future efforts to combine various residential studies will need to be attentive to the intrinsic limitations of studies to detect low levels of risk as well as the unique uncertainties associated with estimating, accurately, cumulative exposure to indoor radon.
A large epidemiologic study on residential radon exposure and lung cancer has been conducted in Sweden. An attempt is now made to quantify the impact of random error in the exposure assessment on the risk estimate for lung cancer in this study. The study included 1,360 lung cancer cases, diagnosed from 1980 to 1984, and 2,847 population controls. Radon measurements were performed in 8,992 dwellings occupied by the study subjects some time since 1947. Questionnaires provided information on smoking and other risk factors. Imprecision in the retrospective exposure assessment for radon was estimated from a Monte Carlo technique modeling Swedish conditions. Adjusted risk estimates were obtained from regression analyses based on expected values for true time-weighted average residential radon concentration (TWA), conditional on observed TWA. Without adjustment for random error in the TWA estimates, the linear excess relative risk coefficient was 0.10 per 100 Bq m(-3), but an excess relative risk of about 0.15 to 0.20 per 100 Bq m(-3) was suggested following adjustment. The potentially significant consequences of errors in the retrospective radon exposure assessment should be taken into consideration in the risk estimation as well as in comparisons of results of different studies and in future pooled analyses.
Comment In: Health Phys. 1997 Aug;73(2):3939228178
Comment In: Health Phys. 1997 Aug;73(2):394-59228179
Comment In: Health Phys. 1997 Jul;73(1):272-39199239
A specific aim of a population-based case-control study of lung cancer in Stockholm, Sweden, was to use emission data, dispersion models, and geographic information systems (GIS) to assess historical exposure to several components of ambient air pollution. Data collected for 1,042 lung cancer cases and 2,364 population controls included information on residence from 1955 to the end of follow-up for each individual, 1990-1995. We assessed ambient air concentrations of pollutants from road traffic and heating throughout the study area for three points in time (1960, 1970, and 1980) using reconstructed emission data for the index pollutants nitrogen oxides (NO(x)/NO(2)) and sulfur dioxide together with dispersion modeling. NO(2) estimates for 1980 compared well with actual measurements, but no independently measured (study-external) data were available for SO(2), precluding similar validation. Subsequently, we used linear intra- and extrapolation to obtain estimates for all other years 1955-1990. Eleven thousand individual addresses were transformed into geographic coordinates through automatic and manual procedures, with an estimated error of
This case-referent study investigated the lung cancer risk from occupational exposure to diesel exhaust, mixed motor exhaust, other combustion products, asbestos, metals, oil mist, and welding fumes. All cases of lung cancer in males aged 40-75 years among stable residents of Stockholm County, Sweden, were identified from 1985 to 1990. Referents were selected as a stratified (age, inclusion year) random sample. Information on lifetime occupational history, residency, and tobacco smoking was obtained from the study subjects or from next of kin. Response rates of 87% and 85% resulted in 1,042 cases and 2,364 referents, respectively. Occupational exposures were assessed by an occupational hygienist who coded the intensity and probability of each exposure. Risk estimates were adjusted for tobacco smoking, other occupational exposures, residential radon, and environmental exposure to traffic-related air pollution. For the highest quartile of cumulative exposure versus no exposure, the relative risk was 1.63 (95% confidence interval (CI): 1.14, 2.33) for diesel exhaust, 1.60 (95% CI: 1.09, 2.34) for combustion products, and 1.68 (95% CI: 1.15, 2.46) for asbestos. Dose-response analyses indicated an increase in lung cancer risk of 14% per fiber-year/ml for asbestos exposure. No increased risk was found for the other exposure factors. An overall attributable proportion of 9.5% (95% CI: 5.5, 13.9) was estimated for lung cancer related to diesel exhaust, other combustion products, and asbestos.
An increased risk for myocardial infarction (MI) related to environmental tobacco smoke (ETS) exposure has previously been reported, but several aspects of the association are still uncertain. We studied the MI risk associated with ETS exposure among 334 nonfatal never-smoking MI cases and 677 population controls, 45-70 years of age, in Stockholm County. A postal questionnaire with a telephone follow-up provided information on ETS exposure and other potential risk factors for MI. After adjustment for age, gender, hospital catchment area, body mass index, socioeconomic status, job strain, hypertension, diet, and diabetes mellitus, the odds ratio for MI was 1.58 (95% confidence interval = 0.97-2.56) for an average daily exposure of 20 cigarettes or more from the spouse. Combined exposure from spouse and work showed an increasing odds ratio for MI, up to 1.55 (95% confidence interval = 1.02-2.34) in the highest category of weighted duration, that is, more than 90 "hour-years" of exposure (1 "hour-year" = 365 hours, or 1 hour per day for 1 year). In addition, more recent exposure appeared to convey a higher risk. Our data confirm an increased risk of MI from exposure to ETS and suggest that intensity of spousal exposure, combined exposure from spouse and work, and time since last exposure are important.
Exposure to elevated levels of ambient air pollutants can lead to adverse cardiovascular effects. Potential mechanisms include systemic inflammation and perturbation of the coagulation balance.
To investigate long- and short-term effects of air pollution exposure on serum levels of inflammatory (IL-6, TNF-alpha and CRP) and coagulation (fibrinogen and PAI-1) markers relevant for cardiovascular pathology.
The study group consisted of a population sample of 1028 men and 508 women aged 45-70 years from Stockholm. Long-term air pollution exposure was assessed using spatial modelling of traffic-related NO(2) and heating-related SO(2) emissions at each subject's residential addresses over retrospective periods of 1, 5 and 30 years. Short-term exposure was assessed as averages of rooftop measurements over 12-120 h before blood sampling.
Long-term exposures to both traffic-NO(2) and heating-SO(2) emissions showed consistent associations with IL-6 levels. 30-year average traffic-NO(2) exposure was associated with a 64.5% (95% CI 6.7% to 153.8%) increase in serum IL-6 per 28.8 microg/m(3) (corresponding to the difference between the 5th and 95th percentile exposure value), and 30-year exposure to heating-SO(2) with a 67.6% (95% CI 7.1% to 162.2%) increase per 39.4 microg/m(3) (5th-95th percentile value difference). The association appeared stronger in non-smokers, physically active people and hypertensive subjects. We observed positive non-significant associations of inflammatory markers with NO(2) and PM(10) during 24 h before blood sampling. Short-term exposure to O(3) was associated with increased, and SO(2) with decreased, fibrinogen levels.
Our results suggest that exposure to moderate levels of air pollution may influence serum levels of inflammatory markers.
Associations between parental educational level and possible risk factors for atopic disease during the first months of life were explored in a cohort of 4089 neonate children born 1994-96 in Stockholm, Sweden. Reports concerning a number of life style factors during pregnancy and after the baby was born were obtained by questionnaire. There was a strong negative association between duration of education and maternal smoking during pregnancy, parental smoking after the baby was born and keeping of cat and dog (p-trend
OBJECTIVES: To investigate whether there is a relation between residential exposure to aircraft noise and hypertension. METHODS: The study population comprised two random samples of subjects aged 19-80 years, one including 266 residents in the vicinity of Stockholm Arlanda airport, and another comprising 2693 inhabitants in other parts of Stockholm county. The subjects were classified according to the time weighted equal energy and maximum aircraft noise levels at their residence. A questionnaire provided information on individual characteristics including history of hypertension. RESULTS: The prevalence odds ratio for hypertension adjusted for age, sex, smoking, and education was 1.6 (95% confidence interval (95% CI) 1.0 to 2.5) among those with energy averaged aircraft noise levels exceeding 55 dBA, and 1.8 (95% CI 1.1 to 2.8) among those with maximum aircraft noise levels exceeding 72 dBA. An exposure-response relation was suggested for both exposure measures. The exposure to aircraft noise seemed particularly important for older subjects and for those not reporting impaired hearing ability. CONCLUSIONS: Community exposure to aircraft noise may be associated with hypertension.
Comment In: Occup Environ Med. 2001 Dec;58(12):76111706140
Environmental issues tend to greater political attention than do environmental health aspects. Therefore, when conflicts of interest occur with other environmental concerns, negative consequences for public health may result. For example, a strategy to substantially reduce indoor ventilation in many dwellings in Scandinavia in order to save energy has led to increased humidity levels and higher prevalences of house dust mites. Wood burning for local heating is promoted because it is a renewable source of energy, and diesel vehicles are promoted because they emit lower levels of carbon dioxide per kilometer compared to conventional gas engines, but both practices lead to increased emissions of fine particulates, which have been associated with adverse health effects. Increasing the level of resources available for research into environmental health is one way to help environmental health issues receive greater attention. Environmental health research initiatives taken by the European Commission, the European Science Foundation, and the World Health Organization's regional office for Europe are noted. Environmental health research is multidisciplinary and should encompass basic science as well as applied research. International collaboration is often very useful in environmental health research.
Seventy similar bungalows constructed between 1968 and 1970 in the same suburban area of Stockholm were investigated regarding the content of house dust mite allergen, absolute indoor humidity, type of ventilation and basement construction. Houses with mechanical exhaust and supply ventilation had an indoor humidity above 7 g/kg less often than houses without this type of ventilation (Odds ratio 0.1, 95% confidence interval 0.0-0.2). Furthermore, only five of the 24 houses with exhaust and supply ventilation contained mattress dust mite allergen concentrations exceeding the median value (98.5 ng/g) compared with 30 of 46 hours which did not have such ventilation (odds ratio = 0.1, C.I. 0.0-0.5). Houses with both natural ventilation and crawl space basement harboured significantly less mattress mite allergen than houses having the same type of ventilation, but with a concrete slab basement. In a cold temperature climate, type of building construction and ventilation seem to be important for the occurrence of house dust mite allergens in dwellings. Our results indicate that modern energy-efficient houses should be equipped with mechanical exhaust and supply ventilation to reduce indoor air humidity during the dry winter months and the risk of mite infestation.
BACKGROUND: The relation between socioeconomic status and allergic diseases in childhood is controversial. Some studies have proposed childhood asthma to be more common in families with low socioeconomic status, while sensitization to airborne allergens seems to be more frequent in individuals with higher socioeconomic status in childhood. OBJECTIVE: To assess the relation between socioeconomic status and asthma, rhinitis and sensitization in an unselected prospective birth cohort. METHODS: Four thousand and eighty-nine families with children born 1994-1996 in predefined areas of Stockholm answered questionnaires on environmental factors, socioeconomic status (parental occupation), and symptoms of allergic disease at birth, 1, 2 and 4 years of age. Blood samples taken at 4 years from 2614 children were analysed for specific IgE to common airborne and food allergens. Odds ratios (OR) and 95% confidence intervals (CI) for various outcomes in relation to socioeconomic status were estimated with a multiple logistic regression model, adjusting for potential confounders such as heredity for allergic diseases, maternal smoking, short duration of breastfeeding and house construction. RESULTS: There was a decreasing risk of asthma and rhinitis with increasing socioeconomic status. The OR for asthma was 0.33 (95% CI 0.17-0.66) and for rhinitis 0.50 (0.32-0.79) comparing the highest and the lowest socioeconomic groups, with a tendency to stronger effects in those with heredity for allergic disease. The risk of sensitization to food allergens also decreased with increasing socioeconomic status; OR 0.65 (0.41-1.02) in the highest socioeconomic group (Ptrend=0.03), which was not clearly seen for airborne allergens. CONCLUSION: Asthma, rhinitis and sensitization is more common in lower than in higher socioeconomic groups after adjustment for traditional risk factors. This may be related to additional uncontrolled differences in life style and environmental exposures between the groups, and calls for further studies.
This study was conducted to examine the impact of building characteristics and indoor air quality on recurrent wheezing in infants. We followed a birth cohort (BAMSE) comprising 4089 children, born in predefined areas of Stockholm, during their first 2 years of life. Information on exposures was obtained from parental questionnaires when the children were 2 months and on symptoms and diseases when the children were 1 and 2 years old. Children with recurrent wheezing, and two age-matched controls per case, were identified and enrolled in a nested case-control study. The homes were investigated and ventilation rate, humidity, temperature and NO2 measured. We found that living in an apartment erected after 1939, or in a private home with crawl space/concrete slab foundation were associated with an increased risk of recurrent wheezing, odds ratio (OR) 2.5 (1.3-4.8) and 2.5 (1.1-5.4), respectively. The same was true for living in homes with absolute indoor humidity >5.8 g/kg, OR 1.7 (1.0-2.9) and in homes where windowpane condensation was consistently reported over several years, OR 2.2 (1.1-4.5). However, air change rate and type of ventilation system did not seem to affect the risk. In conclusion, relatively new apartment buildings, single-family homes with crawl space/concrete slab foundation, elevated indoor humidity, and reported wintertime windowpane condensation were associated with recurrent wheezing in infants. Thus, improvements of the building quality may have potential to prevent infant wheezing.
OBJECTIVE: To assess the effects of living in agreement with allergy preventive guidelines on wheezing and asthma at 2 years of age. DESIGN: Prospective birth cohort study (BAMSE). Questionnaires on heredity and environmental factors were answered when the child was 2 months, and detailed questionnaires on symptoms at 1 and 2 years of age. PARTICIPANTS: 4089 children, born during 1994-1996. SETTING: Child Health Centres in central and north-western parts of Stockholm, Sweden. MAIN OUTCOME MEASURES: Wheezing and asthma up to the age of 2. RESULTS: The effects of preventive guidelines regarding breastfeeding, maternal tobacco smoke and home dampness on wheezing and asthma were assessed in multiple logistic regression models. The cumulative incidence of recurrent wheezing at 2 years of age was 12.6% and of asthma 6.8% among those with a lifestyle in agreement with all guidelines and 24.1 and 17.9%, respectively, in families exposed to at least two of the three risk factors. Among children with no heredity, family lifestyle according to the guidelines gave a twofold reduction of asthma (5.3 vs. 10.5%), while the group with heredity had a threefold reduction (9.1 vs. 27.3%). The attributable fraction for asthma associated with the guidelines was 23% in total and 33% among those with heredity. CONCLUSION: In this observational study, family lifestyle according to preventive guidelines is associated with an important reduction of recurrent wheezing and asthma at 2 years of age, especially among children with allergic heredity. A follow-up will determine whether there still a risk reduction of both symptoms and disease.
AIMS: To investigate the effect of breast feeding on allergic disease in infants up to 2 years of age. METHODS: A birth cohort of 4089 infants was followed prospectively in Stockholm, Sweden. Information about various exposures was obtained by parental questionnaires when the infants were 2 months old, and about allergic symptoms and feeding at 1 and 2 years of age. Duration of exclusive and partial breast feeding was assessed separately. Symptom related definitions of various allergic diseases were used. Odds ratios (OR) and 95% confidence intervals (CI) were estimated in a multiple logistic regression model. Adjustments were made for potential confounders. RESULTS: Children exclusively breast fed during four months or more exhibited less asthma (7.7% v 12%, OR(adj) = 0.7, 95% CI 0.5 to 0.8), less atopic dermatitis (24% v 27%, OR(adj) = 0.8, 95% CI 0.7 to 1.0), and less suspected allergic rhinitis (6.5% v 9%, OR(adj) = 0.7, 95% CI 0.5 to 1.0) by 2 years of age. There was a significant risk reduction for asthma related to partial breast feeding during six months or more (OR(adj) = 0.7, 95% CI 0.5 to 0.9). Three or more of five possible allergic disorders-asthma, suspected allergic rhinitis, atopic dermatitis, food allergy related symptoms, and suspected allergic respiratory symptoms after exposure to pets or pollen-were found in 6.5% of the children. Exclusive breast feeding prevented children from having multiple allergic disease (OR(adj) = 0.7, 95% CI 0.5 to 0.9) during the first two years of life. CONCLUSION: Exclusive breast feeding seems to have a preventive effect on the early development of allergic disease-that is, asthma, atopic dermatitis, and suspected allergic rhinitis, up to 2 years of age. This protective effect was also evident for multiple allergic disease.