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2.  NO2, as a marker of air pollution, and recurrent wheezing in children: a nested case-control study within the BAMSE birth cohort 
Aims: To investigate the association between air pollution, including with NO2, and recurrent wheezing during the first two years of life.
Methods: A birth cohort (BAMSE) comprised 4089 children, for whom information on exposures, symptoms, and diseases was available from parental questionnaires at ages 2 months, and 1 and 2 years. NO2 was measured during four weeks in and outside the dwellings of children with recurrent wheezing and two age matched controls, in a nested case-control study (540 children).
Results: Conditional logistic regression showed an OR of 1.60 (95% CI 0.78 to 3.26) among children in the highest quartile of outdoor NO2 exposure in relation to those in the lowest quartile, adjusted for potential confounders. The corresponding OR for indoor NO2 was 1.51 (95% CI 0.81 to 2.82). An interaction with environmental tobacco smoke (ETS) was indicated with an OR of 3.10 (95% CI 1.32 to 7.30) among children exposed to the highest quartile of indoor NO2 and ETS. The association between NO2 and recurrent wheezing appeared stronger in children who did not fulfil the criteria for recurrent wheezing until their second year.
Conclusions: Although the odds of increased recurrent wheezing are not statistically significantly different from one, results suggest that exposure to air pollution including NO2, particularly in combination with exposure to ETS, increases the risk of recurrent wheezing in children.
PMCID: PMC1740422  PMID: 14573719
3.  Breast feeding and allergic diseases in infants—a prospective birth cohort study 
Archives of Disease in Childhood  2002;87(6):478-481.
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%, ORadj = 0.7, 95% CI 0.5 to 0.8), less atopic dermatitis (24% v 27%, ORadj = 0.8, 95% CI 0.7 to 1.0), and less suspected allergic rhinitis (6.5% v 9%, ORadj = 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 (ORadj = 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 (ORadj = 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.
PMCID: PMC1755833  PMID: 12456543
4.  Radon in homes and risk of lung cancer: collaborative analysis of individual data from 13 European case-control studies 
BMJ : British Medical Journal  2005;330(7485):223.
Objective To determine the risk of lung cancer associated with exposure at home to the radioactive disintegration products of naturally occurring radon gas
Design Collaborative analysis of individual data from 13 case-control studies of residential radon and lung cancer.
Setting Nine European countries.
Subjects 7148 cases of lung cancer and 14 208 controls.
Main outcome measures Relative risks of lung cancer and radon gas concentrations in homes inhabited during the previous 5-34 years measured in becquerels (radon disintegrations per second) per cubic metre (Bq/m3) of household air.
Results The mean measured radon concentration in homes of people in the control group was 97 Bq/m3, with 11% measuring > 200 and 4% measuring > 400 Bq/m3. For cases of lung cancer the mean concentration was 104 Bq/m3. The risk of lung cancer increased by 8.4% (95% confidence interval 3.0% to 15.8%) per 100 Bq/m3 increase in measured radon (P = 0.0007). This corresponds to an increase of 16% (5% to 31%) per 100 Bq/m3 increase in usual radon—that is, after correction for the dilution caused by random uncertainties in measuring radon concentrations. The dose-response relation seemed to be linear with no threshold and remained significant (P = 0.04) in analyses limited to individuals from homes with measured radon < 200 Bq/m3. The proportionate excess risk did not differ significantly with study, age, sex, or smoking. In the absence of other causes of death, the absolute risks of lung cancer by age 75 years at usual radon concentrations of 0, 100, and 400 Bq/m3 would be about 0.4%, 0.5%, and 0.7%, respectively, for lifelong non-smokers, and about 25 times greater (10%, 12%, and 16%) for cigarette smokers.
Conclusions Collectively, though not separately, these studies show appreciable hazards from residential radon, particularly for smokers and recent ex-smokers, and indicate that it is responsible for about 2% of all deaths from cancer in Europe.
PMCID: PMC546066  PMID: 15613366
5.  Increased prevalence of hypertension in a population exposed to aircraft noise 
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.
PMCID: PMC1740076  PMID: 11706142
6.  Mortality among male and female smokers in Sweden: a 33 year follow up 
STUDY OBJECTIVE—It is still unclear if men and women are equally susceptible to the hazards of tobacco smoking. The objective of this study was to examine smoking related mortality among men and women.
DESIGN—In 1963 a questionnaire concerning tobacco smoking habits was sent out to a random sample from the 1960 Swedish census population. Date and cause of death have been collected for the deceased in the cohort through 1996.
PARTICIPANTS—The survey included a total of 27 841 men and 28 089 women, aged 18-69 years. The response rate was 93.1% among the men and 95.4% among the women.
MAIN RESULTS—After adjustment for age and place of residence positive associations were found between cigarette smoking and mortality from ischaemic heart disease, aortic aneurysm, bronchitis and emphysema, cancer of the lung, upper aerodigestive sites, bladder, pancreas in both men and women, but not from cerebrovascular disease. When the effect of amount of the cigarette consumption was considered, female smokers displayed, for example, slightly higher relative death rates from ischaemic heart disease. However, no statistically significant gender differential in relative mortality rates was observed for any of the studied diseases.
CONCLUSIONS—Women and men in this Swedish cohort seem equally susceptible to the hazards of smoking, when the gender differential in smoking characteristics is accounted for. Although the cohort under study is large, there were few female smokers in the high consuming categories and the relative risk estimates are therefore accompanied by wide confidence intervals in these categories.

Keywords: smoking; cause specific mortality
PMCID: PMC1763319  PMID: 11604439
7.  Using geographic information systems to assess individual historical exposure to air pollution from traffic and house heating in Stockholm. 
Environmental Health Perspectives  2001;109(6):633-639.
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 < 100 m for 90% of the addresses. Finally, we linked annual air pollution estimates to annual residence coordinates, yielding long-term residential exposure indices for each individual. There was a wide range of individual long-term average exposure, with an 11-fold interindividual difference in NO(2) and an 18-fold difference in SO(2). The 30-year average for all study subjects was 20 microg/m(3) NO(2) from traffic and 53 microg/m(3) SO(2) from heating. The results indicate that GIS can be useful for exposure assessment in environmental epidemiology studies, provided that detailed geographically related exposure data are available for relevant time periods.
PMCID: PMC1240347  PMID: 11445519
8.  Indoor environmental risk factors in young asthmatics: a case-control study. 
Archives of Disease in Childhood  1995;73(5):408-412.
One hundred and ninety three children with asthma and 318 controls aged 1-4 years were evaluated for atopic heredity and exposure to possible indoor risk factors for asthma-for example exposure to furred pets, tobacco smoke, and home dampness. A subgroup of cases were classified as cat and/or dog allergic on the basis of skin prick tests. Heredity for asthma was a significant risk factor (odds ratio (OR) 3.0, confidence interval (CI) 2.1 to 4.6). Environmental tobacco smoke was associated with an excess risk for asthma (OR 1.7, CI 1.1 to 2.3) and signs of home dampness tended to increase this risk (OR 1.3, CI 0.9 to 2.0). High dose exposure to cat and/or dog resulted in an increased risk only in asthma cases sensitised to cat and/or dog (OR 2.7, CI 1.0 to 7.3). A combination of high dose exposure to cat and/or dog, environmental tobacco smoke and damp housing was associated with an OR of 8.0 (CI 1.9 to 34.1). Raised indoor humidity has been shown to reflect low air exchange, which may also lead to increased doses of inhaled aeroallergens and tobacco smoke, and contribute to the interaction between the three risk factors.
PMCID: PMC1511369  PMID: 8554356
9.  Cancer risk of air pollution: epidemiological evidence. 
Environmental Health Perspectives  1994;102(Suppl 4):187-192.
Epidemiological studies on the effect of urban air pollution on lung cancer were surveyed. Overall, the studies from many countries point to a smoking-adjusted risk in urban areas over countryside areas that is higher by a factor of up to 1.5. The extent to which urban air pollution contributes to this excess remains unknown. Studies on diesel-exposed occupational groups show that urban air pollution may have a causative role in lung cancer. Model calculations on unit risk factors of known human carcinogens were carried out to rank carcinogens according to their current ambient air concentrations.
PMCID: PMC1566938  PMID: 7529702
10.  Health effects of Chernobyl. 
BMJ : British Medical Journal  1988;297(6662):1488-1489.
PMCID: PMC1835228  PMID: 3147040
11.  Histological types of lung cancer among smelter workers exposed to arsenic. 
The histological distribution of lung cancer was investigated in 93 men who had worked at a Swedish smelter with high levels of arsenic. A comparison was made with a group of 136 patients with lung cancer from the county where the smelter was located. Company records provided information on occupational exposure and data on smoking habits were obtained from a next of kin of each subject. No pronounced differences in the histological types of lung carcinomas between smelter workers and the reference group could be seen for smokers. Some analyses indicated an increased proportion of adenocarcinomas among the smelter workers, which confirmed earlier data, but these findings were difficult to interpret. Cases among smelter workers who had never smoked showed a histological distribution resembling that in smokers, indicating that the work environment at the smelter and smoking had a similar influence on the risk for different types of lung cancer.
PMCID: PMC1007859  PMID: 3040072
12.  Mortality in relation to cigarette and pipe smoking: 16 years' observation of 25,000 Swedish men. 
In a random sample of 25,129 Swedish men who responded to a questionnaire on smoking habits in 1963 the cause specific mortality was followed through 1979. In the cohort, 32% smoked cigarettes, 27% a pipe, and 5% cigars. There were clear covariations (p less than 0.001) between the amount of tobacco smoked and the risk of death due to cancer of the oral cavity and larynx, oesophagus, liver, pancreas, lung, and bladder as well as due to bronchitis and emphysema, ischaemic heart disease, aortic aneurysm, and peptic ulcer. Pipe smokers showed similar risk levels to cigarette smokers. There was a close to linear increase in lung cancer risk in relation to the amount of tobacco smoked for cigarette, pipe, and cigar smokers, respectively. An increasing risk of ischaemic heart disease with amount smoked was seen among both cigarette and pipe smokers. A similar fraction of inhalers in Swedish cigarette and pipe smokers may explain the similarity in risks.
PMCID: PMC1052604  PMID: 3655638
13.  Respiratory symptoms and annoyance in the vicinity of coal-fired plants. 
This study constitutes one part of a program for assessing the impact of coal-fired power plants on the surrounding communities. A questionnaire was mailed to a total of 12,000 subjects living in six areas with coal-fired plants and in matched reference areas. The participation rate was 77.3%. In one coal-fired plant/reference area pair, a more detailed medical examination was carried out among subjects who reported symptoms of the respiratory tract. The match between coal-fired plant and reference areas was successful primarily in three pairs. Neither respiratory symptoms nor disease rates were increased among adults or children near any of these plants, but one plant seemed to give rise to annoyance. For the remaining coal-fired plants, consistently higher prevalences of respiratory tract symptoms and annoyance were observed in the surrounding population. The effects cannot, however, conclusively be related to the coal-fired plants. It should be pointed out that the air pollution levels were relatively low, also in the vicinity of most of the plants in this study.
PMCID: PMC1474271  PMID: 3830110
14.  The carcinogenicity of arsenic. 
A carcinogenic role of inorganic arsenic has been suspected for nearly a century. Exposure to inorganic arsenic compounds occurs in some occupational groups, e.g., among smelter workers and workers engaged in the production and use of arsenic containing pesticides. Substantial exposure can also result from drinking water in certain areas and the use of some drugs. Tobacco and wine have had high As concentrations due to the use of arsenic containing pesticides. Inorganic arsenic compounds interfere with DNA repair mechanisms and an increased frequency of chromosomal aberrations have been observed among exposed workers and patients. Epidemiological data show that inorganic arsenic exposure can cause cancer of the lung and skin. The evidence of an etiologic role of arsenic for angiosarcoma of the liver is highly suggestive; however, the association between arsenic and cancer of other sites needs further investigation. No epidemiological data are available on exposure to organic arsenic compounds and cancer. Animal carcinogenicity studies involving exposure to various inorganic and organic arsenic compounds by different routes have been negative, with the possible exception of some preliminary data regarding lung cancer and leukemia. Some studies have indicated an increased mortality from lung cancer in populations living near point emission sources of arsenic into the air. The role of arsenic cannot be evaluated due to lack of exposure data. Epidemiological data suggest that the present WHO standard for drinking water (50 micrograms As/l.) provides only a small safety margin with regard to skin cancer.
PMCID: PMC1568809  PMID: 7023936
15.  Sensitization to inhalant allergens between 4 and 8 years of age is a dynamic process: results from the BAMSE birth cohort 
Clinical and Experimental Allergy  2008;38(9):1507-1513.
There is limited knowledge of the development of IgE-antibody levels over time in childhood, with respect to persistency and co-sensitization to specific inhalant allergens.
Data from 2033 children participating in the BAMSE birth cohort was used. Background factors and clinical parameters were obtained and IgE antibody (ab) levels to eight common airborne allergens were measured (≥0.35 kUA/L) when the children were 4 and 8 years of age.
Between 4 and 8 years the proportion of children sensitized to any of the inhalant allergens tested increased from 15% to 25%. At 4 years IgE-ab to birch and cat dominated, whereas at the age of 8, there was a considerable increase in the proportion of sensitization to timothy and dog. Except for mites and moulds, IgE-ab levels to all aeroallergens increased significantly between 4 and 8 years among those already sensitized at 4. Transient sensitization to inhalant allergen was uncommon. Furthermore, sensitization to birch pollen at 4 years increased the risk for becoming sensitized to timothy, cat and dog later in life. Such an association was not observed among those sensitized primarily to animal dander.
There is a prominent process of sensitization at pre-school age to inhalant allergens, and in Northern Europe sensitization to birch pollen early in life seems to be important for this process. Such a process has a probable impact on the development of allergic disease in the growing child.
Cite this as: A. Asarnoj, E. Östblom, I. Kull, G. Lilja, G. Pershagen, G. Hedlin, M. van Hage and M. Wickman, Clinical and Experimental Allergy, 2008 (38) 1507–1513.
PMCID: PMC2610395  PMID: 18644026
allergy; BAMSE; childhood; IgE; sensitization

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