Biomedical subjects

K Torén

Publications and source records attributed to K Torén.

At least 37 records · Page 2Linked to original sources

PubMed2001

Nasal symptoms among workers exposed to soft paper dust.

OBJECTIVES: To clarify whether occupational exposure to paper-dust is associated with an increased risk of non-infectious rhinitis. METHODS: Thirty-seven workers exposed to paper-dust in a soft-paper mill were compared with 36 unexposed controls. The study was performed under normal working conditions during the non-pollen season. Medical and occupational history was taken down in a comprehensive questionnaire and nasal symptoms were scored on a visual analogue scale (VAS). Pulmonary and nasal function was assessed by spirometry, acoustic rhinometry and peak nasal inspiratory flow. Nasal lavage was analysed for interleukin-8 (IL-8) and nasal transit time was monitored with the saccharine test. Concentrations of inhalable dust for each exposed subject during the day of the clinical study were measured with personal sampling devices. RESULTS: There was an increased prevalence of nasal blockage and crust formation among the exposed workers. However, there was no difference with regard to acoustic rhinometry, nasal transit time or nasal peak inspiratory flow. In the whole population, IL-8 in nasal lavage was higher among men than among women, 193 ng/l vs 132 ng/l, P = 0.006. There was also a positive trend (P = 0.01) with increasing nasal IL-8 going from non-smokers (122 ng/l), ex-smokers (126 ng/l) to current smokers (235 ng/l). CONCLUSIONS: We have found that occupational exposure to paper-dust is associated with symptoms of nasal blockage and nasal crusting. We find no objective signs of nasal inflammation, even among the subgroup with the highest current exposure.

Adult↗

PubMed2001

Adult-onset asthma is associated with self-reported mold or environmental tobacco smoke exposures in the home.

BACKGROUND: In recent years, we have gained better knowledge about the influence of indoor environments on respiratory symptoms and asthma. The purpose of this study was to examine certain exposures in the home environment and the risk of adult-onset asthma. METHODS: A nested case-referent study of adult-onset asthma was performed in a random population sample (n = 15813), aged 20-50 years. Cases for the study included subjects reporting "physician-diagnosed" asthma (n= 174). The referents (n = 870) were randomly selected from the whole population sample. The case-referent sample was investigated with a comprehensive mailed questionnaire about exposures in the home environment, asthma, respiratory symptoms, smoking habits, and atopy. Odds ratios (OR) with 95% confidence intervals (CI) were calculated while controlling for age, sex, smoking, and atopy. RESULTS: Increased adjusted OR for asthma were associated with exposure to molds (OR 2.2, 95%, CI 1.4-3.5), environmental tobacco smoke (OR 2.4, 95%, CI 1.4-4.1), and the presence of a wood stove (OR 1.7, 95% CI 1.2-2.5). CONCLUSIONS: This population-based case-referent study indicates that self-reported domestic exposures to molds or environmental tobacco smoke can be associated with adult-onset asthma.

Adult↗

PubMed2001

Increased nitric oxide in exhaled air after intake of a nitrate-rich meal.

Exhaled and nasal NO (ENO, NNO) have been suggested as markers for inflammation in lower and upper respiratory tract respectively. It is still unknown how a number of factors, apart from airway inflammation, can influence NO levels. The aim of this study was to determine the effect of a nitrate-rich meal on ENO and NNO. Sixteen healthy subjects were observed during 1 week on normal diet before a nitrate-restricted diet was introduced in the next. On day 3 of the second week they were made to ingest a nitrate rich meal. ENO, NNO, plasma nitrate and plasma L-arginine were followed before the meal and afterwards for 3 h. ENO and NNO as well as plasma nitrate and plasma L-arginine were significantly elevated after the nitrate-rich meal. The median maximal increase of ENO and NNO was 47% and 13% respectively. We found a moderate but significant correlation between the rise in plasma nitrate and ENO (r(s)=0.57, P=0.027) but none between plasma nitrate and NNO (r(s)=-0.02, P=0.95). As nitrate in the diet seems to substantially influence the levels of ENO it is important either to restrict or register the intake of nitrate-rich food prior to measuring ENO.

Adult↗

PubMed2001

Nitric oxide (NO) in exhaled air after experimental ozone exposure in humans.

We hypothesized that ozone, a common air pollutant, potent in producing airway inflammation, would increase the production of exhaled nitric oxide (NO). If so, measurement of exhaled NO could potentially be a valuable tool in population studies of air pollution effects. Eleven healthy non-smoking volunteers were exposed to 0.2 ppm ozone (O3) and filtered air for 2h on two separate occasions. Exhaled NO and nasal NO were measured before and on five occasions following the exposures. Changes in exhaled and nasal NO after ozone exposure were adjusted for changes after air exposure. There was a slight decrease in exhaled NO (-0.6; -3.1-1.2 ppb) (median and 95% confidence interval) and of nasal NO (-57; -173-75 ppb) directly after the ozone exposure. No significant changes in exhaled or nasal NO were however found 6 or 24 h after the exposure. Within the examined group, an O3 exposure level proven to induce an airway inflammation caused no significant changes in exhaled or nasal NO levels. Hence, the current study did not yield support for exhaled NO as a useful marker of ozone-induced oxidative stress and airway inflammation after a single exposure. This contrasts with data for workers exposed to repeated high peaks of ozone. The potential for exhaled NO as a marker of oxidative stress therefore deserves to be further elucidated.

Adult↗

PubMed2001

A case-referent study of cancer mortality among sulfate mill workers in Sweden.

OBJECTIVES: To investigate whether workers in Swedish sulfate mills have an increased risk of death from certain malignancies that have previously been linked to the pulping process. METHODS: Subjects of the study (n=2480) were men aged 40-75 at death during 1960-89 in the parishes surrounding four sulfate mills. Exposure assessment was based on information from the personnel files in the mills- 35% of the subjects were recognised there, and work categories were created. RESULTS: Among all sulfate mill workers, the odds ratio (OR) (90% confidence interval (90% CI)) for death from lung cancer was 1.6 (1.1 to 2.3), pleural mesotheliomas 9.5 (1.9 to 48), brain tumours 2.6 (1.2 to 5.3), and liver or biliary tract cancer 2.3 (1.0 to 5.2). There was an increased mortality from leukaemia among workers in the soda recovery plant (5.9 (2.6 to 13)) and bleaching plant and digester house (2.8 (1.0 to 7.5)). CONCLUSIONS: Sulfate mill workers were at increased risk of dying from lung cancer and pleural mesotheliomas, probably due to exposure to asbestos. Increased risks of brain tumours and cancers of the liver or biliary tract were also found but the aetiology is not obvious.

Adult↗

PubMed2000

Asthma on the job: work-related factors in new-onset asthma and in exacerbations of pre-existing asthma.

Occupational asthma (OA) can be defined as variable airways narrowing causally related to exposure in the working environment to airborne dusts, gases, vapours or fumes. There are many agents in the work-place that can induce asthma or cause substantial deterioration in pre-existing asthma. It has been estimated that 5-15% of adult-onset asthma can be attributed to occupational exposures. Hence adult patients, especially those with new-onset asthma, must be investigated with regard to occupational risk factors for disease. The prognosis for OA is improved if the causal exposure is controlled either by controlling the exposure at the workplace or by moving the patient out of the workplace.

Acrylates↗

PubMed2000

The incidence of pregnancy rhinitis.

The purpose of this study was to define the cumulative incidence of pregnancy rhinitis, and to study whether smoking, asthma, hayfever or month of conception are risk factors. A questionnaire was delivered during 1 year in 10 antenatal care centers in one Swedish county. Questions were asked by midwives on the ordinary check-up visits throughout pregnancy. Five centers with response rates of 70% or more, including 599 women, were evaluated. The cumulative incidence of pregnancy rhinitis was 22%. Smokers had a significantly increased incidence with a relative risk enhancement of 69%, whereas hayfever, asthma, and month of conception had no statistically significant influence on incidence. Pregnancy rhinitis was shown to appear at any time during gestation.

Adolescent↗

PubMed1999

Exhaled nitric oxide among pulpmill workers reporting gassing incidents involving ozone and chlorine dioxide.

The aim of the study was to investigate whether measurement of nitric oxide in exhaled air could be used for assessing the effects of irritants on the respiratory system, in this case recurrent ozone gassing in an occupational setting. The study population comprised bleachery workers (n=56) from a Swedish pulpmill carrying out ozone-based pulp bleaching since 1992 and controls (n=39). Both groups were investigated by measuring NO in exhaled air, methacholine challenge test and answers to a questionnaire concerning history of respiratory symptoms and accidental exposure to ozone peaks. There was no significant difference in NO output between exposed subjects and controls (median 67.2 versus 55.0 nL x min(-1), p=0.64). However, among bleachery workers reporting ozone gassings, the median NO output was 90.0 nL x min(-1) compared to 58.8 nL x min(-1) among those not reporting such incidents (p=0.019). There was no relation between exhaled NO and the prevalence of respiratory symptoms or bronchial hyperresponsiveness. In a multiple regression model, only reported ozone gassings were associated (p=0.016) with NO output. The results indicate an association between previous response to ozone gassing and nitric oxide output. The increased nitric oxide output among the bleachery workers reporting peak ozone exposure may indicate that chronic airway inflammation is present. Further studies are needed to evaluate the extent to which nitric oxide can be used for biological monitoring of respiratory health effects, and to relate it to other markers of airway inflammation.

Adult↗

PubMed1999

Asthma-related work disability in Sweden. The impact of workplace exposures.

Work disability due to respiratory disease, especially asthma, is common and costly among working age adults. The goal of this analysis was to characterize the risk factors for such disability. We analyzed data from the Swedish part of the European Community Respiratory Health Survey (ECRHS), a random population-based sample of adults age 20 to 44, enriched with symptomatic subjects at increased likelihood of having asthma. We analyzed structured interview data available for 2,065 subjects and further analyzed methacholine challenge and skin prick test data for 1,562 of these. We defined respiratory work disability as reported job change or work loss due to breathing affected by a job. We used binary generalized linear modeling with a log link to estimate disability risk. Eighty-four subjects (4%) reported such work disability. This increased to 13% among those with asthma (45 of 350 subjects). Adjusting for covariates, occupations at high risk for asthma were associated with disability (prevalence ratio [PR] 1.8; 95% confidence interval [CI] 1.1 to 3.0), as was self-reported regular exposure to environmental tobacco smoke (ETS) at work (PR 1.8; 95% CI 1.1 to 3.1) and self- reported job exposure to vapors, gases, dust, or fumes (VGDF) (PR 4.3; 95% CI 2.2 to 8.6). Workplace ETS exposure was also associated with methacholine challenge-positive asthma reported to be symptomatic at work among male subjects (PR 4. 2; 95% CI 1.8 to 9.8), whereas high asthma-risk occupations were associated with this outcome among female subjects (PR 2.7; 95% CI 1. 05 to 7.1). Respiratory work disability, defined as breathing-related job change due to work loss, was associated with workplace exposures themselves, even after taking into account other covariates. Better control of workplace exposures, including workplace ETS, may reduce work disability caused by respiratory conditions, especially adult asthma.

Adult↗

PubMed1999

The risk of asthma in relation to occupational exposures: a case-control study from a Swedish city.

The purpose of this study was to estimate the risk of adult asthma in relation to certain occupational exposures. The study was designed as a case-control study in Göteborg, including 321 subjects with asthma, born between 1926 and 1970. Controls (n=1,459) were randomly selected from the same area from registers of the 1986 population. Questionnaire information was collected in 1996, and included occupational exposures and smoking habits. Odds ratios were calculated for exposure before asthma onset, stratified by sex and age-class. The highest risks for asthma were associated with exposure to grain dust (odds ratio (OR) 4.2, 95% confidence interval (CI) 1.6-10.7) and flour dust (OR 2.8, 95% CI 1.1-7.2). Among males, significantly increased risks were observed after exposure to flour dust, welding fumes, man-made mineral fibres, and solvents. Among females, increased risks for asthma were associated with exposures to paper dust and textile dust. In logistic regression models controlling for age, smoking, sex and interacting exposures, increased risks were seen for welding fumes (OR 2.0, 95% CI 15-3.4), man-made mineral fibres (OR 2.6, 95% CI 1.4-7.3) and solvents (OR 2.2, 95% CI 1.2-3.2). The fraction of asthma attributed to occupational exposures after adjusting for sex, smoking and age was 11% (95% CI 7-14%). In conclusion, exposure to welding fumes, man-made mineral fibres, solvents and textile dust is associated with increased risk for asthma.

Adult↗

PubMed1999

Adult-onset asthma and occupational exposures.

OBJECTIVES: This study examined certain occupational exposures and the risk for adult-onset asthma. METHODS: A nested case-referent study of adult-onset asthma was performed on a random population sample (N=15813), aged 21 to 51 years. Cases for the study included 2 groups: subjects reporting "physician-diagnosed" asthma (N=251) and a broader "asthma" group (N=362). The "asthma" group consisted of subjects with "physician-diagnosed" asthma (N=251) and subjects reporting asthma-like symptoms without having "physician-diagnosed" asthma (N=111). The referents (N=2044) were randomly selected from the whole population sample. The case-referent sample was investigated with a comprehensive questionnaire about occupational exposures, asthma, respiratory symptoms, smoking, and atopy. Odds ratios were calculated with stratification for gender, year of diagnosis, and birth year. RESULTS: The highest odds ratio for "physician-diagnosed" asthma was associated with exposure to flour dust [odds ratio (OR) 2.8, 95% confidence interval (95% CI) 1.5-5.2] and the occupational handling of resin-based paints (isocyanates) (OR 3.0, 95% CI 1.6-5.9). Exposure to welding fumes, textile dust, and work with glues containing acrylates was also associated with an increased odds ratio for "physician-diagnosed" asthma. Including persons with asthma-like symptoms (ie, the asthma group) showed similar results. CONCLUSION: This population-based case-referent study from Sweden indicates that occupational exposure to acrylate-based compounds and welding fumes is associated with increased risk for adult-onset asthma.

Adult↗

PubMed1999

Challenges for the new century in the epidemiology of adult asthma.

Numerous risk factors are associated with asthma. To achieve adequate precision in epidemiologic studies of asthma, large populations and specific diagnostic methods are to be preferred. The association between air pollution (in a wide sense) and adult-onset asthma is well-known, but little is known about the actual risks. In published studies the fraction of adult-onset asthma caused by occupational exposures ranges from 4.8% to 36%. Whether subjects with preexisting asthma are at an increased risk for impairment due to asthma when they are exposed to irritants is an issue of great relevance. The literature addressing these problems is scant. The challenge facing us is to design epidemiologic studies on adult asthma that lead to answers to the following questions: (i) has the incidence of asthma increased among adults, (ii) to what extent is adult-onset asthma caused by occupational exposure, (iii) does preexisting asthma get worse due to exposures in the workplace?

Adult↗

PubMed1999

Incidence rate of adult-onset asthma in relation to age, sex, atopy and smoking: a Swedish population-based study of 15813 adults.

SETTING: Our knowledge about asthma incidence in an adult population is limited. The aim of the present investigation was to estimate the incidence rate of adult-onset asthma in relation to age, sex, atopy and smoking in a random population sample. METHODS: A random sample of 20000 subjects 20 to 50 years of age was investigated using a short respiratory questionnaire. It was answered by 15813 persons. Adult-onset asthma was defined as a positive response to 'physician-diagnosed' asthma from 16 years of age. Subjects were also asked to report the year of asthma diagnosis, and also, when relevant, the year of smoke-start and smoke-stop. Incidence rates of adult-onset asthma and incidence rate ratios (IRR) were calculated. RESULTS: The incidence rate of adult-onset asthma among females was 1.3 cases/1000 person-years compared with 1.0/1000 person-years for males (IRR 1.3, 95% confidence interval [CI] 1.0-1.6). The incidence rate was high (3.0/1000 person-years) among females aged 16-20 years. There was a strong association between the incidence rate of adult-onset asthma and hay fever, atopic dermatitis and family history of atopy. Compared with never-smokers, the IRR for female smokers was 1.6 (95% CI 1.1-2.2), while for male smokers it was unity. Both male and female ex-smokers had moderately increased rate ratios, of 1.5 and 1.1, respectively. CONCLUSIONS: In this retrospective study, reported atopic symptoms and family history of atopy were strongly associated with incidence of adult-onset asthma. Tobacco smoking may be associated with an increased incidence rate of adult-onset asthma, especially among women.

Adolescent↗

PubMed1998

Nasal symptoms and indices of nasal inflammation in flour-dust-exposed bakers.

OBJECTIVE: To analyze whether indices of nasal airway inflammation in bakers were related to nasal symptoms and exposure to airborne flour dust. METHODS: A cross-sectional study was performed in 12 currently flour-exposed bakers. They were examined by nasal lavage (NAL), visual inspection, a test of mucociliary clearance, and nasal peak expiratory flow (nasal PEF). NAL fluid was analyzed according to the inflammatory markers eosinophil cationic protein (ECP), indicating eosinophilic activity; myeloperoxidase (MPO), indicating active neutrophils; hyaluronic acid (HA) from active fibroblasts; tryptase, indicating activation of mast cells; and albumin, indicating plasma exudation. The bakers were also questioned about respiratory symptoms and working history. Their current and cumulative exposure to inhalable flour dust was estimated after exposure measurements and information about earlier work tasks. Office workers (n=16) without occupational exposure to dust or any other known nasal irritant or sensitizer served as controls. RESULTS: Personal inhalable dust measurements among the bakers working as dough makers or bread formers ranged from 1.0 to 3.8 mg/m3. Of the 12 bakers, 10 reported at least 1 nasal symptom (crusts, blockage, or a runny nose), a proportion significantly greater than that of the controls (P=0.009). Bakers with nasal symptoms had higher concentrations of markers of inflammation in their NALs as compared with nonsymptomatic bakers. The difference was significant for MPO (P=0.02) and HA (P=0.04) in relation to a runny nose. Tryptase was detected in only one NAL of the bakers. There was a positive correlation between the cumulative dose of inhalable flour dust and concentrations of MPO and HA in NAL. Two bakers were sensitized to wheat; they had the highest NAL concentrations of inflammatory markers. CONCLUSIONS: Our results indicate that flour dust exposure in bakers at levels below the current occupational exposure limit causes nasal mucosal inflammation, which, in turn, is related to nasal symptoms. We propose that the inflammation may be nonallergic, characterized by activation of neutrophils and fibroblasts.

Adult↗

PubMed1998

Predictors of self-assessed work ability among subjects with recent-onset asthma.

The objective of the study was to find predictors for work disability among adults with recent-onset asthma. The study was performed in a group of 332 subjects with recent-onset asthma. The predictors were ascertained by structured interviews, pulmonary function measurements, methacholine challenge tests and skin prick tests. Asthma severity was classified into mild, moderate or severe, based on the minimum medication required to maintain asthma control. Work ability was based on self-assessment by inquiring about the subjects' present work ability, expressed in percent. The self-reported work ability decreased significantly with increasing number of days off work, indicating that self-reported work ability reflects the actual work ability. The majority (56%) of the subjects reported 100% working ability. Among women, but not among men, working ability was negatively correlated (rs = -0.33) with age. Among subjects with PC20 < 16 mg ml-1 work ability increased with increasing PC20. There was no relation between FEV1, FVC and working ability. Asthma severity and current respiratory symptoms at the work place showed a significant negative relation with work ability. In a logistic regression model, when controlling for age, gender, smoking and weekly working hours, decreased work ability was associated with asthma severity, respiratory symptoms at the workplace and PC20 < or = 4 mg ml-1. In conclusion, the work ability was assessed as normal in most asthmatic subjects. Significant predictors for decreased work ability were asthma severity, workplace-associated respiratory symptoms and bronchial hyperresponsiveness. The results indicate that work ability among asthmatics could be improved by reducing the workplace-associated symptoms, either by reducing the exposure to triggers or by improving the asthma therapy.

Adolescent↗

PubMed1998

Mortality from asthma and cancer among sulfite mill workers.

OBJECTIVES: The aims of the present case-referent study were to investigate whether sulfite workers show increased mortality from asthma, chronic obstructive pulmonary disease or certain malignancies of interest in relation to sulfite mill work. The main exposure from the pulping processes is from sulfur dioxide, wood dust and terpenes. METHODS: The subjects of the study were all the men who died between 1960 and 1989 and who were aged 40 to 75 years at death (N = 780) in the parishes surrounding 3 sulfite mills. The men who died from asthma (N = 13), COPD (N = 20), lung cancer (N = 33), stomach cancer (N = 35), or brain tumor (N = 10) formed the case group. All the subjects, except the cases in question, were used as referents. As a proxy variable of exposure, job titles from the registers of deaths and burials were used, and 24% of the subjects were classified as exposed. RESULTS: There was an increased mortality from asthma [odds ratio(OR) 2.8, 90% confidence interval (90% CI) 1.1-6.8] and brain tumors (OR 3.3, 90% CI 1.2-8.9) among the sulfite workers. The mortality due to lung cancer was not significantly increased (OR 1.4, 90% CI 0.7-2.6), and there was a reduced mortality from stomach cancer (OR 0.4, 90% CI 0.2-0.9). CONCLUSIONS: The increased asthma mortality may be due to accidental exposure to irritating gases, such as sulfur dioxide. The increased risk for brain tumors has no obvious explanation.

Adult↗

PubMed1998

Nasal nitric oxide and its relationship to nasal symptoms, smoking and nasal nitrate.

Nitric oxide (NO) is produced in the nasal mucosa and in the paranasal sinuses. Increased nasal NO concentrations have been found in patients with asthma and/or rhinitis, and nasal NO has been suggested to be a marker of nasal inflammation. Measuring the stable end products of NO, nitrate and nitrite in nasal lavage fluid have been proposed as an indirect method for measuring NO concentration. The aim of this study was to measure nasal NO concentration, and to find out its relationship to nasal nitrate concentration and clinical parameters. 73 paper-mill workers were investigated with nasal and exhaled NO, nitrate in nasal lavage fluid and were given a respiratory questionnaire. Nasal air was sampled directly from a nasal mask and NO concentration was measured with a chemiluminescence analyser. Exhaled NO was measured with the subjects breathing tidal volumes and wearing nose clips. The nitric oxide metabolites were analysed as nitrate, after reduction of nitrite to nitrate. Smokers had lower nasal NO concentration (264 ppb) as compared to NO concentrations of 340 ppb among non-smokers (p = 0.02). There was no statistically significant relationship between nasal NO concentration and nitrate in nasal lavage fluid or nasal symptoms. Nasal NO concentration was significantly related to FVC (p = 0.047) and there was a relationship with borderline statistical significance (p = 0.06) to FEV1. In conclusion, we found no relationship between nitrate in nasal lavage and nasal NO, and neither of these were correlated to nasal symptoms or to nasal PIF. Nasal NO was significantly lower among smokers. Further controlled studies on subjects with rhinitis are needed, to evaluate the relation between nasal NO and nasal inflammation. In addition, there is also a need to develop methods for measuring nasal NO that minimise contamination from sinuses.

Adult↗

PubMed1998

The association between epidemiological measures of the occurrence of asthma.

SETTING: The prevalence of asthma is useful for studying the causes of asthma. OBJECTIVE: To ascertain whether there is a relationship between the prevalence and incidence of asthma. DESIGN: The association between age and the occurrence of asthma was analysed in an epidemiological study of 15,813 persons. RESULTS: Different conclusions were reached depending on whether the point prevalence, cumulative prevalence or the incidence rates were studied. The relation between the incidence and prevalence of asthma is described in two epidemiological models, and none of the models seem to fit empirical data. Furthermore, it is shown that estimating incidence rates by prospectively measuring the point prevalences may introduce a considerable bias if the reliability of the diagnosis of asthma is around or below an agreement of 99%, which is probably usually the case. Including asthmatic symptoms during the last year in the definition of point prevalence means that there is no simple relation between incidence rates and point prevalences. CONCLUSION: The point prevalence may be a biased measure in the study of the etiology of asthma, as there is no simple relationship between the incidence and prevalence of asthma.

Adult↗