No longitudinal studies exist on the natural history of food hypersensitivity and IgE sensitisation to food allergens in adults.
To examine the natural history of food hypersensitivity, the natural history of IgE sensitisation to food allergens and to investigate the risk factors for new onset food hypersensitivity.
Food hypersensitivity was questionnaire-assessed in 2307 individuals (aged 20–45 years) from Iceland and Sweden during the European Community Respiratory Health Survey both at baseline and follow-up 9 years later. IgE food and aeroallergen sensitisation were assessed in a subgroup of these individuals (n = 807). Values of 0.35 kU/L and above were regarded as positive sensitisation.
Food hypersensitivity was reported by 21% of the subjects and this proportion remained unchanged at follow-up (p = 0.58). Fruits, nuts and vegetables were the three most common causes of food hypersensitivity, with a similar prevalence at baseline and follow-up. The prevalence IgE sensitisation to food allergens decreased in general by 56% (p<0.001) and IgE sensitisation to peanut decreased in particular by 67% (p = 0.003). The prevalence of timothy grass IgE sensitisation decreased by 15% (p = 0.003) while cat, mite and birch IgE sensitisation did not decrease significantly. Female sex, rhinitis, eczema and presence of IgE sensitisation to aeroallergens were independently associated with new onset food hypersensitivity.
The prevalence of food hypersensitivity remained unchanged while the prevalence of IgE sensitisation to food allergens decreased in adults over a 9-year follow-up period. The decrease in prevalence of IgE sensitisation to food allergens was considerably larger than the change in prevalence of IgE sensitisation to aeroallergens.
To estimate the effects of smoking, gender and occupational exposure on the risk of developing severe pulmonary fibrosis (PF), including dose-response and interaction effects.
National case–control study of 171 patients (cases) who had started a long-term oxygen therapy for PF in Sweden between February 1997 and April 2000, and 719 random control participants from the general population. Of these cases, 137 had probable idiopathic PF (IPF). The ORs for smoking, gender and occupational exposure were estimated using Mantel-Haenszel analysis and conditional logistic regression, controlling for age and year of diagnosis.
The adverse effect of smoking was amplified by male gender and occupational exposure, OR 4.6 (95% CI 2.1 to 10.3) for PF, and OR 3.0 (1.3 to 6.5) for IPF, compared with in non-exposed women. Higher cumulative smoking exposure was linearly associated with increased risks. Compared with smoking less than 10 pack-years, smoking ≥20 pack-years was associated with increased risk of PF and IPF, OR 2.6 (1.4 to 4.9) and OR 2.5 (1.3 to 5.0), respectively.
Smoking has a dose-related association with increased risk of severe PF. Men with a history of smoking and occupational exposure is a particular risk group for developing severe PF.
Occupational exposure to irritants is associated with chronic bronchitis. The aim of this study was to elucidate whether repeated peak exposures with respiratory symptoms, gassings, to sulphur dioxide (SO2) and other irritant gases could increase the risk of chronic bronchitis.
The study population comprised 3,060 Swedish pulp mill workers (84% males) from a cohort study, who completed a comprehensive questionnaire with items on chronic bronchitis symptoms, smoking habit, occupational history, and specific exposures, including gassings. 2,037 have worked in sulphite mills. Incidence rates and hazard ratios (HRs) for the observation period, 1970–2000, in relation to exposure and the frequency of repeated gassings to SO2 and other irritant gases were calculated.
The incidence rate for chronic bronchitis among workers with repeated gassings was 3.5/1,000 person-years compared with 1.5/1,000 person-years among unexposed workers (HR 2.1, 95% confidence interval (CI) 1.4-3.1). The risk was even higher in the subgroup with frequent gassings (HR 3.2, 95% CI 2.0-5.2), particularly among never-smokers (HR 8.7, 95% CI 3.5-22).
Repeated gassings to irritant gases increased the incidence of chronic bronchitis in our study population during and after work in pulp mills, supporting the hypothesis that occupational exposures to irritants negatively affect the airways. These results underscore the importance of preventive actions in this work environment.
(MeSH); Bronchitis; Chronic; Irritants; Sulphur dioxide; Paper
Some previous studies have proposed potential explanatory factors for the social gradient in sickness absence. Yet, this research area is still in its infancy and in order to comprise the full range of socioeconomic positions there is a need for studies conducted on random population samples. The main aim of the present study was to investigate if somatic and mental symptoms, mental wellbeing, job strain, and physical work environment could explain the association between low socioeconomic position and belonging to a sample of new cases of sick-listed employees.
This study was conducted on one random working population sample (n = 2763) and one sample of newly sick-listed cases of employees (n = 3044), drawn from the same random general population in western Sweden. Explanatory factors were self-rated 'Somatic and mental symptoms', 'Mental well-being', 'job strain', and 'physical work conditions' (i.e. heavy lifting and awkward work postures). Multiple logistic regression analyses were used.
Somatic and mental symptoms, mental well-being, and job strain, could not explain the association between socioeconomic position and sickness absence in both women and men. However, physical work conditions explained the total association in women and much of this association in men. In men the gradient between Non-skilled manual OR 1.76 (1.24;2.48) and Skilled manual OR 1.59 (1.10;2.20), both in relation to Higher non-manual, remained unexplained.
The present study strengthens the scientific evidence that social differences in physical work conditions seem to comprise a key element of the social gradient in sickness absence, particularly in women. Future studies should try to identify further predictors for this gradient in men.
Women who smoke have higher risk of lung function impairment, COPD and lung cancer than smoking men. An influence of sex hormones has been demonstrated, but the mechanisms are unclear and the associations often subject to confounding. This was a study of wheeze in relation to smoking and sex with adjustment for important confounders.
In 2008 the Global Allergy and Asthma European Network (GA2LEN) questionnaire was mailed to 45.000 Swedes (age 16–75 years), and 26.851 (60%) participated. “Any wheeze”: any wheeze during the last 12 months. “Asthmatic wheeze”: wheeze with breathlessness apart from colds.
Any wheeze and asthmatic wheeze was reported by 17.3% and 7.1% of women, vs. 15.8% and 6.1% of men (both p<0.001). Although smoking prevalence was similar in both sexes, men had greater cumulative exposure, 16.2 pack-years vs. 12.8 in women (p<0.001). Most other exposures and characteristics associated with wheeze were significantly overrepresented in men. Adjusted for these potential confounders and pack-years, current smoking was a stronger risk factor for any wheeze in women aged <53 years, adjusted odds ratio (aOR) 1.85 (1.56–2.19) vs. 1.60 (1.30–1.96) in men. Cumulative smoke exposure and current smoking each interacted significantly with female sex, aOR 1.02 per pack-year (p<0.01) and aOR 1.28 (p = 0.04) respectively. Female compared to male current smokers also had greater risk of asthmatic wheeze, aOR 1.53 vs. 1.03, interaction aOR 1.52 (p = 0.02). These interactions were not seen in age ≥53 years.
In addition to the increased risk of COPD and lung cancer female, compared to male, smokers are at greater risk of significant wheezing symptoms in younger age. This became clearer after adjustment for important confounders including cumulative smoke exposure. Estrogen has previously been shown to increase the bioactivation of several compounds in tobacco smoke, which may enhance smoke-induced airway inflammation in fertile women.
The aim of this study was to examine the short-term and long-term cumulative risk of coronary heart disease (CHD) and stroke separately based on age, sex, smoking status, systolic blood pressure, and total serum cholesterol.
Methods and results
The Primary Prevention Study comprising 7174 men aged between 47 and 55 free from a previous history of CHD, stroke, and diabetes at baseline examination (1970–73) was followed up for 35 years. To estimate the cumulative effect of CHD and stroke, all participants were stratified into one of five risk groups, defined by their number of risk factors. The estimated 10-year risk for high-risk individuals when adjusted for age and competing risk was 18.1% for CHD and 3.2% for stroke which increased to 47.8 and 19.6%, respectively, after 35 years. The estimates based on risk factors performed well throughout the period for CHD but less well for stroke.
The prediction of traditional risk factors (systolic blood pressure, total serum cholesterol, and smoking status) on short-term risk (0–10 years) and long-term risk (0–35 years) of CHD of stroke differs substantially. This indicates that the cumulative risk in middle-aged men based on these traditional risk factors can effectively be used to predict CHD but not stroke to the same extent.
Score models; Stroke; CHD; Risk prediction; Risk factors
This cross-sectional study explored relationships between psychosocial work environment, captured by job demand-control (JDC) and effort-reward imbalance (ERI), and seven cardiovascular heart disease (CHD) risk factors in a general population.
The sampled consists of randomly-selected men and women from Gothenburg, Sweden and the city’s surrounding metropolitan areas. Associations between psychosocial variables and biomarkers were analysed with multiple linear regression adjusted for age, smoking, education and occupational status.
The study included 638 men and 668 women aged 24–71. Analysis between JDC and CHD risk factors illustrated that, for men, JDC was associated with impaired scores in several biomarkers, especially among those in high strain jobs. For women, there were no relationships between JDC and biomarkers. In the analysis of links between ERI and CHD risk factors, most associations tested null. The only findings were raised triglycerides and BMI among men in the fourth quartile of the ERI-ratio distribution, and lowered LDL-cholesterol for women. An complementary ERI analysis, combining high/low effort and reward into categories, illustrated lowered triglycerides and elevated HDL-cholesterol values among women reporting high efforts and high rewards, compared to women experiencing low effort and high reward.
There were some associations between psychosocial stressors and CHD risk factors. The cross-sectional design did not allow conclusions about causality but some results indicated gender differences regarding sensitivity to work stressors and also how the models might capture different psychosocial dimensions.
Psychosocial work environment; Cardiovascular heart disease risk factors; Job demand-control; Effort-reward imbalance; Gender
In a large population-based study among adults in northern Europe the relation between occupational exposure and new-onset asthma was studied.
The study comprised 13 284 subjects born between 1945 and 1973, who answered a questionnaire 1989–1992 and again 1999–2001. Asthma was defined as ‘Asthma diagnosed by a physician’ with reported year of diagnose. Hazard ratios (HR), for new-onset adult asthma during 1980–2000, were calculated using a modified job-exposure matrix as well as high-risk occupations in Cox regression models. The analyses were made separately for men and women and were also stratified for atopy.
During the observation period there were 429 subjects with new-onset asthma with an asthma incidence of 1.3 cases per 1000 person-years for men and 2.4 for women. A significant increase in new-onset asthma was seen for men exposed to plant-associated antigens (HR = 3.6; 95% CI [confidence interval] = 1.4–9.0), epoxy (HR = 2.4; 95% CI = 1.3–4.5), diisocyanates (HR = 2.1; 95% CI = 1.2–3.7) and accidental peak exposures to irritants (HR = 2.4; 95% CI = 1.3–4.7). Both men and women exposed to cleaning agents had an increased asthma risk. When stratifying for atopy an increased asthma risk were seen in non-atopic men exposed to acrylates (HR = 3.3; 95% CI = 1.4–7.5), epoxy compounds (HR = 3.6; 95% CI = 1.6–7.9), diisocyanates and accidental peak exposures to irritants (HR = 3.0; 95% CI = 1.2–7.2). Population attributable risk for occupational asthma was 14% for men and 7% for women.
This population-based study showed that men exposed to epoxy, diisocyanates and acrylates had an increased risk of new-onset asthma. Non-atopics seemed to be at higher risk than atopics, except for exposure to high molecular weight agents. Increased asthma risks among cleaners, spray painters, plumbers, and hairdressers were confirmed.
Atopics and non-atopics; high molecular weight agent; high-risk occupations; irritating agents; job-exposure matrix; low molecualr weight agent; occupational asthma; population attributable risk
There is conflicting evidence whether nasal nitric oxide (NO) is associated with current rhinitis and with other possible predictors. Most studies have been performed in clinical cohorts and there is a lack of studies based on a general population sample. The aim of the present study was to investigate predictors for levels of nasal nitric oxide (NO) in a general population.
The population consisted of 357 subjects from Gothenburg participating in the follow-up of the European Respiratory Health Survey in 1999–2001. All subjects completed an extensive respiratory questionnaire. Nasal NO was measured from one nostril at a time with a sampling rate of 50 mL/s for 16 seconds and the nasal NO concentration was determined as the mean value within the plateau phase. Mattress dust samples were collected for cats and mites in a subsample of subjects. Ambient and exhaled NO was also measured. The predictors for nasal NO were analyzed in multiple linear regression models.
There was no relation between the levels of nasal NO and reporting current rhinitis. Nasal NO was significantly increased among those with high levels of IgE against cats and current smokers had significantly lower nasal NO. There was also a positive association between ambient NO and nasal NO. There were no significant associations between nasal NO and sex, age, or height, or between nasal NO and measured levels of cat antigen.
In this general population sample we found no relation between current rhinitis and nasal NO levels. There was a clear association between sensitization to cat and nasal NO, but there was no relation to current exposure to cat allergen. Our data support that nasal NO has a limited value in monitoring upper airway inflammation.
Allergic rhinitis; epidemiology; FENO; nasal nitric oxide; nNO; rhinitis; sensitization
Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FENO), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchoprotective role.
To investigate how the relation between FENO and bronchial responsiveness is modulated by atopy and smoking habits.
Exhaled NO measurements and methacholine challenge were performed in 468 subjects from the random sample of three European Community Respiratory Health Survey II centers: Turin (Italy), Gothenburg and Uppsala (both Sweden). Atopy status was defined by using specific IgE measurements while smoking status was questionnaire-assessed.
Increased bronchial responsiveness was associated with increased FENO levels in non-smokers (p = 0.02) and decreased FENO levels in current smokers (p = 0.03). The negative association between bronchial responsiveness and FENO was seen only in the group smoking less <10 cigarettes/day (p = 0.008). Increased bronchial responsiveness was associated with increased FENO in atopic subjects (p = 0.04) while no significant association was found in non-atopic participants. The reported interaction between FENO and smoking and atopy, respectively were maintained after adjusting for possible confounders (p-values<0.05).
The present study highlights the interactions of the relationship between FENO and bronchial responsiveness with smoking and atopy, suggesting different mechanisms behind atopy- and smoking-related increases of bronchial responsiveness.
Understanding the reasons for the social gradient in sickness absence might provide an opportunity to reduce the general rates of sickness absence. The complete explanation for this social gradient still remains unclear and there is a need for studies using randomized working population samples. The main aim of the present study was to investigate if self-reported work ability could explain the association between low socioeconomic position and belonging to a sample of new cases of sick-listed employees.
The two study samples consisted of a randomized working population (n = 2,763) and a sample of new cases of sick-listed employees (n = 3,044), 19-64 years old. Both samples were drawn from the same randomized general population. Socioeconomic status was measured with occupational position and physical and mental work ability was measured with two items extracted from the work ability index.
There was an association between lower socioeconomic status and belonging to the sick-listed sample among both women and men. In men the crude Odds ratios increased for each downwards step in socioeconomic status, OR 1.32 (95% CI 0.98-1.78), OR 1.53 (1.05-2.24), OR 2.80 (2.11-3.72), and OR 2.98 (2.27-3.90). Among women this gradient was not as pronounced. Physical work ability constituted the strongest explanatory factor explaining the total association between socioeconomic status and being sick-listed in women. However, among men, the association between skilled non-manual, OR 2.07 (1.54-2.78), and non-skilled manual, OR 2.03 (1.53-2.71) positions in relation to being sick-listed remained. The explanatory effect of mental work ability was small. Surprisingly, even in the sick-listed sample most respondents had high mental and physical work ability.
These results suggest that physical work ability may be an important key in explaining the social gradient in sickness absence, particularly in women. Hence, it is possible that the factors associated with the social gradient in sickness absence may differ, to some extent, between women and men.
The association between chronic respiratory diseases and work disability has been demonstrated a number of times over the past 20 years, but still little is known about work disability in occupational cohorts of workers exposed to respiratory irritants. This study investigated job or task changes due to respiratory problems as an indicator of work disability in pulp mill workers occupationally exposed to irritants.
Data about respiratory symptoms and disease diagnoses, socio-demographic variables, occupational exposures, gassing episodes, and reported work changes due to respiratory problems were collected using a questionnaire answered by 3226 pulp mill workers. Information about work history and departments was obtained from personnel files. Incidence and hazard ratios for respiratory work disability were calculated with 95% confidence intervals (CI).
The incidence of respiratory work disability among these pulp mill workers was 1.6/1000 person-years. The hazard ratios for respiratory work disability were increased for workers reporting gassings (HR 5.3, 95% CI 2.7-10.5) and for those reporting physician-diagnosed asthma, chronic bronchitis, and chronic rhinitis, when analyzed in the same model.
This cohort study of pulp mill workers found that irritant peak exposure during gassing episodes was a strong predictor of changing work due to respiratory problems, even after adjustment for asthma, chronic bronchitis, and chronic rhinitis.
The primary aim of the present study was to investigate if exposure to dust from absorbent hygiene products containing superabsorbent polymer is related to symptoms from the airways and from the eyes. The secondary aim was to estimate the current exposure to superabsorbent polymer among production and maintenance workers in a plant producing hygiene products.
The cohort comprised 1043 workers of whom 689 were exposed to super absorbent polymer and 804 were exposed to paper dust (overlapping groups). There was 186 workers not exposed to either superabsorbent polymer or to paper dust They were investigated with a comprehensive questionnaire about exposure, asthma, rhinitis and symptoms from eyes and airways. The results were analyzed with logistic regression models adjusting for sex, age, atopy and smoking habits. An aerosol sampler equipped with a polytetrafluoroethylene filter with 1 μm pore size was used for personal samplings in order to measure inhalable dust and superabsorbent polymer.
The prevalence of nasal crusts (OR 1.4, 95% CI 1.01-2.0) and nose-bleeding (OR 1.7, 95% CI 1.2-2.4) was increased among the paper dust exposed workers (adjusted for superabsorbent polymer exposure). There were no significant effects associated with exposure to superabsorbent polymer (adjusted for paper dust exposure). The average exposure to inhalable levels of total dust (paper dust) varied between 0.40 and 1.37 mg/m3. For superabsorbent polymer dust the average exposure varied between 0.02 and 0.81 mg/m3.
In conclusion, our study shows that workers manufacturing diapers in the hygiene industry have an increased prevalence of symptoms from the nose, especially nose-bleeding. There was no relation between exposure to superabsorbent polymer and symptoms from eyes, nose or respiratory tract, but exposure to paper dust was associated with nose-bleeding and nasal crusts. This group of workers had also a considerable exposure to superabsorbent polymer dust.
The increase in asthma prevalence until 1990 has been well described. Thereafter, time trends are poorly known, due to the low number of high quality studies. The preferred method for studying time trends in prevalence is repeated surveys of similar populations. This study aimed to compare the prevalence of asthma symptoms and their major determinants, rhinitis and smoking, in Swedish young adults in 1990 and 2008.
In 1990 the European Community Respiratory Health Survey (ECRHS) studied respiratory symptoms, asthma, rhinitis and smoking in a population-based sample (86% participation) in Sweden. In 2008 the same symptom questions were included in the Global Allergy and Asthma European Network (GA2LEN) survey (60% participation). Smoking questions were however differently worded. The regions (Gothenburg, Uppsala, Umeå) and age interval (20–44 years) surveyed both in 1990 (n = 8,982) and 2008 (n = 9,156) were analysed.
The prevalence of any wheeze last 12 months decreased from 20% to 16% (p<0.001), and the prevalence of “asthma-related symptoms” was unchanged at 7%. However, either having asthma attacks or using asthma medications increased from 6% to 8% (p<0.001), and their major risk factor, rhinitis, increased from 22% to 31%. Past and present smoking decreased.
From 1990 to 2008 the prevalence of obstructive airway symptoms common in asthma did not increase in Swedish young adults. This supports the few available international findings suggesting the previous upward trend in asthma has recently reached a plateau. The fact that wheeze did not increase despite the significant increment in rhinitis, may at least in part be due to the decrease in smoking.
There are few studies about school-environment in relation to pupils' respiratory health, and Korean school-environment has not been characterized. All pupils in 4th grade in 12 selected schools in three urban cities in Korea received a questionnaire (n = 2,453), 96% participated. Gaseous pollutants and ultrafine particles (UFPs) were measured indoors (n = 34) and outdoors (n = 12) during winter, 2004. Indoor dampness at home was investigated by the questionnaire. To evaluate associations between respiratory health and environment, multiple logistic- and multi-level regression models were applied adjusting for potential confounders. The mean age of pupils was 10 yr and 49% were boys. No school had mechanical ventilation and CO2-levels exceeded 1,000 ppm in all except one of the classrooms. The indoor mean concentrations of SO2, NO2, O3 and formaldehyde were 0.6 µg/m3, 19 µg/m3, 8 µg/m3 and 28 µg/m3, respectively. The average level of UFPs was 18,230 pt/cm3 in the classrooms and 16,480 pt/cm3 outdoors. There were positive associations between wheeze and outdoor NO2, and between current asthma and outdoor UFPs. With dampness at home, pupils had more wheeze. In conclusion, outdoor UFPs and even low levels of NO2 may adversely contribute to respiratory health in children. High CO2-levels in classrooms and indoor dampness/mold at home should be reduced.
Asthma; Indoor Dampness; Mold Nitrogen Dioxide; Ultrafine Particles
Snakebites are a public health problem in Nicaragua: it is a tropical developing country, venomous snakes are present and there are reports of snakebites treated both in the formal and informal health care system. We aimed to produce an incidence map using data reported by the health care system that would be used to allocate resources. However, this map may suffer from case detection bias and decisions based on this map will neglect snakebite victims who do not receive healthcare. To avoid this error, we try to identify where underreporting is likely based on available information.
Method and Findings
The Nicaraguan municipalities are categorized by precipitation, altitude and geographical location into regions of assumed homogenous snake prevalence. Socio-economic and healthcare variables hypothesized to be related to underreporting of snakebites are aggregated into an index. The environmental region variable, the underreporting index and three demographic variables (rurality, sex and age distribution) are entered in a Poisson regression model of municipality-level snakebite incidence. In this model, the underreporting index is non-linearly associated with snakebite incidence, a finding we attribute to underreporting in the most deprived municipalities. The municipalities with the worst scoring on the underreporting index and those with combined low reported incidence and large rural population are identified as likely underreporting. 3,286 snakebite cases were reported in 2005–2009, corresponding to a 5-year incidence of 56 bites per 100,000 inhabitants (municipality range: 0–600 cases per 100,000 inhabitants).
Using publicly available data, we identified areas likely to be underreporting snakebites and highlighted these areas instead of leaving them “white” on the incidence map. The effects of the case detection bias on the distribution of resources against snakebites could decrease. Although not yet verified empirically, our study provides an example of how snake bite epidemiology may be investigated in similar settings worldwide at a low cost.
Snakebites have recently been recognized as a neglected cause of human suffering and death worldwide. Many bites are treated by traditional practitioners and thereby not recorded by the health care system. This leads to a lack of reliable epidemiological data and is identified as a major obstacle in dealing with this health problem. Household surveys are recommended for finding the true snakebite incidence, but the countries where snakebites are frequent are usually poor, meaning that this method is often too expensive. The usage of data reported by the health care system could then provide a necessary option when locating and estimating the snakebite problem. However, this data could be biased and lead to implementation of unfair policies. In this study, we use publicly available data about environmental, socioeconomic and health-care related variables and incidence reported from health care facilities to create a map of where underreporting could be suspected, either because of the presence of factors favouring underreporting or by a comparatively low reported incidence. By high-lighting these areas, the reported statistics are put into a context and the decision-maker is able to make a less biased decision on where to locate research, preventive and therapeutic resources.
A growing number of epidemiological studies are showing that ambient exposure to particulate matter air pollution is a risk factor for cardiovascular disease; however, whether occupational exposure increases this risk is not clear. The aim of the present study was to examine whether occupational exposure to particulate air pollution increases the risk for ischaemic heart disease and cerebrovascular disease.
The study population was a cohort of 176 309 occupationally exposed Swedish male construction workers and 71 778 unexposed male construction workers. The definition of exposure to inorganic dust (asbestos, man‐made mineral fibres, dust from cement, concrete and quartz), wood dust, fumes (metal fumes, asphalt fumes and diesel exhaust) and gases and irritants (organic solvents and reactive chemicals) was based on a job‐exposure matrix with focus on exposure in the mid‐1970s. The cohort was followed from 1971 to 2002 with regard to mortality to ischaemic heart disease and cerebrovascular disease. Relative risks (RR) were obtained by the person‐years method and from Poisson regression models adjusting for baseline values of blood pressure, body mass index, age and smoking habits.
Any occupational particulate air pollution was associated with an increased risk for ischemic heart disease (RR 1.13, 95% CI 1.07 to 1.19), but there was no increased risk for cerebrovascular disease (RR 0.97, 95% CI 0.88 to 1.07). There was an increased risk for ischaemic heart disease and exposure to inorganic dust (RR 1.07, 95% CI 1.03 to 1.12) and exposure to fumes (RR 1.05, 95% CI 1.00 to 1.10), especially diesel exhaust (RR 1.18, 95% CI 1.13 to 1.24). There was no significantly increased risk for cerebrovascular disease and exposure to inorganic dust, fumes or wood dust.
Occupational exposure to particulate air pollution, especially diesel exhaust, among construction workers increases the risk for ischaemic heart disease.
The authors examined the relations between self‐reported work tasks, use of cleaning products and latex glove use with new‐onset asthma among nurses and other healthcare workers in the European Community Respiratory Health Survey (ECRHS II).
In a random population sample of adults from 22 European sites, 332 participants reported working in nursing and other related healthcare jobs during the nine‐year ECRHS II follow‐up period and responded to a supplemental questionnaire about their principal work settings, occupational tasks, products used at work and respiratory symptoms. Poisson regression models with robust error variances were used to compare the risk of new‐onset asthma among healthcare workers with each exposure to that of respondents who reported professional or administrative occupations during the entire follow‐up period (n = 2481).
Twenty (6%) healthcare workers and 131 (5%) members of the referent population reported new‐onset asthma. Compared to the referent group, the authors observed increased risks among hospital technicians (RR 4.63; 95% CI 1.87 to 11.5) and among those using ammonia and/or bleach at work (RR 2.16; 95% CI 1.03 to 4.53).
In the ECRHS II cohort, hospital technicians and other healthcare workers experience increased risks of new‐onset current asthma, possibly due to specific products used at work.
Diseases of the skin are important and often preventable conditions occurring among workers with dermal exposures to irritant and sensitizing agents.
We conducted this analysis to assess the associations between metalworking exposures and current, persistent skin symptoms among male and female participants in two population-based epidemiologic studies.
We pooled data from the European Community Respiratory Health Survey II (ECRHS II) and the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults 2 (SAPALDIA 2), two prospective cohort studies in Europe. Participants each completed interviewer-administered questionnaires to provide information about symptoms and exposures related to selected occupations, including metalworking, during the follow-up periods. We assessed associations between skin symptoms and the frequency of metalworking exposures among 676 ECRHS II/SAPALDIA 2 respondents.
Current skin symptoms were reported by 10% of metalworkers and were associated with frequent use, defined as 4+days/week, of oil-based metalworking fluids (prevalence ratio (PR): 1.76, 95% confidence interval (CI): 1.25, 2.49) and organic solvent degreasing agents (PR: 2.06, 95% CI: 1.21, 3.50).
Skin symptom prevalence is associated with increasing frequency of oil-based metalworking fluid and degreasing agent use. Our findings justify assessing strategies for reducing the frequency of metal-related exposures.
contact dermatitis; epidemiology; metals; occupational diseases; occupational exposure
To estimate the occurrence of hand eczema in hairdressers in Sweden.
The occurrence of hand eczema was estimated in a Swedish longitudinal retrospective cohort study including all female graduates from vocational schools for hairdressers from 1970 to 1995. A stratified sample from the general population acted as controls. A self‐administered questionnaire including questions on the occurrence of hand eczema, skin atopy, working periods and number of hair treatments performed per week was sent to the participants. Incidence rate ratios (IRRs) of hand eczema were estimated.
The incidence rate of hand eczema in hairdressers was 23.8 cases/1000 person‐years, whereas in hairdressers who were aged <25 years it was 37.1/1000 person‐years. The corresponding IRR for hairdressers compared with controls was 2.5 (95% confidence interval (CI) 2.2 to 2.8), and that for younger hairdressers was 3.1 (95% CI 2.6 to 3.5). The mean age at onset of hand eczema was 21.6 years for hairdressers and 21.2 years for controls. The 1‐year prevalence of hand eczema was 18.0% for hairdressers and 12.1% for controls. A large number of hair treatments involving exposure to skin irritants and sensitisers were reported. The incidence rate of hand eczema was higher among individuals with a history of childhood eczema, both for hairdressers and for controls, giving an (age‐adjusted) IRR of 1.9 and 2.2, respectively. The attributable fraction of hand eczema from skin atopy was 9.6%. A synergistic effect of skin atopy and hairdressing was found on the occurrence of hand eczema. The relative excess risk due to interaction was 1.21 (95% CI 0.21 to 2.21; p = 0.01).
Hairdressers are highly exposed to skin‐damaging substances. The self‐reported incidence of hand eczema was substantially higher in female hairdressers than in controls from the general population and than that found previously in register‐based studies. For many individuals, onset of hand eczema occurs early in life. Only about 10% of the hand eczema cases among hairdressers would be prevented if no one with skin atopy entered the trade.
Asthma prevalence has increased over the last fifty years, but the more recent changes have not been conclusively determined. Studies in children indicate that a plateau in the prevalence of asthma may have been reached, but this has not yet been confirmed in adults. Epidemiological studies have suggested that the prevalence of asthma in adults is approximately 7-10% in different parts of the western world.
We have now performed a large-scale epidemiological evaluation of the prevalence of asthma and respiratory symptoms in adults between the ages of 16-75 in West Sweden. Thirty thousand randomly chosen individuals were sent a detailed questionnaire focusing on asthma and respiratory symptoms, as well possible risk factors. Sixty-two percent of the contacted individuals responded to the questionnaire. Asthma prevalence, defined as asthma diagnosed by a physician, was 8.3%. Moreover, the prevalence of respiratory symptoms was lower compared to previous studies. The most common respiratory symptom was any wheeze (16.6%) followed by sputum production (13.3%). In comparison with studies performed 18 years ago, the prevalence of asthma has not increased, and the prevalence of most respiratory symptoms has decreased. Therefore, our data argues that the continued increase in asthma prevalence that has been observed over the last half century is over.
Inhalation incidents are an important cause of acute respiratory symptoms, but little is known about how these incidents affect chronic respiratory health.
We assessed reported inhalation incidents among 3,763 European Community Respiratory Health Survey (ECRHS) participants with and without cough, phlegm, asthma, wheezing or bronchial hyperresponsiveness. We then examined whether inhalation incidents during the 9-year ECRHS follow-up period were associated with a new onset of any of these respiratory outcomes among 2,809 participants who were free of all five outcomes at the time of the baseline ECRHS survey.
Inhalation incidents were reported by 5% of participants, with higher percentages reported among individuals with asthma-related outcomes at the time of the baseline survey. Among participants without symptoms at baseline, our analyses generated non-statistically significant elevated estimates of the risk of cough, phlegm, asthma and wheezing and a non-statistically significant inverse estimate of the risk of bronchial hyperresponsiveness among participants who reported an inhalation incident compared to those without such an event reported.
Our findings provide limited evidence of an association between inhalation incidents and asthma-related symptoms. These data could be affected by differences in the reporting of inhalation incidents according to symptom status at the time of the baseline survey; they should thus be interpreted with caution.
accident; asthma; epidemiology; inhalation; respiratory health
The aim of this paper is to highlight emerging data on occupational attributable risk in asthma. Despite well documented outbreaks of disease and the recognition of numerous specific causal agents, occupational exposures previously had been relegated a fairly minor role relative to other causes of adult onset asthma. In recent years there has been a growing recognition of the potential importance of asthma induced by work-related exposures
We searched Pub Med from June 1999 through December 2007. We identified six longitudinal general population-based studies; three case-control studies and eight cross-sectional analyses from seven general population-based samples. For an integrated analysis we added ten estimates prior to 1999 included in a previous review.
The longitudinal studies indicate that 16.3% of all adult-onset asthma is caused by occupational exposures. In an overall synthesis of all included studies the overall median PAR value was 17.6%.
Clinicians should consider the occupational history when evaluating patients in working age who have asthma. At a societal level, these findings underscore the need for further preventive action to reduce the occupational exposures to asthma-causing agents.
Rationale: Cleaning work and professional use of certain cleaning products have been associated with asthma, but respiratory effects of nonprofessional home cleaning have rarely been studied.
Objectives: To investigate the risk of new-onset asthma in relation to the use of common household cleaners.
Methods: Within the follow-up of the European Community Respiratory Health Survey in 10 countries, we identified 3,503 persons doing the cleaning in their homes and who were free of asthma at baseline. Frequency of use of 15 types of cleaning products was obtained in a face-to-face interview at follow-up. We studied the incidence of asthma defined as physician diagnosis and as symptoms or medication usage at follow-up. Associations between asthma and the use of cleaning products were evaluated using multivariable Cox proportional hazards or log-binomial regression analysis.
Measurements and Main Results: The use of cleaning sprays at least weekly (42% of participants) was associated with the incidence of asthma symptoms or medication (relative risk [RR], 1.49; 95% confidence interval [CI], 1.12−1.99) and wheeze (RR, 1.39; 95% CI, 1.06−1.80). The incidence of physician-diagnosed asthma was higher among those using sprays at least 4 days per week (RR, 2.11; 95% CI, 1.15−3.89). These associations were consistent for subgroups and not modified by atopy. Dose–response relationships (P < 0.05) were apparent for the frequency of use and the number of different sprays. Risks were predominantly found for the commonly used glass-cleaning, furniture, and air-refreshing sprays. Cleaning products not applied in spray form were not associated with asthma.
Conclusions: Frequent use of common household cleaning sprays may be an important risk factor for adult asthma.
airway irritants; epidemiology; incidence; ECRHS