Biomedical subjects
Publications and source records attributed to R Rylander.
The amount of (1-->3)-beta-D-glucan in pollen from different plants was evaluated using the Limulus assay with a specific lysate. The amount ranged from 79 to 1800 ng/10(6) pollen. A calculation of the inhaled dose suggests that the amount of (1-->3)-beta-D-glucan present during periods with a high pollen content in the air exceeds levels that cause airways inflammation.
OBJECTIVES: To further assess the presence of fatigue, symptoms of diarrhoea, and inflammation of airways among people working in sewage plants and the relation to airborne bacterial endotoxin at the workplace. METHODS: 34 Employees in sewage treatment plants and 35 controls were selected. They underwent a questionnaire investigation, and spirometry and airway responsiveness were measured. Measurements were made of airborne endotoxin at different workplaces. RESULTS: The amount of airborne endotoxin varied between 3.8 and 32,170 ng/m3. Workers reported significantly higher nose irritation, tiredness, and diarrhoea. Airway responsiveness was increased among sewage workers, but no differences between the groups were found for spirometry. CONCLUSIONS: The results confirm previous studies on the presence of airways and intestinal inflammation among workers in sewage treatment plants. The most likely causative agent is endotoxin, and at 14 of 23 workplaces, concentrations exceeded recommended guidelines.
Reactive airways disease in children is increasing in many countries around the world. The clinical diagnosis of asthma or reactive airways disease includes a variable airflow and an increased sensitivity in the airways. This condition can develop after an augmented reaction to a specific agent (allergen) and may cause a life-threatening situation within a very short period of exposure. It can also develop after a long-term exposure to irritating agents that cause an inflammation in the airways in the absence of an allergen. (paragraph) Several environmental agents have been shown to be associated with the increased incidence of childhood asthma. They include allergens, cat dander, outdoor as well as indoor air pollution, cooking fumes, and infections. There is, however, increasing evidence that mold growth indoors in damp buildings is an important risk factor. About 30 investigations from various countries around the world have demonstrated a close relationship between living in damp homes or homes with mold growth, and the extent of adverse respiratory symptoms in children. Some studies show a relation between dampness/mold and objective measures of lung function. Apart from airways symptoms, some studies demonstrate the presence of general symptoms that include fatigue and headache and symptoms from the central nervous system. At excessive exposures, an increased risk for hemorraghic pneumonia and death among infants has been reported. (paragraph) The described effects may have important consequences for children in the early years of life. A child's immune system is developing from birth to adolescence and requires a natural, physiologic stimulation with antigens as well as inflammatory agents. Any disturbances of this normal maturing process will increase the risk for abnormal reactions to inhaled antigens and inflammagenic agents in the environment. (paragraph) The knowledge about health risks due to mold exposure is not widespread and health authorities in some countries may not be aware of the serious reactions mold exposure can provoke in some children. Individual physicians may have difficulty handling the patients because of the lack of recognition of the relationship between the often complex symptoms and the indoor environment (paragraph) The workshop was organized to develop a basis for risk assessment and formulation of recommendations, particularly for diagnostic purposes and prevention, and to formulate priorities for future research. The participants were all active researchers with current experience in child health, molds, and respiratory disease. They were engaged in free and intensive discussions on a scientific basis throughout the duration of the 3-day workshop (paragraph) This monograph contains peer-reviewed papers based on individual presentations at the workshop as well as the workshop conclusions. They are offered to the public health community, administrators, research agencies, physicians, particularly pediatricians, nurses and health workers as information and encouragement to engage themselves in this health problem of importance for the next generation in our population. (paragraph) Acknowledgments: The workshop received financial support from the U.S. Environmental Protection Agency, the National Center for Environmental Assessment at the U.S. EPA, the Vardal Foundation (Sweden), Astra Corp (Sweden), the Committee on Organic Dusts, International Commission on Occupational Health. The printing of this document was made possible by a grant from the Center for Indoor Air Research (U.S.). Yvonne Peterson, research secretary, provided excellent and invaluable assistance in the organization and publication efforts.
To evaluate the health consequences for children of indoor exposure to molds, an international workshop was organized with 15 scientists from eight countries. The participants agreed that exposure to molds may constitute a health threat to children resulting in respiratory symptoms in both the upper and lower airways, an increased incidence of infections, and skin symptoms. Allergy, either to molds or to other indoor agents, also presents a health risk. At very high exposure levels to specific molds, nose bleeding, hemoptysis, and pulmonary hemorrhage have been documented. Pediatricians and allergists need to obtain information about mold and dampness in the home environment when examining children with chronic respiratory symptoms, recurrent infections, or persistent fatigue and headache. Measurement techniques are available to determine exposure. Most important, the source of dampness must be eliminated and the indoor environment must be thoroughly cleaned of molds.
In studies on the relation between indoor mold exposure and symptoms/disease, the exposure should be described in terms of biomass and not viability. This paper reviews field studies in which (1--> 3)-ss-d-glucan was measured as a marker of biomass and was related to the extent of symptoms and measures of inflammation among exposed subjects. Increased levels of (1-->3)-ss-d-glucan were related to an increased extent of symptoms and markers of inflammation. The data suggest that (1-->3)-ss-d-glucan can be used as a risk marker in indoor environments.
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A relation between water hardness and cardiovascular death has been shown in previous studies. In this case-control study, we investigated the levels of magnesium and calcium in drinking water and death from acute myocardial infarction among women. The study population encompassed 16 municipalities in southern Sweden. Cases were women who had died from acute myocardial infarction between the ages of 50 and 69 years during 1982-1993 (N = 378), and controls were women who had died from cancer (N = 1,368). We obtained magnesium and calcium concentrations of the individual water sources. We divided the subjects into quartiles and found that odds ratios (ORs) were lower at higher levels of both magnesium and calcium. For the quartile with the highest magnesium levels (> or =9.9 mg/liter), the OR adjusted for age and calcium was 0.70 (95% confidence interval = 0.50-0.99). For calcium, the adjusted OR for the quartile with the highest level (> or =70 mg/liter) was 0.66 (95% confidence interval = 0.47-0.94). The results suggest that magnesium and calcium in drinking water are important protective factors for death from acute myocardial infarction among women.
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Three children living in a house affected by mould manifested severe airways and general symptoms indicative of non-specific airways inflammation. Measurement of airborne (1-->3)-beta-D-glucan, a cell wall constituent in moulds, yielded values ranging from 22 to 115 ng/m3, as compared to normal values of some few ng/m3. On moving to relatives, all three children improved and could terminate medication after 2-3 weeks. The findings are consistent with previous reports of symptoms induced by exposure to mould, and suggest that quantification of viable organisms may not adequately reflect the exposure risk.
A field study was made on 17 workers collecting unsorted household waste, eight workers collecting organic/nonorganic separated waste, and 24 controls. Measurements of airborne endotoxin and (1-->3)-beta-D-glucan were made in their working environments. Examinations consisted of a questionnaire for symptoms, spirometry, airway responsiveness, and blood and sputum sampling for determination of cell counts, eosinophilic cationic protein (ECP), and myeoloperoxidase (MPO). A higher proportion of waste collectors reported diarrhea, congested nose, and unusual tiredness as compared to controls. The number of blood lymphocytes was higher among waste collectors and were dose-related to the amount of airborne (1-->3)-beta-D-glucan at the workplaces. The amount of ECP and the number of macrophages were lower in sputum among waste collectors as compared with controls. The results suggest that certain dusts from household waste may cause airway inflammation as well as general symptoms, and the effects were associated with higher (1-->3)-beta-D-glucan levels.
Epidemiological studies have shown an inverse relationship between magnesium in drinking water and death from ischaemic heart disease. The question is whether magnesium in drinking water can be critical for the body magnesium status. The aim of this study was to investigate, using an oral loading test, whether a change in body magnesium status could be found among people who change from drinking water with a low magnesium concentration to water with higher concentrations. The subjects participating in the study were 9 men and 3 women 65-70 years old, living in the city of Göteborg, Sweden, where the magnesium concentration in the tap water is low (1.6 mg/l). Drinking water was prepared with 200 mg MgCl2 x 6H2O added per litre to a level of 25 mg/l, and was distributed to the subjects twice a week for 6 weeks. Excretion of magnesium, potassium and creatinine, basal and after oral magnesium loading (tablets containing 575 mg), was measured in 24 h urine before and after the supplementation period. Calculations were made for the total excretion (mmol/24 h), and in relation to creatinine. The subjects' intake of magnesium via food and water was estimated using a questionnaire. There was a difference between the post load excretion of magnesium, expressed as the magnesium/creatinine ratio, before and after the supplementation period. The mean percentage change was a 14.6% (p=0.047) increase. No changes were found for potassium. In summary, the results indicate that magnesium in drinking water can affect body magnesium status.
Exposure to dust may involve co-exposure to agents which are allergens, together with those which are pro-inflammatory. To study the effects of such a co-exposure, the humoral and inflammatory responses were studied in guinea pigs inhaling the T-cell-dependent antigen ovalbumin (OVA) and the inflammatory agents (1 --> 3)-beta-D-glucan and lipopolysaccharide (LPS). The effects were evaluated as inflammatory cells in the lung and serum antibodies to OVA. LPS caused a stimulation of the OVA-induced antibody production which was abolished by simultaneous exposure to (1 --> 3)-beta-D-glucan. An increase of eosinophils after OVA exposure was decreased by co-exposure to (1 --> 3)-beta-D-glucan. The results demonstrate a complex interaction between adaptive and innate immune mechanisms in the lung, determined by exposure to common contaminants in airborne dust.
BACKGROUND: Organic dusts may cause inflammation in the airways. This study was performed to assess the usefulness of the induced sputum technique for evaluating the presence of airways inflammation using inhaled endotoxin (lipopolysaccharide) as the inducer of inflammation. METHODS: To characterise the inflammatory response after inhalation of endotoxin, 21 healthy subjects inhaled 40 micrograms lipopolysaccharide and were examined before and 24 hours after exposure. Examinations consisted of a questionnaire for symptoms, spirometric testing, blood sampling, and collection of induced sputum using hypertonic saline. Eleven of the subjects inhaled hypertonic saline without endotoxin exposure as controls. Cell counts, eosinophilic cationic protein (ECP), and myeloperoxidase (MPO) were determined in blood and sputum. RESULTS: A significantly higher proportion of subjects reported respiratory and general symptoms after endotoxin inhalation. MPO and the number of neutrophils in the blood were higher and spirometric values were decreased after the lipopolysaccharide challenge. In the sputum MPO, ECP, and the numbers of neutrophils and lymphocytes were higher after the lipopolysaccharide challenge. No significant differences were found after the inhalation of hypertonic saline compared with before, except for a significantly lower number of lymphocytes in the sputum. CONCLUSIONS: The results support previous studies that inhaled endotoxin causes an inflammation at the exposure site itself, as well as general effects. Sampling of sputum seems to be a useful tool for assessing the presence of airways inflammation, and the inhalation of hypertonic saline used to induce sputum did not significantly interfere with the results found after inhalation of lipopolysaccharide.
A study was undertaken in a number of rowhouses, some of which had had previous problems related to dampness and water leakage. The aim of the study was to assess the relation between exposure to airborne (1--> 3)-beta-D-glucan, a cell-wall substance in molds, and airways inflammation. The study involved 75 houses with indoor (1--> 3)-beta-D-glucan levels ranging from 0 to 19 ng/m3. Of 170 invited tenants, 129 (76%) participated in the study. A questionnaire relating to symptoms was used, and measurements were made of lung function and airway responsiveness. Myeloperoxidase (MPO), eosinophilic cationic protein (ECP), and C-reactive protein (CRP) were measured in serum. Atopy was determined with the Phadiatop test. The major findings were a relation between exposure to (1--> 3)- beta-D-glucan and an increased prevalence of atopy, a slightly increased amount of MPO, and a decrease in FEV1 over the number of years lived in the house. The results suggests the hypothesis that exposure to (1--> 3)-beta-D-glucan or molds indoors could be associated with signs of a non-specific inflammation.
This study investigated two schools, one of which had previous mold problems. Pupils aged 6 to 13 yr were investigated using a questionnaire on symptoms and a skin prick test. The amount of airborne (1--> 3)-beta-D-glucan was measured in the classrooms. The levels were significantly higher in the problem school than in the control school (15.3 versus 2.9 ng/m3). The extent of respiratory as well as general symptoms was higher among the pupils in the problem school. Among the atopics, the extent of symptoms of dry cough, cough with phlegm, and hoarseness was similar to the nonatopics in the control school, but significantly higher in the problem school. The results suggest that (1--> 3)-beta-D-glucan, either by itself or as an indicator of molds, is a risk indicator of airways inflammation.
OBJECTIVE AND DESIGN: To evaluate the effect of a microbial cell wall component--(1-->3)-beta-D-glucan--on the inflammatory effect induced by cigarette smoke in a subchronic exposure situation. MATERIAL: Groups of guinea-pigs were exposed 5 days/week to cigarette smoke, an aerosol of (1-->3)-beta-D-glucan, or to both. METHODS: The numbers of different inflammatory cells were studied in histological sections, enzyme digested lung tissue and in lung lavage. Cell enzyme production was measured. RESULTS: Exposure to (1-->3)-beta-D-glucan or cigarette smoke caused only minor alterations in inflammatory cells. Given together they caused an increase in cellularity in the tissue with significantly increased numbers of macrophages, lymphocytes, neutrophils and eosinophils. There was also an increase in subepithelial eosinophils. Lung lavage cell enzyme production was slightly lower in the combined exposure group. CONCLUSION: The results demonstrate that (1-->3)-beta-D-glucan synergistically increases the inflammation induced by cigarette smoke. The mechanism may be a downregulation of the macrophage control of inflammatory cell migration into the lung tissue.
From epidemiologic studies in several countries, passive smoking has been associated with increased risk for lung cancer, respiratory diseases, and coronary heart disease. Since the relative risks derived from those studies are weak, i.e. relative risk less than two, we investigated whether poorer diets and less healthy lifestyles might act as confounders and be correlated with having a smoking husband on a cross-cultural basis. Characteristics of never-smoked wives with or without smoking husbands were compared between 530 women from Hong Kong, 13,047 from Japan, 87 from Sweden, and 144 from the U.S. In all four sites, wives with smoking husbands generally ate less healthy diets. They had a tendency to eat more fried food but less fruit than wives with nonsmoking husbands. Other healthy traits, e.g. avoiding obesity, dietary cholesterol and alcohol, or taking vitamins and participating in preventive screening were also less prevalent among wives with smoking husbands. These patterns suggest that never-smoked wives with smoking husbands tend to share the same less healthy dietary traits characteristic of smokers, and to have dietary habits associated with increased risk for lung cancer and heart disease in their societies. These results emphasize the need to take into account the potential confounding effects of diet and lifestyle in studies evaluating the health effects of passive smoking, especially since it is known that the current prevalence rates of smoking among men is indirectly associated with social class and education in affluent urban societies.
It has been implicated that high vegetable intake is associated with a decreased risk for various forms of cancer in epidemiological studies. A major defense system against cancer has shown to be antioxidants. Glutathione S-transferases (GSTs), one of the major defense ststems against oxidative damage, can be induced by antioxidant and addition of vegetables to their normal diet. Serum retinol and a-tocopherol were determined by HPLC and the gene expression of GST pi in lymphocytes was measured by reverse transcription-polymerase chain reaction (RT-PCR) techniques. The results showed that there was on significant difference in the levels of serum retinol and a-tocopherol before and after the addition of vegetables. GST pi mRNA levels in lymphocytes were higher in four out of five subjects after addition of vegetables. The results suggested that it might be other antioxidants than vitamin A and E in the vegetables that induced the gene transcription of GST pi.