Outdoor Factors

General Ozone Particulates Dust/Molds Pollens Pesticides

General

Author(s): Peden DB
Affiliation: Department of Pediatrics, and Center for Environmental Medicine and Lung Biology, School of Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7310, USA. peden@med.unc.edu

Title: Pollutants and asthma: role of air toxics. Source: Environ Health Perspect (Environmental health perspectives.) 2002 Aug; 110 Suppl 4: 565-8

Abstract: Asthma is a disease characterized by intermittent bronchoconstriction due to increased airway reactivity to both allergic and nonallergic stimuli. Most asthma exacerbations that result in hospitalization are associated with viral upper respiratory tract infections. Such infections typically induce T-helper type 1 (T(H)1) responses in the airway, involving activation of nuclear factor-kappaB (NF-Kappa B). However, a more recently appreciated cause of asthma exacerbation is exposure to pollutants, including ozone and various components of particulate matter (PM), including transition metals, diesel exhaust, and biologicals such as endotoxin. Although the role of air toxics in asthma pathogenesis remains incompletely examined, many components of PM that are active exacerbants of asthma are also prominent air toxics (metal ions and organic residues). These agents have been observed to activate NF-Kappa B. Reviewed in this article are the actions of specific air pollutants on airway inflammation in humans and potential common response pathways for ozone, PM, and several air toxics.

Author(s): Dales RE ; Cakmak S ; Judek S ; Dann T ; Coates F ; Brook JR ; Burnett RT
Affiliation: University of Ottawa, Ottawa, Ontario, Canada.

Title: Influence of outdoor aeroallergens on hospitalization for asthma in Canada. Source: J Allergy Clin Immunol (The Journal of allergy and clinical immunology.) 2004 Feb; 113(2): 303-6

Abstract: BACKGROUND: The risk of hospitalization for asthma caused by outdoor aeroallergens is largely unknown. OBJECTIVE: The objective of this study was to determine the association between changes in outdoor aeroallergens and hospitalizations for asthma from the Pacific coast to the Atlantic coast of Canada. METHODS: A daily time series analysis was done to test the association between daily changes in aeroallergens and daily changes in hospitalizations for asthma during a 7-year period between 1993 and 2000 in 10 of the largest cities in Canada. Results were adjusted for long-term trends, day of the week, climate, and air pollution. RESULTS: A daily increase, equivalent to the mean value of each allergen, was associated with the following percentage increase in asthma hospitalizations: 3.3% (95% CI, 2.3 to 4.1) for basidiomycetes, 3.1% (95% CI, 2.8 to 5.7) for ascomycetes, 3.2% (95% CI, 1.6 to 4.8) for deuteromycetes, 3.0% (95% CI, 1.1 to 4.9) for weeds, 2.9% (95% CI, 0.9 to 5.0) for trees, and 2.0% (95% CI, 1.1 to 2.8) for grasses. After accounting for the independent effects of trees and ozone, the combination of the 2 was associated with an additional 0.22% increase in admissions averaged across cities (P <.05). CONCLUSION: These findings provide evidence for the hypothesis that aeroallergens are an important cause of severe asthma morbidity across Canada, and in some situations there might be a modest synergistic adverse effect of ozone and aeroallergens combined.

Author(s): Koenig JQ
Affiliation: Department of Environmental Health, University of Washington, Seattle, Wash. 98195, USA.

Title: Air pollution and asthma. Source: J Allergy Clin Immunol (The Journal of allergy and clinical immunology.) 1999 Oct; 104(4) Pt 1: 717-22

Abstract: Asthma is a disease syndrome that has captured a great deal of attention for several years. One of the perplexing aspects to asthma is that the prevalence is increasing in most industrialized countries. The reasons for this widespread increase are largely unknown. Another aspect of industrialization is the persistence of air pollution in urban areas. Because much air pollution is due to vehicles, no solution appears in sight. The topic of this article is the association between air pollution and various signs and symptoms of asthma. Air pollution is convincingly associated with many signs of asthma aggravation. These include pulmonary function decrements, increased bronchial hyperresponsiveness, visits to emergency departments, hospital admissions, increased medication use and symptom reporting, inflammatory changes, interactions between air pollution and allergen challenges, and immune system changes. With the exception of exposure to environmental tobacco smoke, common air pollutants have not been shown to cause asthma. It seems prudent for clinicians to counsel their patients about the potential risks of asthma aggravation from common outdoor air pollutants.

Author(s): Anderson HR
Affiliation: Department of Public Health Sciences, St. George's Hospital Medical School, London, UK.

Title: Air pollution and trends in asthma. Source: Ciba Found Symp (Ciba Foundation symposium.) 1997; 206: 190-202; discussion 203-7

Abstract: There is considerable concern about possible links between ambient air pollution and the upward trend in asthma. This chapter reviews the mechanistic and epidemiological evidence concerning air pollution and asthma and examines the hypothesis that trends in asthma could be explained by air pollution. It is concluded that existing evidence is not sufficient to link air pollution with the initiation of asthma in healthy subjects. Although there is better evidence that air pollution can provoke or aggravate asthma, it probably plays a minor role at a public health level, in comparison with other factors. It is therefore unlikely that trends in asthma could be explained by air pollution. Furthermore, correlations between some air pollutants and asthma over time are not consistent with the hypothesis. The possibility of a specific effect of motor vehicle pollution needs further investigation but this factor is unlikely to be the main cause of the worldwide increase in asthma.

Author(s): Koenig JQ
Affiliation: Department of Environmental Health, University of Washington, Seattle, Wash. 98195, USA.

Title: Air pollution and asthma. Source: J Allergy Clin Immunol (The Journal of allergy and clinical immunology.) 1999 Oct; 104(4) Pt 1: 717-22

Author(s): Hiltermann TJ ; Stolk J ; van der Zee SC ; Brunekreef B ; de Bruijne CR ; Fischer PH ; Ameling CB ; Sterk PJ ; Hiemstra PS ; van Bree L
Affiliation: Dept of Pulmonology, Leiden University Medical Centre, The Netherlands.

Title: Asthma severity and susceptibility to air pollution. Source: Eur Respir J (The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology.) 1998 Mar; 11(3): 686-93

Abstract: Exacerbations of asthma have been associated with exposure to ozone or particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10). We postulated in this study that the association of summertime air pollution (i.e. ozone and PM10) with acute respiratory symptoms, medication use and peak expiratory flow differs among patients grouped according to asthma severity. During the summer of 1995, effects of ambient air pollution on these parameters were studied in a panel of 60 nonsmoking patients with intermittent to severe persistent asthma. These patients were recruited from our Pulmonary Out-patient Clinic. Subgroup analysis was performed on the degree of hyperresponsiveness and lung steroid use before the start of the study, as indictors for the severity of asthma. Associations of the parameters studied with ozone, PM10, nitrogen dioxide (NO2), sulphur dioxide (SO2) and black smoke were evaluated using time series analysis. Several episodes with increased summertime air pollution occurred during the 96 day study period. Eight hour average ozone concentrations exceeded the World Health Organization (WHO) Air Quality Guidelines (120 microg x m(-3)) on 16 occasions. Daily mean levels of PM10 were moderately elevated (range 16-98 microg x m(-3)). Levels of the other measured pollutants were low. There was a consistent, positive association of the prevalence of shortness of breath (maximal relative risk (RRmax) 1.18) with ozone, PM10, black smoke and NO2. In addition, bronchodilator use was associated with both ozone and PM10 levels (RRmax 1.16). Stratification by airway hyperresponsiveness and steroid use did not affect the magnitude of the observed associations. No associations with peak expiratory flow measurements were found. We conclude that the severity of asthma is not an indicator for the sensitivity to air pollution.

Author(s): Slaughter JC ; Lumley T ; Sheppard L ; Koenig JQ ; Shapiro GG
Affiliation: Department of Biostatistics, University of Washington, Seattle, Washington 98195-7232, USA.

Title: Effects of ambient air pollution on symptom severity and medication use in children with asthma. Source: Ann Allergy Asthma Immunol (Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.) 2003 Oct; 91(4): 346-53

Abstract: BACKGROUND: Exposure to air pollutants has been investigated as a possible cause of asthma attacks in children. OBJECTIVE: To investigate the short-term effects of air pollutants on a panel of 133 children with asthma who enrolled in the Childhood Asthma Management Program. METHODS: During screening, the children completed daily diary cards for an average of 58 days to indicate their medication use and asthma severity. We used ordinal logistic regression to compare the odds of a more serious relative to a less serious asthma attack, and we used a Poisson model to analyze medication use. In both analyses we accommodate dependence in the data and different periods of observation for study subjects. RESULTS: Our results indicate that a 10-microg/m3 increase in particulate matter less than or equal to 2.5 microm (PM2.5) lagged 1 day was associated with a 1.20 times increased odds of having a more serious asthma attack [95% confidence interval (CI), 1.05 to 1.37] and a 1.08-fold increase in medication use (95% CI, 1.01 to 1.15). A 10-microg/m3 increase in particulate matter less than or equal to 10 microm (PM10) increased the odds of a more serious asthma attack (odds ratio = 1.12; 95% CI, 1.04 to 1.22) and also increased medication use (relative risk = 1.05; 95% CI, 1.00 to 1.09). CONCLUSIONS: Increases in PM2.5 and PM10 are significantly associated with an increased risk of more severe asthma attacks and medication use in Seattle area children with asthma. We also found associations with carbon monoxide, but we believe that carbon monoxide is a marker for exposure to combustion byproducts.

Ozone

General Ozone Particulates Dust/Molds Pollens Pesticides

Author(s): Thurston GD ; Lippmann M ; Scott MB ; Fine JM
Affiliation: Nelson Institute of Environmental Medicine, New York University School of Medicine, Tuxedo 10987, USA.

Title: Summertime haze air pollution and children with asthma. Source: Am J Respir Crit Care Med (American journal of respiratory and critical care medicine.) 1997 Feb; 155(2): 654-60

Abstract: In order to investigate associations between summertime haze air pollution and asthma at an individual level, 52, 58, and 56 children (ages 7 to 13) attending a summer "asthma camp" were followed during the last week of June in 1991, 1992, and 1993, respectively. Most of the subjects had moderate to severe asthma. Daily records were kept of the environmental conditions, as well as of subject medication use, lung function, and medical symptoms. Air pollution was found to be significantly and consistently correlated with acute asthma exacerbations, chest symptoms, and lung function decrements. The pollutant most consistently associated with adverse health consequences was ozone (O3), although associations with sulfates and hydrogen ion suggest a possible role by fine particles as well. Effects were found to be roughly monotonic as a function of O3 concentration. Regression of morning (8:00 A.M.) to afternoon (5:00 P.M.) peak flow change on O3 indicated pulmonary function reductions similar to those previously reported for more active children without asthma. Moreover, analyses also indicated an increased risk of an asthma exacerbation and of experiencing chest symptoms of approximately 40% on the highest pollution day, relative to the mean. Based on these relative risk estimates, a rise in the 1-h daily maximal O3 from 84 ppb to 160 ppb was associated in this group with an increase from 20 to 28 (+/- 2) in the expected number of unscheduled medications administered/day, and from 29 to 41 (+/- 3) in the expected total number of chest symptoms/day. Thus, air pollution can be a major contributor to the respiratory problems experienced by children with asthma during the summer months.

Author(s): Jörres R ; Nowak D ; Magnussen H
Affiliation: Krankenhaus Grosshansdorf, Zentrum für Pneumologie und Thoraxchirurgie, Germany.

Title: The effect of ozone exposure on allergen responsiveness in subjects with asthma or rhinitis. Source: Am J Respir Crit Care Med (American journal of respiratory and critical care medicine.) 1996 Jan; 153(1): 56-64

Abstract: The aim of this study was to determine whether ozone enhances bronchial responsiveness to allergens in subjects with allergic asthma, or facilitates a bronchial response in subjects with allergic rhinitis. Twenty-four subjects with mild stable allergic asthma, 12 subjects with allergic rhinitis without asthma, and 10 healthy subjects participated in the study. Subjects breathed 250 ppb ozone or filtered air (FA) for 3 h of intermittent exercise. Airway responsiveness to methacholine was determined 1 h before and after exposures, and allergen responsiveness 3 h after exposures. We determined the concentration of methacholine (PC20FEV1) and the dose of allergen (PD20FEV1) producing a 20% fall in FEV1. In the subjects with asthma, FEV1 decreased by 12.5 +/- 2.2% (mean +/- SEM; p = 0.0001), PC20FEV1 of methacholine by 0.91 +/- 0.19 doubling concentrations (p = 0.0001) and PD20FEV1 of allergen by 1.74 +/- 0.25 doubling doses (p < 0.0001) after ozone compared with FA. The changes in lung function, methacholine, and allergen responsiveness did not correlate with each other. In the subjects with rhinitis, mean FEV1 decreased by 7.8% and 1.3% when ozone or FA, respectively, were followed by allergen inhalation (p = 0.035). Therefore, our data suggest that short-term exposure to ozone can increase bronchial allergen responsiveness in subjects with mild allergic asthma or rhinitis.

Author(s): Chen LL ; Tager IB ; Peden DB ; Christian DL ; Ferrando RE ; Welch BS ; Balmes JR
Affiliation: Lung Biology Center, Center for Occupational and Environmental Health, Cardiovascular Research Institute, and Medical Service, San Francisco General Hospital, University of California, San Francisco, CA, USA.

Title: Effect of ozone exposure on airway responses to inhaled allergen in asthmatic subjects. Source: Chest (Chest.) 2004 Jun; 125(6): 2328-35

Abstract: BACKGROUND: Controlled human exposure studies have produced conflicting results regarding the effect of ozone on the early bronchoconstrictor response to inhaled allergen in specifically sensitized asthmatic subjects. Spirometric parameters do not necessarily reflect the airway inflammatory effects of inhaled ozone or allergen. OBJECTIVE: This study was designed to investigate whether exposure to ozone enhances the late airway inflammatory response, as well as the early bronchoconstrictor response, to inhaled house dust mite allergen in sensitized asthmatic subjects. DESIGN: Randomized, counter-balanced, cross-over study. SETTING: Human exposure laboratory. METHODS: Fourteen subjects were exposed to 0.2 ppm O(3) or filtered air, on separate days, for 1 h during exercise. After each exposure, the subjects were challenged with doubling doses of Dermatophagoides farinae (DF) allergen (provocative concentration of DF causing a 15% decrease in FEV(1) [PC(15)]). At 6 h after allergen challenge, bronchoscopy with BAL, proximal airway lavage (PAL), and endobronchial biopsy were performed. The second exposure/allergen challenge/bronchoscopy sequence was performed at least 4 weeks after the first sequence. RESULTS: No significant difference in cellular or biochemical markers of the late inflammatory response after allergen was found between the ozone and air exposures (although a trend toward increased neutrophils was noted after ozone exposure in the PAL fluid, p = 0.06). For the group as a whole, no significant difference in PC(15) was demonstrated after ozone exposure compared to air exposure. However, subjects with the greatest ozone-induced decrements in FEV(1) tended to have lower PC(15) values after ozone exposure. CONCLUSION: Exposure to a relatively low-level concentration of ozone does not enhance the late inflammatory or early bronchoconstrictor response to inhaled antigen in most allergic asthmatic subjects. Our results do suggest, however, that a subgroup of asthmatics may acquire increased sensitivity to aeroallergens after exposure to ozone.

Author(s): Jalaludin BB ; O'Toole BI ; Leeder SR
Affiliation: Epidemiology Unit, South Western Sydney Area Health Services, Liverpool BC, NSW, Australia. b.jalaudin@unsw.edu.au

Title: Acute effects of urban ambient air pollution on respiratory symptoms, asthma medication use, and doctor visits for asthma in a cohort of Australian children. Source: Environ Res (Environmental research.) 2004 May; 95(1): 32-42

Abstract: We enrolled a cohort of primary school children with a history of wheeze (n=148) in an 11-month longitudinal study to examine the relationship between ambient air pollution and respiratory morbidity. We obtained daily air pollution (ozone, particulate matter less than 10 microm, and nitrogen dioxide), meteorological, and pollen data. One hundred twenty-five children remained in the final analysis. We used logistic regression models to determine associations between air pollution and respiratory symptoms, asthma medication use, and doctor visits for asthma. There were no associations between ambient ozone concentrations and respiratory symptoms, asthma medication use, and doctor visits for asthma. There was, however, an association between PM(10) concentrations and doctor visits for asthma (RR=1.11, 95% CI=1.04-1.19) and between NO(2) concentration and wet cough (RR=1.05, 95% CI=1.003-1.10) in single-pollutant models. The associations remained significant in multipollutant models. There was no consistent evidence that children with wheeze, positive histamine challenge, and doctor diagnosis of asthma reacted differently to air pollution from children with wheeze and doctor diagnosis of asthma and children with wheeze only. There were significant associations between PM(10) levels and doctor visits for asthma and an association between NO(2) levels and the prevalence of wet cough. We were, however, unable to demonstrate that current levels of ambient air pollution in western Sydney have a coherent range of adverse health effects on children with a history of wheezing.

Author(s): Sunyer J ; Basagaña X ; Belmonte J ; Antó JM
Affiliation: Respiratory and Environmental Research Unit, IMIM, Barcelona, Catalonia, Spain. jsunyer@imim.es Title: Effect of nitrogen dioxide and ozone on the risk of dying in patients with severe asthma. Source: Thorax (Thorax.) 2002 Aug; 57(8): 687-93
Additional Info: England Standard No: ISSN: 0040-6376; 1468-3296; NLM Unique Journal Identifier: 0417353 Language: English Abstract: BACKGROUND: A study was performed to assess the acute association between air pollution, pollen and spores, and mortality in a population based cohort of subjects with asthma recruited from emergency room admissions for an asthma exacerbation using a case crossover design. METHODS: Patients in Barcelona aged over 14 years who died during the period 1985-95 who had visited the emergency department of one of the four largest hospitals in the city for asthma during 1985-9 were included in the study (a total of 467 men and 611 women). Deaths were identified by record linkage of the cohort individuals with the Catalonia mortality registry. Causes of death were based on the underlying cause on the death certificate. Air pollution, pollen and spore levels were measured at the city monitoring stations which provide an average for the entire city. RESULTS: Nitrogen dioxide was associated with mortality for all causes of death (adjusted odds ratio (OR) for an increase of the interquartile range = 1.50, 95% confidence interval (CI) 1.09 to 2.64) in asthmatic patients with more than one emergency room admission for asthma. The association was particularly strong for respiratory causes (OR 1.63, 95% CI 0.93 to 2.86). Ozone also increased the risk of death in asthmatic patients (OR 1.90, 95% CI 1.09 to 3.30) during spring and summer. The association with particles, pollen, and spores was not significant, and no interactions between air pollutants and pollen and spores were found. CONCLUSION: Nitrogen dioxide and ozone may exacerbate severe asthma and even cause death among asthmatic subjects.

Author(s): Olin AC ; Andersson E ; Andersson M ; Granung G ; Hagberg S ; Torén K
Affiliation: Section of Occupational and Environmental Medicine, Sahlgrenska University Hospital, Göteborg, Sweden. Anna-Carin.Olin@ymk.gu.se

Title: Prevalence of asthma and exhaled nitric oxide are increased in bleachery workers exposed to ozone. Source: Eur Respir J (The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology.) 2004 Jan; 23(1): 87-92

Abstract: The aims of the present study were to determine whether exposure to high peaks of ozone resulted in an increased prevalence of asthma or respiratory symptoms among bleachery workers and whether nitric oxide (NO) was elevated in the exhaled air of these workers. Bleachery workers (n=228) from three Swedish pulp mills who had been exposed to ozone, together with 63 unexposed control subjects, were investigated by means of spirometry, Phadiatop, exhaled and nasal NO and answers to a questionnaire concerning respiratory symptoms and exposure. Exposure to an ozone peak that gave rise to respiratory symptoms was defined as a "gassing". Bleachery workers reporting four or more gassings involving ozone had an increased prevalence of adult-onset asthma, wheeze, and current asthma symptoms. They also had a higher median concentration of exhaled NO in comparison with those who reported no such gassings (19.2 versus 15.7 parts per billion). No such associations were found in respect of nasal NO. The results from this study show that bleachery workers who have been repeatedly exposed to ozone gassings have an increased prevalence of adult-onset asthma. The results also indicate exhaled nitric oxide may be a marker of airway inflammation in bleachery workers who have been exposed to high peaks of ozone.

Author(s): Donoghue AM ; Thomas M
Affiliation: Medical Centre, Mount Isa, Queensland, Australia.

Title: Point source sulphur dioxide peaks and hospital presentations for asthma. Source: Occup Environ Med (Occupational and environmental medicine.) 1999 Apr; 56(4): 232-6

Abstract: OBJECTIVE: To examine the effect on hospital presentations for asthma of brief exposures to sulphur dioxide (SO2) (within the range 0-8700 micrograms/m3) emanating from two point sources in a remote rural city of 25,000 people. METHODS: A time series analysis of SO2 concentrations and hospital presentations for asthma was undertaken at Mount Isa where SO2 is released into the atmosphere by a copper smelter and a lead smelter. The study examined 5 minute block mean SO2 concentrations and daily hospital presentations for asthma, wheeze, or shortness of breath. Generalised linear models and generalised additive models based on a Poisson distribution were applied. RESULTS: There was no evidence of any positive relation between peak SO2 concentrations and hospital presentations or admissions for asthma, wheeze, or shortness of breath. CONCLUSION: Brief exposures to high concentrations of SO2 emanating from point sources at Mount Isa do not cause sufficiently serious symptoms in asthmatic people to require presentation to hospital.

Author(s): Hiltermann TJ ; Peters EA ; Alberts B ; Kwikkers K ; Borggreven PA ; Hiemstra PS ; Dijkman JH ; van Bree LA ; Stolk J
Affiliation: Department of Pulmonology, Leiden University Hospital, The Netherlands.

Title: Ozone-induced airway hyperresponsiveness in patients with asthma: role of neutrophil-derived serine proteinases. Source: Free Radic Biol Med (Free radical biology & medicine.) 1998 Apr; 24(6): 952-8

Abstract: Proteinase inhibitors may be of potential therapeutic value in the treatment of respiratory diseases such as chronic obstructive pulmonary disease (COPD) or asthma. Our aim was to study the role of neutrophils, and neutrophil-derived serine proteinases in an acute model in patients with asthma. Exposure to ozone induces an acute neutrophilic inflammatory reaction accompanied by an increase in airway hyperresponsiveness. It is thought that these two effects of ozone are linked, and that neutrophil-derived serine proteinases (i.e. elastase) may play a role in the ozone-induced airway hyperresponsiveness. Therefore, we examined the effect of recombinant antileukoprotease (rALP), one of the major serine proteinase inhibitors in the lung, on ozone-induced changes in airway hyperresponsiveness in this model. We observed that 16 h after exposure to ozone, airway hyperresponsiveness to methacholine was increased both following placebo and rALP treatment. There was no significant difference between placebo and rALP treatment (change in area under the dose-response curve to methacholine: 117.3+/-59.0 vs 193.6+/-59.6 % fall x DD; p=.12). Moreover, the immediate decrease in FEV1 after ozone exposure was not significantly different between the two groups (placebo: -29.6+/-6.7%; rALP: -20.9+/-3.8%; p=.11). In addition, no significant differences were observed in plasma levels of fibrinogen degradation products generated by neutrophil serine proteinases before and after exposure to ozone. We conclude that neutrophil-derived serine proteinases are not important mediators for ozone-induced hyperresponsiveness.

Author(s): Hirabayashi K ; Kubo K ; Yamaguchi S ; Fujimoto K ; Murakami G ; Nasu Y
Affiliation: Department of Biology, Yamanashi Women's College, Kofu, Japan.

Title: Studies of bronchial asthma induced by chironomid midges (Diptera) around a hypereutrophic lake in Japan. Source: Allergy (Allergy.) 1997 Feb; 52(2): 188-95

Abstract: There have been few reports on hypersensitivity to chironomid midges in bronchial asthmatic patients around the area of hypereutrophic natural lakes, which have been notorious as an environmental hazard due to the massive occurrence of adult chironomids during several periods of the year. Our study investigated IgE antibodies to chironomid midges in bronchial asthmatic patients around the Lake Suwa area in comparison with those of the Matsumoto area (control area). A total of 123 adult patients with bronchial asthma were investigated by measurement of IgE antibodies with extracts of three chironomid midges (Chironomus yoshimatsui, C. plumosus, and Tokunagayusurika akamusi), mite, and silkworm. In addition, in the allergy testing, 12 common inhalant antigens were used. Of 123 adult patients with bronchial asthma, 65 (52.8%) produced positive allergy tests. Thirty-three (50.8%) were positive to mite, 28 (43.1%) to silkworm, 11 (16.9%) to C. yoshimatsui, eight (12.3%) to C. plumosus, and three (4.6%) to T. akamusi. We compared our results with the previous reports. The number of positive tests to silkworm in the Lake Suwa area was higher than in other areas. However, C. plumosus and T. akamusi showed a lower number of positive reactions. We considered the lower positive number of C. plumosus and T. akamusi tests in the Lake Suwa area to be related to the advanced age of patients in this area. The chironomids are an important cause of asthma, together with mite and silkworm, in the Lake Suwa area, but affect old asthmatic patients less than asthmatic children.

Author(s): Chauhan AJ ; Inskip HM ; Linaker CH ; Smith S ; Schreiber J ; Johnston SL ; Holgate ST
Affiliation: Respiratory, Cell, and Molecular Biology Research Division, University of Southampton, Southampton, UK. anoop.chauhan@porthosp.nhs.uk <anoop.chauhan@porthosp.nhs.uk>

Title: Personal exposure to nitrogen dioxide (NO2) and the severity of virus-induced asthma in children. Source: Lancet (Lancet.) 2003 Jun 7; 361(9373): 1939-44

Abstract: BACKGROUND: A link between exposure to the air pollutant nitrogen dioxide (NO2) and respiratory disease has been suggested. Viral infections are the major cause of asthma exacerbations. We aimed to assess whether there is a relation between NO2 exposure and the severity of asthma exacerbations caused by proven respiratory viral infections in children. METHODS: A cohort of 114 asthmatic children aged between 8 and 11 years recorded daily upper and lower respiratory-tract symptoms, peak expiratory flow (PEF), and measured personal NO2 exposures every week for up to 13 months. We took nasal aspirates during reported episodes of upper respiratory-tract illness and tested for infection by common respiratory viruses and atypical bacteria with RT-PCR assays. We used generalised estimating equations to assess the relation between low (<7.5 microg/m3), medium (7.5-14 microg/m3 ), and high (>14 microg/m3) tertiles of NO2 exposure in the week before or after upper respiratory-tract infection and the severity of asthma exacerbation in the week after the start of an infection. FINDINGS: One or more viruses were detected in 78% of reported infection episodes, and the medians of NO2 exposure were 5 (IQR 3.6-6.3), 10 (8.7-12.0), and 21 microg/m3 (16.8-42.9) for low, medium, and high tertiles, respectively. There were significant increases in the severity of lower respiratory-tract symptom scores across the three tertiles (0.6 for all viruses [p=0.05] and >2 for respiratory syncytial virus [p=0.01]) and a reduction in PEF of more than 12 L/min for picornavirus (p=0.04) for high compared with low NO2 exposure before the start of the virus-induced exacerbation. INTERPRETATION: High exposure to NO2 in the week before the start of a respiratory viral infection, and at levels within current air quality standards, is associated with an increase in the severity of a resulting asthma exacerbation.

Author(s): Eggleston PA ; Buckley TJ ; Breysse PN ; Wills-Karp M ; Kleeberger SR ; Jaakkola JJ
Affiliation: School of Medicine, Department of Pediatrics, The Johns Hopkins University, Baltimore, MD 21287-3923, USA. pegglest@welchlink.welch.jhu.edu

Title: The environment and asthma in U.S. inner cities. Source: Environ Health Perspect (Environmental health perspectives.) 1999 Jun; 107 Suppl 3: 439-50

Abstract: The prevalence and severity of asthma has increased in the last 20 years, and the greatest increase has been seen among children and young adults living in U.S. inner cities. The reasons for this increase are obviously complex, but include environmental exposures to allergens and pollutants, changing patterns of medication, and the psychosocial stresses of living in poor inner-city neighborhoods. This paper presents an overview of environmental, immunologic, and genetic factors associated with asthma morbidity and mortality. This overview can be used to provide a framework for designing an interdisciplinary research program to address the complexities of asthma etiology and exacerbation. The strongest epidemiologic association has been found between asthma morbidity and the exposure of immunologically sensitive asthmatic patients to airborne allergens. Our current understanding of the process of sensitization suggests that there is a strong genetic predisposition to form IgE to allergenic proteins on airborne particles. Much of this work has been conducted with animal models, but in a number of instances, specific confirmation has been reported in humans. Sensitized individuals respond to inhaled exposure with immediate mast-cell dependent inflammation that may be augmented by pollutant particles, especially diesel exhaust particles. Relatively little is known about the methods of assessing exposure to airborne pollutants, especially biologically active particulates. However, to examine the relationship of morbidity in genetically predisposed individuals, it will be important to determine the most relevant method of making this assessment.

Particulates

General Ozone Particulates Dust/Molds Pollens Pesticides

Author(s): Glovsky MM ; Miguel AG ; Cass GR
Affiliation: Huntington Memorial Hospital Asthma and Allergy Center, Pasadena, California, USA.

Title: Particulate air pollution: possible relevance in asthma. Source: Allergy Asthma Proc (Allergy and asthma proceedings : the official journal of regional and state allergy societies.) 1997 May-Jun; 18(3): 163-6

Abstract: The relative importance of air pollution in the pathogenesis of bronchial asthma has been of interest for several decades. Numerous studies on the role of gaseous air pollution containing ozone, nitrogen dioxide, sulfur dioxide, and carbon monoxide have been published. Very little attention has been focused on the role of respirable particles in the causation of asthma. In this article we summarize some of our ongoing investigations into the sources and composition of airborne particles in the Los Angeles and Pasadena atmosphere, including the search for biologically active particles that may induce asthma attacks. If is found that the urban atmosphere contains not only combustion-derived particles from diesel engine exhaust and gasoline-powered motor vehicle exhaust, but also particles formed from biological starting materials including plant debris, cigarette smoke, wood smoke, and meat smoke as well as tire debris containing some natural rubber and paved road dust. Paved road dust is a very complex mixture of particles including garden soil, tire dust, plant fragments, redeposited atmospheric particles of all types, and pollen fragments presumably ground up by passing traffic. We have shown previously that latex allergen can be extracted from tire dust, from roadside dust, and from respirable air samples taken at Los Angeles and Long Beach. At present, work is underway to identify the larger range of allergens that may be contributed by the entrainment of paved road dust into the atmosphere. The possible importance of pollen fragments present in paved road dust in very small particle sizes is discussed as well as their potential relevance in asthma.

Author(s): Pirie RS ; Collie DD ; Dixon PM ; McGorum BC
Affiliation: Wellcome Trust Centre for Research in Comparative Respiratory Medicine, Easter Bush Veterinary Centre, Roslin, Midlothian, UK. scottp@staffmail.ed.ac.uk

Title: Inhaled endotoxin and organic dust particulates have synergistic proinflammatory effects in equine heaves (organic dust-induced asthma). Source: Clin Exp Allergy (Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.) 2003 May; 33(5): 676-83

Abstract: BACKGROUND: Equine heaves is a naturally occurring organic dust-induced asthma characterized by airway neutrophilia, mucus hypersecretion and obstructive lung dysfunction. However, the relative role of different dust components in disease severity remains unclear. OBJECTIVE: This study investigated the relative contribution of inhaled endotoxin and organic dust particulates (mainly mould spores) in inducing heaves in heaves-susceptible horses. METHODS: Control and heaves-susceptible horses received inhalation challenges with hay dust suspension (HDS) before and after lipopolysaccharide (LPS) depletion. Heaves-susceptible horses also received inhalation challenge with HDS particulates with and without the addition of LPS and were housed in two separate dusty environments during which mould and endotoxin exposure was measured. The airway inflammatory and functional response to each challenge was measured. RESULTS: Depletion of endotoxin from HDS attenuated the airway neutrophilia and abrogated the airway dysfunction induced in heaves horses by inhaled HDS. The airway response was re-established by adding back LPS to the depleted HDS, confirming that the attenuation in airway response was due specifically to endotoxin depletion. Interestingly, the magnitude of alteration in airway response following endotoxin depletion and add-back was greater than that which could be attributed solely to endotoxin per se, indicating that the LPS activity was enhanced by the other dust components. Consistent with this possibility, washed particulates harvested from HDS enhanced the airway response to inhaled LPS in heaves horses. Heaves horses given two different hay/straw challenges had a significantly different severity of airway inflammation and dysfunction, despite airborne dust and endotoxin concentrations in the horses' breathing zones being similar. CONCLUSION: Although inhaled endotoxin appears not to be the only determinant of disease severity in heaves, it does contribute significantly to the induction of airway inflammation and dysfunction. This contribution is largely via the synergistic action of inhaled endotoxin and organic dust particulates, although other soluble dust components also contribute to a lesser degree.

Author(s): Johnston FH ; Kavanagh AM ; Bowman DM ; Scott RK
Affiliation: Menzies School of Health Research, PO Box 41096 Casuarina, NT 0811, Australia. fjohns@tedgp.org.au

Title: Exposure to bushfire smoke and asthma: an ecological study. Source: Med J Aust (The Medical journal of Australia.) 2002 Jun 3; 176(11): 535-8

Abstract: OBJECTIVE: To examine the relationship between the mean daily concentration of respirable particles arising from bushfire smoke and hospital presentations for asthma. DESIGN AND SETTING: An ecological study conducted in Darwin (Northern Territory, Australia) from 1 April - 31 October 2000, a period characterised by minimal rainfall and almost continuous bushfire activity in the proximate bushland. The exposure variable was the mean atmospheric concentration of particles of 10 microns or less in aerodynamic diameter (PM(10)) per cubic metre per 24-hour period. OUTCOME MEASURE: The daily number of presentations for asthma to the Emergency Department of Royal Darwin Hospital. RESULTS: There was a significant increase in asthma presentations with each 10-microg/m(3) increase in PM(10) concentration, even after adjusting for weekly rates of influenza and for weekend or weekday (adjusted rate ratio, 1.20; 95% CI, 1.09-1.34; P < 0.001). The strongest effect was seen on days when the PM(10) was above 40 microg/m(3) (adjusted rate ratio, 2.39; 95% CI, 1.46-3.90), compared with days when PM(10) levels were less than 10 microg/m(3). CONCLUSION: Airborne particulates from bushfires should be considered as injurious to human health as those from other sources. Thus, the control of smoke pollution from bushfires in urban areas presents an additional challenge for managers of fireprone landscapes.

Author(s): Delfino RJ ; Quintana PJ ; Floro J ; Gastañaga VM ; Samimi BS ; Kleinman MT ; Liu LJ ; Bufalino C ; Wu CF ; McLaren CE
Affiliation: Epidemiology Division, Department of Medicine, College of Medicine, University of California at Irvine, 224 Irvine hall, Irvine, CA 92697-7550, USA. rdelfino@uci.edu

Title: Association of FEV1 in asthmatic children with personal and microenvironmental exposure to airborne particulate matter. Source: Environ Health Perspect (Environmental health perspectives.) 2004 Jun; 112(8): 932-41

Abstract: Exposure to particulate matter (PM) air pollution has been shown to exacerbate children's asthma, but the exposure sources and temporal characteristics are still under study. Children's exposure to PM is likely to involve both combustion-related ambient PM and PM related to a child's activity in various indoor and outdoor microenvironments. Among 19 children with asthma, 9-17 years of age, we examined the relationship of temporal changes in percent predicted forced expiratory volume in 1 sec (FEV1) to personal continuous PM exposure and to 24-hr average gravimetric PM mass measured at home and central sites. Subjects were followed for 2 weeks during either the fall of 1999 or the spring of 2000, in a southern California region affected by transported air pollution. FEV(subscript)1(/subscript) was measured by subjects in the morning, afternoon, and evening. Exposure measurements included continuous PM using a passive nephelometer carried by subjects; indoor, outdoor home, and central-site 24-hr gravimetric PM2.5 (PM of aerodynamic diameter < 2.5 microm) and PM10; and central-site hourly PM10, nitrogen dioxide, and ozone. Data were analyzed with linear mixed models controlling for within-subject autocorrelation, FEV1 maneuver time, and exposure period. We found inverse associations of FEV1 with increasing PM exposure during the 24 hr before the FEV1 maneuver and with increasing multiday PM averages. Deficits in percent predicted FEV1 (95% confidence interval) for given PM interquartile ranges measured during the preceding 24-hr were as follows: 128 microg/m3 1-hr maximum personal PM, -6.0% (-10.5 to -1.4); 30 microg/m3 24-hr average personal PM, -5.9% (-10.8 to -1.0); 6.7 microg/m3 indoor home PM2.5, -1.6% (-2.8 to -0.4); 16 microg/m3 indoor home PM10, -2.1% (-3.7 to -0.4); 7.1 microg/m3 outdoor home PM2.5, -1.1% (-2.4 to 0.1); and 7.5 microg/m3 central-site PM2.5, -0.7% (-1.9 to 0.4). Stronger associations were found for multiday moving averages of PM for both personal and stationary-site PM. Stronger associations with personal PM were found in boys allergic to indoor allergens. FEV1 was weakly associated with NO2 but not with O3. Results suggest mixed respiratory effects of PM in asthmatic children from both ambient background exposures and personal exposures in various microenvironments.

Author(s): Delfino RJ ; Gong H ; Linn WS ; Hu Y ; Pellizzari ED
Affiliation: Epidemiology Division, Department of Medicine, College of Medicine, University of California, Irvine, California 92697, USA. rdelfino@uci.edu

Title: Respiratory symptoms and peak expiratory flow in children with asthma in relation to volatile organic compounds in exhaled breath and ambient air. Source: J Expo Anal Environ Epidemiol (Journal of exposure analysis and environmental epidemiology.) 2003 Sep; 13(5): 348-63

Abstract: Indoor volatile organic compounds (VOCs) have been associated with asthma, but there is little epidemiologic work on ambient exposures, and no data on relationships between respiratory health and exhaled breath VOCs, which is a biomarker of VOC exposure. We recruited 26 Hispanic children with mild asthma in a Los Angeles community with high VOC levels near major freeways and trucking routes. Two dropped out, three had invalid peak expiratory flow (PEF) or breath VOC data, leaving 21. Children filled out symptom diaries and performed PEF maneuvers daily, November 1999-January 2000. We aimed to collect breath VOC samples on asthma episode and baseline symptom-free days, but six subjects only gave samples on symptom-free days. We analyzed 106 breath samples by GC-MS. Eight VOCs were quantifiable in >75% of breath samples (benzene, methylene chloride, styrene, tetrachloroethylene, toluene, m,p-xylene, o-xylene, and p-dichlorobenzene). Generalized estimating equation and mixed linear regression models for VOC exposure-response relationships controlled for temperature and respiratory infections. We found marginally positive associations between bothersome or more severe asthma symptoms and same day breath concentrations of benzene [odds ratio (OR) 2.03, 95% confidence interval (CI) 0.80, 5.11] but not other breath VOCs. Ambient petroleum-related VOCs measured on the same person-days as breath VOCs showed notably stronger associations with symptoms, including toluene, m,p-xylene, o-xylene, and benzene (OR 5.93, 95% CI 1.64, 21.4). On breath sample days, symptoms were also associated with 1-h ambient NO(2), OR 8.13 (1.52, 43.4), and SO(2), OR 2.36 (1.16, 4.81). Consistent inverse relationships were found between evening PEF and the same ambient VOCs, NO(2), and SO(2). There were no associations with O(3). Given the high traffic density of the region, stronger associations for ambient than for breath VOCs suggest that ambient VOC measurements were better markers for daily exposure to combustion-related compounds thought to be causally related to acute asthma. Alternatively, the low sample size of symptom responses (15-21 responses per 108 breath samples) may have led to the nonsignificant results for breath VOCs.

Author(s): Delfino RJ
Affiliation: Epidemiology Division, Department of Medicine, University of California, Irvine, California 92697-7550, USA. rdelfino@uci.edu

Title: Epidemiologic evidence for asthma and exposure to air toxics: linkages between occupational, indoor, and community air pollution research. Source: Environ Health Perspect (Environmental health perspectives.) 2002 Aug; 110 Suppl 4: 573-89

Abstract: Outdoor ambient air pollutant exposures in communities are relevant to the acute exacerbation and possibly the onset of asthma. However, the complexity of pollutant mixtures and etiologic heterogeneity of asthma has made it difficult to identify causal components in those mixtures. Occupational exposures associated with asthma may yield clues to causal components in ambient air pollution because such exposures are often identifiable as single-chemical agents (e.g., metal compounds). However, translating occupational to community exposure-response relationships is limited. Of the air toxics found to cause occupational asthma, only formaldehyde has been frequently investigated in epidemiologic studies of allergic respiratory responses to indoor air, where general consistency can be shown despite lower ambient exposures. The specific volatile organic compounds (VOCs) identified in association with occupational asthma are generally not the same as those in studies showing respiratory effects of VOC mixtures on nonoccupational adult and pediatric asthma. In addition, experimental evidence indicates that airborne polycyclic aromatic hydrocarbon (PAH) exposures linked to diesel exhaust particles (DEPs) have proinflammatory effects on airways, but there is insufficient supporting evidence from the occupational literature of effects of DEPs on asthma or lung function. In contrast, nonoccupational epidemiologic studies have frequently shown associations between allergic responses or asthma with exposures to ambient air pollutant mixtures with PAH components, including black smoke, high home or school traffic density (particularly truck traffic), and environmental tobacco smoke. Other particle-phase and gaseous co-pollutants are likely causal in these associations as well. Epidemiologic research on the relationship of both asthma onset and exacerbation to air pollution is needed to disentangle effects of air toxics from monitored criteria air pollutants such as particle mass. Community studies should focus on air toxics expected to have adverse respiratory effects based on biological mechanisms, particularly irritant and immunological pathways to asthma onset and exacerbation.

Author(s): Reed CE ; Milton DK
Affiliation: Allergic Disease Research Laboratory, Mayo Clinic, Rochester, MN, USA.

Title: Endotoxin-stimulated innate immunity: A contributing factor for asthma. Source: J Allergy Clin Immunol (The Journal of allergy and clinical immunology.) 2001 Aug; 108(2): 157-66

Abstract: Exposure to airborne endotoxin in infancy may protect against asthma by promoting enhanced T(H)1 response and tolerance to allergens. On the other hand, later in life, it adversely affects patients with asthma. Endotoxin binding to receptors on macrophages and other cells generates IL-12, which inhibits IgE responses. It also generates cytokines like IL-1, TNF-alpha, and IL-8, which cause inflammation. These signal transduction pathways resemble those leading to the generation of cytokines, such as IL-4, IL-13, and IL-5, which are responsible for the inflammation of IgE-mediated allergic disease. The main difference seems to be that endotoxin recruits neutrophils, but IgE recruits eosinophils, and the details of the tissue injury from these granulocytes differ. Sources of airborne endotoxin include many agricultural dusts, aerosols from contaminated water in many industrial plants, contaminated heating and air-conditioning systems, mist-generating humidifiers, and damp or water-damaged homes. Acute inhalation of high concentrations of endotoxin can cause fever, cough, and dyspnea. Chronic inhalation of lesser amounts causes chronic bronchitis and emphysema and is associated with airway hyperresponsiveness. Airborne endotoxin adversely affects patients with asthma in 3 ways: (1) by increasing the severity of the airway inflammation; (2) by increasing the susceptibility to rhinovirus-induced colds; and (3) by causing chronic bronchitis and emphysema with development of irreversible airway obstruction after chronic exposure of adults. The most effective management is mitigating exposure. The potential of drug treatments requires further clinical

Author(s): Goldsmith CA ; Hamada K ; Ning Y ; Qin G ; Catalano P ; Krishna Murthy GG ; Lawrence J ; Kobzik L
Affiliation: Harvard School of Public Health, Bldg. II-221, 665 Huntington Ave, Boston, MA 02115, USA.

Title: Effects of environmental aerosols on airway hyperresponsiveness in a murine model of asthma. Source: Inhal Toxicol (Inhalation toxicology.) 1999 Nov; 11(11): 981-98

Abstract: Increased morbidity in persons suffering from inflammatory lung diseases, such as asthma and bronchitis, has been associated with air pollution particles. One hypothesis is that particles can cause an amplification of the pulmonary inflammation associated with these diseases, thus worsening affected individuals' symptoms. This hypothesis was tested in a murine model of asthma by inhalation exposure to (1) concentrated air particles (CAPs), (2) the leachate of residual oil fly ash (ROFA-S), and (3) lipopolysaccharide (LPS). Allergen-sensitized mice (ip ovalbumin, OVA) were 21 days old when challenged with an aerosol of 3% OVA in phosphate-buffered saline (PBS) for 10 min (controls were challenged with PBS only) for 3 days. On the same days, mice were further exposed to 1 of 3 additional agents: CAPs (or filtered air) for 6 h/day; LPS (5 microg/ml, or PBS) for 10 min/day; or ROFA-S (leachate of 50 mg/ml, or PBS) for 30 min on day 2 only. At 24 h later, mice challenged with OVA aerosol showed airway inflammation and airway hyperresponsiveness (AHR) to methacholine (Mch), features absent in mice challenged with PBS alone. Both OVA- and PBS-challenged mice subsequently exposed to ROFA-S showed increased AHR to Mch when compared to their respective controls (OVA only or PBS only). In contrast, when OVA-challenged mice were further exposed to CAPs or LPS, no changes in AHR were seen in comparison to mice challenged with OVA only. Bronchoalveolar lavage (BAL) analysis and histopathology 48 h postexposure showed OVA-induced allergic inflammation. No significant additional effects were caused by CAPs or ROFA-S. LPS, in contrast, caused significant increases in total cell, macrophage, and polymorphonuclear cell numbers. The data highlight discordance between airway inflammation and hyperresponsiveness.

Affiliation: Asthma Control Program, Division of Disease Prevention and Control, Rhode Island Department of Health, USA.

Title: Asthma, particulates, and diesel exhaust. Source: Med Health R I (Medicine and health, Rhode Island.) 2002 Apr; 85(4): 140-2
No abstract available

Author(s): Sagai M ; Furuyama A ; Ichinose T
Affiliation: National Institute for Environmental Studies, Research Team for Health Effects of Air Pollutants, Ibaraki, Japan.

Title: Biological effects of diesel exhaust particles (DEP). III. Pathogenesis of asthma like symptoms in mice. Source: Free Radic Biol Med (Free radical biology & medicine.) 1996; 21(2): 199-209

Abstract: Chronic airway inflammation, mucus hypersecretion, reversible airway constriction, and bronchial hyperresponsiveness are important pathogenic features of asthma. We found that diesel exhaust particles (DEP) instilled intratracheally and repeatedly to mice (once/week for 16 weeks) caused marked infiltration of inflammatory cells, proliferation of goblet cells, increased mucus secretion, respiratory resistance, and airway constriction. Eosinophils in the submucosa of the proximal bronchi and medium bronchioles increased eightfold following instillation. Eosinophil infiltration was significantly suppressed by pretreatment with polyethyleneglycol-conjugated superoxide dismutase (PEG-SOD). Bound sialic acid concentrations in bronchial alveolar lavage fluids, an index of mucus secretion, increased with DEP, but were suppressed by pretreatment with PEG-SOD. Goblet cell hyperplasia, airway narrowing, and airway constriction also were observed with DEP. Respiratory resistance in the DEP-group to acetylcholine was 11 times higher than in controls, and the increased resistance was significantly suppressed by PEG-SOD pretreatment. These findings suggest that DEP and/or oxygen radicals derived from DEP cause bronchial asthma in mice.

Dust/Molds

General Ozone Particulates Dust/Molds Pollens Pesticides

Author(s): Sigsgaard T ; Schlunssen V
Affiliation: Department of Environmental and Occupational Medicine, Aarhus University, Vennelyst Boulevard 6, DK 8000 Aarhus C, Denmark. ts@mil.au.dk

Title: Occupational asthma diagnosis in workers exposed to organic dust. Source: Ann Agric Environ Med (Annals of agricultural and environmental medicine : AAEM.) 2004; 11(1): 1-7

Abstract: The clinical evaluation of newly developed asthma in an adult should always include consideration of his occupational environment, since an abundance of different exposures, which are known causes of asthma, occur in workplaces. Two types of occupational asthma (OA) are distinguished, by whether they appear after a latency period: 1)Immunological OA, characterised by a latency period, caused by high and low-molecular-weight agents, with or without an IgE mechanism 2) Non-immunological, i.e. irritant induced asthma. The first step of the clinical evaluation is to confirm a diagnosis of asthma. Second step is to find out if there is a temporo-spatial distribution of symptoms and lung function that are indicative of OA. Third step is to determine if the disease at hand is an IgE or a non-IgE mediated disease. Last step is a challenge test that can be either unspecific, in order to assess the responsiveness of the lung, or specific challenge test, especially for the non-IgE mediated OA. The depth of clinical evaluation may vary from a situation in which a classical history confirms the clinical symptoms in e.g. a baker with confirmed allergy towards well-known allergens and a characteristic pattern in serial measurements of lung function, to more elaborate investigations in a situation with no or unknown allergen. In the latter situation, a specific challenge test might be necessary in order to find the offending agent. Finally, challenge tests are important in order to distinguish a causal relation from unspecific hyperresponsiveness in persons with pre-existing asthma. In these situations, extended sick leave and challenge tests can be the only way to find the answer.

Author(s): Rodrigo MJ ; Cruz MJ ; García MD ; Antó JM ; Genover T ; Morell F
Affiliation: Unitat de Recerca en Neumologia i Unitat Immunologia, Servei de Pneumologia, Hospital Universitario Vall d'Hebrón, Universidal Autónoma de Barcelona, Passeig Vall d'Hebrón 119-129, ES-08035 Barcelona, Spain. mjrodrigo@vhebron.net

Title: Epidemic asthma in Barcelona: an evaluation of new strategies for the control of soybean dust emission. Source: Int Arch Allergy Immunol (International archives of allergy and immunology.) 2004 Jun; 134(2): 158-64

Abstract: BACKGROUND: Asthma attacks and mortality due to inhalation of soybean antigens in Barcelona have been well documented. Strict protective measures in the unloading process were established in 1998 to avoid the release of soybean dust into the atmosphere. The present study was undertaken to assess the effectiveness of these latest environmental measures, and, if effective, to recommend their implementation in the many harbours where soybean is unloaded. METHODS: Levels of soybean aeroallergen were analysed daily during a period of 5 years and 2 months in a total of 1,854 samples, 125 from the pre-intervention period and 1,729 from the postintervention period. Additionally, the number of asthma admissions to the emergency rooms of the city's three largest hospitals was recorded. Asthma patients attended at home by the public home emergency service and judicial autopsies registering asthma deaths were also investigated. RESULTS: The mean concentration of soybean aeroallergen was 159 U/m(3) in the pre-intervention period and 39 U/m(3) in the postintervention period (p < 0.0001). Significant differences in postintervention aeroallergen concentrations were found between days of soybean unloading (42 U/m(3)) and days of no unloading (33 U/m(3)), with p < 0.0001. No significant relationship was found between concentrations of environmental soybean aeroallergens and the number of emergency room admissions for asthma. CONCLUSIONS: Implementation of stricter protective measures in silos for the soybean unloading process has reduced the concentration of soybean dust in the atmosphere and evidences the effectiveness of the measures adopted.

Author(s): Delfino RJ ; Zeiger RS ; Seltzer JM ; Street DH ; Matteucci RM ; Anderson PR ; Koutrakis P
Affiliation: Graduate School of Public Health, San Diego State University, CA 92120, USA.

Title: The effect of outdoor fungal spore concentrations on daily asthma severity. Source: Environ Health Perspect (Environmental health perspectives.) 1997 Jun; 105(6): 622-35

Abstract: The relationship between day-to-day changes in asthma severity and combined exposures to community air pollutants and aeroallergens remains to be clearly defined. We examined the effects of outdoor air pollutants, fungi, and pollen on asthma. Twenty-two asthmatics ages 9-46 years were followed for 8 weeks (9 May-3 July 1994) in a semirural Southern California community around the air inversion base elevation (1,200 ft). Daily diary responses included asthma symptom severity (6 levels), morning and evening peak expiratory flow rates (PEFR), and as-needed beta-agonist inhaler use. Exposures included 24-hr outdoor concentrations of fungi, pollen, and particulate matter with a diameter < 10 microns (PM10; maximum = 51 micrograms/m3) and 12-hour day-time personal ozone (O3) measurements (90th percentile = 38 ppb). Random effects longitudinal regression models controlled for autocorrelation and weather. Higher temperatures were strongly protective, probably due to air conditioning use and diminished indoor allergens during hot, dry periods. Controlling for weather, total fungal spore concentrations were associated with all outcomes: per minimum to 90th percentile increase of nearly 4,000 spores/m3, asthma symptom scores increased 0.36 (95% CI, 0.16-0.56), inhaler use increased 0.33 puffs (95% CI, -0.02-0.69), and evening PEFR decreased 12.1 l/min (95% CI, -1.8-22.3). These associations were greatly enhanced by examining certain fungal types (e.g., Alternaria, basidiospores, and hyphal fragments) and stratifying on 16 asthmatics allergic to tested deuteromycete fungi. There were no significant associations to low levels of pollen or O3, but inhaler use was associated with PM10 (0.15 inhaler puffs/10 micrograms/m3; p < 0.02). These findings suggest that exposure to fungal spores can adversely effect the daily respiratory status of some asthmatics.

Author(s): Freye HB ; King J ; Litwin CM
Affiliation: Department of Pediatrics, Brown University Medical School, Rhode Island, USA.

Title: Variations of pollen and mold concentrations in 1998 during the strong El Niño event of 1997-1998 and their impact on clinical exacerbations of allergic rhinitis, asthma, and sinusitis. Source: Allergy Asthma Proc (Allergy and asthma proceedings : the official journal of regional and state allergy societies.) 2001 Jul-Aug; 22(4): 239-47

Abstract: Previous studies of pollen and mold dispersal have not correlated meteorological phenomena with clinical exacerbations of asthma, allergic rhinitis, and sinusitis. We utilized the resources of 11 New England Society of Allergy (NESA) pollen collectors, a certified palynologist, over a dozen weather stations for meteorological data, and 10 emergency rooms to explore the effects of the strong "El Niño" of 1997-1998 on our region during the 1998 pollen season. There was a marked increase in the number of clinical exacerbations of asthma, allergic rhinitis, and sinusitis in April, May, and June of 1998. Several emergency rooms reported a greater increase in visits for sinusitis as compared to asthma. In addition, maximum mold counts occurred two to three months earlier than in 1997. Maximum pollen counts were also higher than in 1997, and occurred two to four weeks earlier for most tree pollen types.

Author(s): Targonski PV ; Persky VW ; Ramekrishnan V
Affiliation: University of Illinois, School of Public Health, Chicago 60612, USA.

Title: Effect of environmental molds on risk of death from asthma during the pollen season. Source: J Allergy Clin Immunol (The Journal of allergy and clinical immunology.) 1995 May; 95(5) Pt 1: 955-61

Abstract: OBJECTIVE: Many studies have noted an association of ambient aeroallergen levels with exacerbation of asthma. This study was undertaken to examine the relationship of aeroallergen levels with asthma-related mortality in Chicago. METHODS: The association of environmental aeroallergen levels with death caused by asthma among 5- to 34-year-olds in Chicago was examined for the period of 1985 through 1989. Logistic regression analysis was used to compare the probability of a death caused by asthma occurring on the basis of environmental tree, grass, or ragweed pollen and mold spore levels. RESULTS: Mean mold spore levels but not tree, grass, or ragweed pollen levels were significantly higher for days on which asthma-related death occurred than for days on which no deaths occurred (z = 2.80, p < 0.005). The odds of a death caused by asthma occurring on days with mold spore counts of 1000 spores per cubic meter or greater was 2.16 times higher (95% confidence interval = 1.31, 3.56, p = 0.003) than on days on which mold spore counts were less than 1000 spores per cubic meter. The association with mold spore levels remained significant on multivariate logistic regression with mold spore counts measured as a continuous variable and controlling for pollens, with the odds of an asthma-related death occurring being 1.2 times higher (95% confidence interval = 1.07-1.34) for every increase of 1000 spores per cubic meter in daily mold spore levels. CONCLUSION: Although death caused by asthma also involves personal, social, and medical access factors, these data suggest that exposure to environmental molds may play a role in asthma-related mortality and should be considered in prevention strategies.

Author(s): Lin RY ; Williams KD
Affiliation: Department of Medicine, Saint Vincents Hospital, Manhattan, USA.

Title: Hypersensitivity to molds in New York City in adults who have asthma. Source: Allergy Asthma Proc (Allergy and asthma proceedings : the official journal of regional and state allergy societies.) 2003 Jan-Feb; 24(1): 13-8

Abstract: Molds have been linked epidemiologically to asthma as a key aeroallergen in several studies. Other allergens such as cockroach have been linked to asthma in New York City (NYC). To our knowledge, however, the pattern of mold hypersensitivity has never been examined systematically in the NYC area. Thus, we sought to determine the association between mold hypersensitivity and asthma in a large group of ambulatory patients evaluated for allergic disease for the years 1993 through 2001 at a single medical center. Serological testing for mold-specific immunoglobulin E (IgE) as well as IgE specific for other aeroallergens was performed and the associations between allergen-specific IgE and the presence of asthma were examined using bivariate and multivariate analysis. Factor analysis showed that three distinct groupings of aeroallergen-specific IgE existed within the panel of allergens used. Group 1 consisted of cat dander and dust mites (Dermatophagoides farinae). Group 2 consisted of tree, grass, and ragweed pollen. Group 3 consisted of the Deuteromycetes molds, Alternaria tenuis, Aspergillus fumigatus, and Cladosporium herbarum. Patients with asthma had a highly significant increase in the incidence of hypersensitivity to cat/dust mites and to the molds. Multivariate analysis showed that the presence of hypersensitivity to either A. tenuis or C. herbarum had a significant independent association with asthma after adjustment for cat/dust mite hypersensitivity and after adjustment for other clinical factors. On the other hand, pollen hypersensitivity was not associated independently with asthma. Mold hypersensitivity was strongly correlated with hypersensitivity to cat or dust mites in patients who did not have asthma but not in patients who did have asthma. In the NYC area, recent pollen and spore counts show that mold spores are measurable in at least 75% of the year. Thus it is conceivable that mold hypersensitivity plays a contributing and independent role in initiating or perpetuating the allergic response in patients with asthma in the New York area.

Author(s): Rutherford S ; Clark E ; McTainsh G ; Simpson R ; Mitchell C
Affiliation: School of Public Health, Griffith University, Logan, Australia.

Title: Characteristics of rural dust events shown to impact on asthma severity in Brisbane, Australia. Source: Int J Biometeorol (International journal of biometeorology.) 1999 Apr; 42(4): 217-25

Abstract: Wind erosion in arid inland Australia leads to dust plumes which can pass over populated coastal areas in Eastern Australia, such as Brisbane. Such events can lead to concerns about respiratory health problems because they significantly increase the fine particle component of atmospheric aerosols. This paper examines the particulate characteristics of 11 dust events in Brisbane and associations with daily diary records (peak expiratory flow, symptoms) of people with asthma, and hospital emergency attendances for asthma during a number of seasons between 1992 and 1994. These dust events are frequently, but not always, characterised by higher particulate levels and higher ratios of fine to coarse particulates. The results indicate that a number of dust events were significantly associated with changes in asthma severity, but general relationships could not be determined. Given that the phenomenon of wind-blown dust is not isolated to the Australian continent, these findings raise important questions about the effects of wind-blown dust in other parts of the world.

Author(s): Taivainen AI ; Tukiainen HO ; Terho EO ; Husman KR
Affiliation: Department of Pulmonary Diseases, Kuopio University Hospital, Finland. antti.taivainen@kuh.fi

Title: Powered dust respirator helmets in the prevention of occupational asthma among farmers. Source: Scand J Work Environ Health (Scandinavian journal of work, environment & health.) 1998 Dec; 24(6): 503-7

Abstract: OBJECTIVES: This study investigated the value of powered dust respirator helmets in the treatment of farmers with occupational asthma. METHODS: The study population consisted of 33 asthmatic agricultural workers, 24 with occupational asthma induced by cow dander or grains, 2 with other forms of atopic asthma, and 7 with nonatopic asthma. The efficiency of a powered dust respirator helmet with a P2-class filter in preventing asthmatic symptoms was assessed for 1 year. Morning and evening peak expiratory flow rates and daily symptoms of the subjects were monitored for 3 months without the use of the helmet and for 10 months with the helmet. RESULTS: Objective evidence of protection was obtained for farmers with occupational asthma. The morning peak flow rate increased and the variation in daily peak flow rate and the symptoms of cow-barn rhinitis diminished significantly during the helmet period. In the group of farmers with nonatopic asthma there was no improvement in peak flow rate or symptoms of asthma, although some of these farmers also seemed to benefit from helmet use. CONCLUSIONS: The results of this study suggest that especially dairy farmers with occupational asthma benefit from the use of a powered dust respirator helmet.

Pollens

General Ozone Particulates Dust/Molds Pollens Pesticides

Author(s): Arilla MC ; Ibarrola I ; García R ; de la Hoz B ; Martínez A ; Asturias JA
Affiliation: Research and Development Department, Bial-Arístegui, Bilbao, Spain.

Title: Quantification of the major allergen from cypress (Cupressus arizonica) pollen, Cup a 1, by monoclonal antibody-based ELISA. Source: Int Arch Allergy Immunol (International archives of allergy and immunology.) 2004 May; 134(1): 10-6

Abstract: BACKGROUND: Cypress pollen allergy is an important cause of rhinoconjunctivitis and asthma in Mediterranean countries. Cypress allergenic extracts are difficult to produce since they have low protein and high carbohydrate content, thus accurate standardization of them is essential to guarantee their quality. The aim of this study is to develop a sandwich ELISA for the quantification of Cup a 1, the major allergen of cypress (Cupressus arizonica) pollen extract. METHODS: Monoclonal antibodies directed to purified Cup a 1 were produced. Two of them (9C7 as capture antibody and 3D2 as the tracer) were selected to develop a quantitative sandwich ELISA. This ELISA was subsequently evaluated and compared with other techniques. RESULTS: The described ELISA is very sensitive with a detection limit of 8.7 ng/ml and a practical working range of 62.5-1,000 ng/ml. The assay is also highly reproducible with intra-assay and interassay coefficients of variation of less than 10%. The purified Cup a 1, used as standard, presents pectate lyase enzymatic activity. The assay also detected Cup a 1-like proteins in pollen from other Cupressaceae. A good correlation was obtained between Cup a 1 content of 12 C. arizonica pollen extracts and their IgE-binding activity. CONCLUSIONS: The described Cup a 1 ELISA is sensitive, specific and reproducible and can be used for the quantification of Cup a 1 in C. arizonica and other related pollen extracts. It also provides a reliable indication of the allergenic activity of the whole cypress pollen extract.

Author(s): Galdi E ; Perfetti L ; Calcagno G ; Marcotulli MC ; Moscato G
Affiliation: Servizio Autonomo di Allergologia e Immunologia Clinica, Fondazione S. Maugeri, Clinica del Lavoro e della Riabilitazione, IRCCS, Istituto Scientifico di Pavia, Italy. egaldi@fsm.it

Title: Exacerbation of asthma related to Eucalyptus pollens and to herb infusion containing Eucalyptus. Source: Monaldi Arch Chest Dis (Monaldi archives for chest disease = Archivio Monaldi per le malattie del torace / Fondazione clinica del lavoro, IRCCS [and] Istituto di clinica tisiologica e malattie apparato respiratorio, Universita di Napoli, Secondo ateneo.) 2003 Jul-Sep; 59(3): 220-1

Abstract: Eucalyptus is known as a potential cause of cutaneous diseases due to contact with oil or pollens, and of respiratory allergic diseases due to exposure to pollens. We report the case of a 30-year-old woman with asthma and rhinoconjunctivitis in which symptoms appeared to be exacerbated by Eucalyptus pollens and by ingestion of an infusion containing Eucalyptus. Specific IgE were positive for Eucalyptus pollens and negative for common aeroallergens. Our report shows that Eucalyptus may elicit asthma and rhinitis with an IgE-mediated mechanism both by inhalation of pollens and by ingestion of herb infusions, and suggests that care should be taken in administering herbal medications in asthmatic subjects.

Author(s): Motta A ; Peltre G ; Dormans JA ; Withagen CE ; Lacroix G ; Bois F ; Steerenberg PA
Affiliation: National Institute of Public Health and the Environment, Bilthoven, The Netherlands.

Title: Phleum pratense pollen starch granules induce humoral and cell-mediated immune responses in a rat model of allergy. Source: Clin Exp Allergy (Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.) 2004 Feb; 34(2): 310-4

Abstract: BACKGROUND: Timothy grass (Phleum pratense) pollen allergens are an important cause of allergic symptoms. However, pollen grains are too large to penetrate the deeper airways. Grass pollen is known to release allergen-bearing starch granules (SG) upon contact with water. These granules can create an inhalable allergenic aerosol capable of triggering an early asthmatic response and are implicated in thunderstorm-associated asthma. OBJECTIVE: We studied the humoral (IgE) and bronchial lymph node cells reactivities to SG from timothy grass pollen in pollen-sensitized rats. METHODS: Brown-Norway rats were sensitized (day 0) and challenged (day 21) intratracheally with intact pollen and kept immunized by pollen intranasal instillation by 4 weeks intervals during 3 months. Blood and bronchial lymph nodes were collected 7 days after the last intranasal challenge. SG were purified from fresh timothy grass pollen using 5 microm mesh filters. To determine the humoral response (IgE) to SG, we developed an original ELISA inhibition test, based on competition between pollen allergens and purified SG. The cell-mediated response to SG in the bronchial lymph node cells was determined by measuring the uptake of [3H]thymidine in a proliferation assay. RESULTS: An antibody response to SG was induced, and purified SG were able to inhibit the IgE ELISA absorbance by 45%. Pollen extract and intact pollen gave inhibitions of 55% and 52%, respectively. A cell-mediated response was also found, as pollen extract, intact pollen and SG triggered proliferation of bronchial lymph node cells. CONCLUSIONS: It was confirmed that timothy grass pollen contains allergen-loaded SG, which are released upon contact with water. These granules were shown to be recognized by pollen-sensitized rats sera and to trigger lymph node cell proliferation in these rats. These data provide new arguments supporting the implication of grass pollen SG in allergic asthma.

Author(s): García BE ; Lombardero M ; Echechipía S ; Olaguibel JM ; Díaz-Perales A ; Sánchez-Monge R ; Barber D ; Salcedo G ; Tabar AI
Affiliation: Sección de Alergología, Hospital Virgen del Camino, Pamplona, Spain. bgarciaf@cfnavarra.es

Title: Respiratory allergy to peach leaves and lipid-transfer proteins. Source: Clin Exp Allergy (Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.) 2004 Feb; 34(2): 291-5

Abstract: BACKGROUND: Several lipid-transfer proteins (LTPs) have been identified as important food allergens, especially in fruits of the Rosaceae family. The major peach (Prunus persica) allergen has been identified, sequenced and designated Pru p 3. OBJECTIVE: To present Pru p 3 as an aeroallergen able to induce occupational asthma. METHODS: A thorough investigation was performed in a fruit grower with occupational asthma. Skin prick-prick tests with peach leaves and prick tests with perennial respiratory allergens and pollens, fruits and peach leaf extracts were done. Serum-specific IgE was tested for peach leaf, peach fruit, peach skin and respiratory allergens that were positive in skin prick tests. Specific bronchial provocation tests (BPTs) with extracts of peach leaf were also done. Before and 24 h after the BPT, BPTs with methacholine and sputum induction were done. The IgE reactivity pattern to peach leaf and fruit extracts and to Pru p 3 was identified by using SDS-PAGE and immunoblotting. Blotting inhibition of peach leaf extract by Pru p 3 was also performed. The putative allergen was quantified in leaf and fruit skin extracts with ELISA based on an anti-Pru p 3 antibody. RESULTS: Skin tests were positive for peach leaf and fruit. The BPT was positive, with immediate and delayed response. This test induced a decrease in PD20 (dose of agonist that induces a 20% fall in FEV1) methacholine and an increase in eosinophils and eosinophil cationic protein in sputum. Peach leaf extract contained concentrations of Pru p 3 similar to those found in peach skin. Specific IgE immunodetection showed that patient's sera reacted with Pru p 3, and with a single major band from the peach leaf extract fully inhibited by Pru p 3. CONCLUSION: Pru p 3 from peach leaves can act as a respiratory allergen and cause occupational rhinoconjunctivitis and asthma.

Author(s): Schäppi GF ; Taylor PE ; Pain MC ; Cameron PA ; Dent AW ; Staff IA ; Suphioglu C
Affiliation: Pollen and Allergen Research Group, School of Botany, The University of Melbourne, Australia.

Title: Concentrations of major grass group 5 allergens in pollen grains and atmospheric particles: implications for hay fever and allergic asthma sufferers sensitized to grass pollen allergens. Source: Clin Exp Allergy (Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.) 1999 May; 29(5): 633-41

Abstract: BACKGROUND: Grass pollen allergens are the most important cause of hay fever and allergic asthma during summer in cool temperate climates. Pollen counts provide a guide to hay fever sufferers. However, grass pollen, because of its size, has a low probability of entering the lower airways to trigger asthma. Yet, grass pollen allergens are known to be associated with atmospheric respirable particles. OBJECTIVE: We aimed (1) to determine the concentration of group 5 major allergens in (a) pollen grains of clinically important grass species and (b) atmospheric particles (respirable and nonrespirable) and (2) to compare the atmospheric allergen load with clinical data to assess different risk factors for asthma and hay fever. METHODS: We have performed a continuous 24 h sampling of atmospheric particles greater and lower than 7.2 microm in diameter during the grass pollen season of 1996 and 1997 (17 October 1996-16 January 1997) by means of a high volume cascade impactor at a height of about 15 m above ground in Melbourne. Using Western analysis, we assessed the reactivity of major timothy grass allergen Phl p 5 specific monoclonal antibody (MoAb) against selected pollen extracts. A MoAb-based ELISA was then employed to quantify Phl p 5 and cross-reactive allergens in pollen extracts and atmospheric particles larger and smaller than 7.2 microm. RESULTS: Phl p 5-specific MoAb detected group 5 allergens in tested grass pollen extracts, indicating that the ELISA employed here determines total group 5 allergen concentrations. On average, 0.05 ng of group 5 allergens were detectable per grass pollen grain. Atmospheric group 5 allergen concentrations in particles > 7.2 microm were significantly correlated with grass pollen counts (rs = 0.842, P < 0. 001). On dry days, 37% of the total group 5 allergen load, whereas upon rainfall, 57% of the total load was detected in respirable particles. After rainfall, the number of starch granule equivalents increased up to 10-fold; starch granule equivalent is defined as a hypothetical potential number of airborne starch granules based on known pollen count data. This indicates that rainfall tended to wash out large particles and contributed to an increase in respirable particles containing group 5 allergens by bursting of pollen grains. Four day running means of group 5 allergens in respirable particles and of asthma attendances (delayed by 2 days) were shown to be significantly correlated (P < 0.001). CONCLUSION: Here we present, for the first time, an estimation of the total group 5 allergen content in respirable and nonrespirable particles in the atmosphere of Melbourne. These results highlight the different environmental risk factors for hay fever and allergic asthma in patients, as on days of rainfall following high grass pollen count, the risk for asthma sufferers is far greater than on days of high pollen count with no associated rainfall. Moreover, rainfall may also contribute to the release of allergens from fungal spores and, along with the release of free allergen molecules from pollen grains, may be able to interact with other particles such as pollutants (i.e. diesel exhaust carbon particles) to trigger allergic asthma.

Pesticides

General Ozone Particulates Dust/Molds Pollens Pesticides

Author(s): Fryer AD ; Lein PJ ; Howard AS ; Yost BL ; Beckles RA ; Jett DA
Affiliation: National Institutes of Health National Institute of Neurological Disorders and Stroke, 6001 Executive Blvd. NSC, Suite 2149, MSC 9535, Bethesda, MD 20892-9835, USA.

Title: Mechanisms of organophosphate insecticide-induced airway hyperreactivity. Source: Am J Physiol Lung Cell Mol Physiol (American journal of physiology. Lung cellular and molecular physiology.) 2004 May; 286(5): L963-9

Abstract: It has been suggested that pesticide exposure may be a contributing factor underlying the increased incidence of asthma in the United States and other industrialized nations. To test this hypothesis, airway hyperreactivity was measured in guinea pigs exposed to chlorpyrifos, a widely used organophosphate pesticide. Electrical stimulation of the vagus nerves caused frequency-dependent bronchoconstriction that was significantly potentiated in animals 24 h or 7 days after a single subcutaneous injection of either 390 mg/kg or 70 mg/kg of chlorpyrifos, respectively. Mechanisms by which chlorpyrifos may cause airway hyperreactivity include inhibition of acetylcholinesterase (AChE) or dysfunction of M3 muscarinic receptors on airway smooth muscle or of autoinhibitory M2 muscarinic receptors on parasympathetic nerves in the lung. AChE activity in the lung was significantly inhibited 24 h after treatment with 390 mg/kg of chlorpyrifos, but not 7 days after injection of 70 mg/kg of chlorpyrifos. Acute exposure to eserine (250 microg/ml) also significantly inhibited lung AChE but did not potentiate vagally induced bronchoconstriction. Neuronal M2 receptor function was tested using the M2 agonist pilocarpine, which inhibits vagally induced bronchoconstriction in control animals. In chlorpyrifos-treated animals, pilocarpine dose-response curves were shifted significantly to the right, demonstrating decreased responsiveness of neuronal M2 receptors. In contrast, chlorpyrifos treatment did not alter methacholine-induced bronchoconstriction, suggesting that chlorpyrifos does not alter M3 muscarinic receptor function on airway smooth muscle. These data demonstrate that organophosphate insecticides can cause airway hyperreactivity in the absence of AChE inhibition by decreasing neuronal M2 receptor function.

Author(s): Bryant DH

Title: Asthma due to insecticide sensitivity. Source: Aust N Z J Med (Australian and New Zealand journal of medicine.) 1985 Feb; 15(1): 66-8

Abstract: Two patients are reported in whom asthma was precipitated by exposure to synthetic organophosphorous insecticides. Investigation showed no evidence of systemic poisoning or cholinesterase inhibition and indicated that the asthmatic reactions may have been due to a sensitivity response. The mechanism of this response is unknown but it was inhibited by corticosteroids in one patient. A history of insecticide exposure was obtained from the affected patients only after careful questioning and indicates the need for awareness that sensitivity to insecticides may precipitate asthma and that little exposure is necessary to elicit a response.

Author(s): Ernst P

Title: Pesticide exposure and asthma. Source: Am J Respir Crit Care Med (American journal of respiratory and critical care medicine.) 2002 Mar 1; 165(5): 563-4
No abstract available

Author(s): Jones SM ; Burks AW ; Spencer HJ ; Lensing S ; Roberson PK ; Gandy J ; Helm RM
Affiliation: Department of Pediatrics, University of Arkansas for Medical Sciences, Arkansas 72202, USA. JonesStacieM@uams.edu

Title: Occupational asthma symptoms and respiratory function among aerial pesticide applicators. Source: Am J Ind Med (American journal of industrial medicine.) 2003 Apr; 43(4): 407-17

Abstract: BACKGROUND: Pesticide exposure has been suggested as one causal factor for the rise in asthma prevalence. The goal of this investigation was to determine the effect of pesticide exposure on respiratory symptoms and lung function in workers with occupational exposure to pesticides. METHODS: A prospective, case-controlled study was conducted among pesticide aviators (AV) and community controls (Con). In Phase I, subjects completed an asthma survey and baseline spirometry. In Phase II, subjects reported symptoms, lung function monitoring, and pesticide exposure during two, 14-day periods. RESULTS: Phase I-Self-reported asthma and symptoms were similar among AV (n = 135) and Con (n = 118) with 4-6% prevalence reported but with higher rates among smokers. Baseline lung function was similar; although, a higher proportion of AV had forced expiratory volume in one second (FEV(1)) <80% predicted (8% vs. 2%, P = 0.02). Phase II-Self-reported symptoms were similar with 80% of AV (n = 50) and 73% of Con (n = 49) reporting no symptoms. Only 4% of AV and 6% of controls reported increased symptoms from baseline to spray season. Serial lung function did not differ between group and mean diurnal variation in peak expiratory flow improved in both groups between sampling times (AV 18% vs. 14%; Con 19% vs. 16%, P < 0.001). CONCLUSIONS: This study suggests that among workers with occupational pesticide exposure.

Author(s): Pearce M ; Habbick B ; Williams J ; Eastman M ; Newman M
Affiliation: University of Saskatchewan, Saskatoon, SK. marty.pearce@caphealth.org

Title: The effects of aerial spraying with Bacillus thuringiensis Kurstaki on children with asthma. Source: Can J Public Health (Canadian journal of public health. Revue canadienne de sante publique.) 2002 Jan-Feb; 93(1): 21-5

Abstract: OBJECTIVE: To determine if aerially spraying a biological pesticide was associated with an increase in the symptoms or change in the Peak Expiratory Flow Rate of children with asthma. METHODS: A pre/post matched pairs cohort design was used. Children living in the spray zone were matched with children outside of the spray zone. Peak Expiratory Flow Rates, asthma symptoms and non-asthma symptoms were recorded in diaries. RESULTS: There were no differences in asthma symptom scores between subjects and controls, neither before nor after the spray; nor were there significant changes in Peak Expiratory Flow Rates for subjects after the spray period. CONCLUSIONS: No evidence of adverse effects from the use of the biological pesticide was found. We believe that this is the first paper to address the issue of whether or not aerial spraying with Btk has a harmful effect on children with asthma.

Author(s): Senthilselvan A ; McDuffie HH ; Dosman JA
Affiliation: Department of Medicine, University of Saskatchewan, Saskatoon, Canada.

Title: Association of asthma with use of pesticides. Results of a cross-sectional survey of farmers. Source: Am Rev Respir Dis (The American review of respiratory disease.) 1992 Oct; 146(4): 884-7

Abstract: We investigated the association of self-reported asthma and pesticide use in 1,939 male farmers. Regardless of age, smoking pack-years, and nasal allergic reactions, the prevalence of asthma was significantly associated with the use of carbamate insecticides (prevalence odds ratio = 1.8, 95% confidence interval: 1.1 to 3.1, p = 0.02). Self-reported asthmatics, in comparison with nonasthmatics, had significantly lower mean values for lung function test variables after adjusting for age and height and a higher prevalence of respiratory symptoms. These findings raise the possibility that exposure to agriculture chemicals could be related to lung dysfunction in exposed farmers.