Allergens in Paved Road Dust and Airborne Particles

Paved road dust present on the surface of streets in Southern California consists of a complex mixture of soil dust, deposited motor vehicle exhaust particles, tire dust, brake lining wear dust, plant fragments, and other biological materials. The research presented here shows that allergens from at least 20 different source materials are found in the paved road dust. These include pollens and pollen fragments, animal dander, and molds. When paved road dust is resuspended into the atmosphere by passing vehicle traffic, allergen concentrations in the air are increased above the levels that would prevail without the vehicle traffic. Using immunological assays that measure the proteins extracted from environmental samples that bind to IgE antibodies present in the blood serum of allergenic patients, it is possible to measure the allergen concentrations present in paved road dust and in airborne particle samples. Total protein contributions to monthly average airborne TSP and PM_(10) concentrations are found to be in the range from 1 to 5.8 μg m^(-3), potentially accounting for a significant fraction of the airborne particulate organic material that has not been identified to date by GC/MS techniques. Results show that up to 5−12% of the allergenicity of atmospheric total suspended particulate matter samples at Long Beach and Rubidoux, CA, is attributable to paved road dust emissions. In an industrial area of urban central Los Angeles where there is less proximity to vegetation and domestic activities, the paved road dust contribution to airborne allergen concentrations is lower, accounting for approximately 0.5% of the total allergenic activity of the atmospheric particle samples. In conclusion, paved road dust when entrained into the atmosphere by passing traffic is a source of allergen exposure for the general population and could be more important in areas with more abundant vegetation or with closer proximity of populations to major highways than is the case for the Southern California air monitoring sites studied here

Allergens in Paved Road Dust and Airborne Particles

Paved road dust present on the surface of streets in Southern California consists of a complex mixture of soil dust, deposited motor vehicle exhaust particles, tire dust, brake lining wear dust, plant fragments, and other biological materials. The research presented here shows that allergens from at least 20 different source materials are found in the paved road dust. These include pollens and pollen fragments, animal dander, and molds. When paved road dust is resuspended into the atmosphere by passing vehicle traffic, allergen concentrations in the air are increased above the levels that would prevail without the vehicle traffic. Using immunological assays that measure the proteins extracted from environmental samples that bind to IgE antibodies present in the blood serum of allergenic patients, it is possible to measure the allergen concentrations present in paved road dust and in airborne particle samples. Total protein contributions to monthly average airborne TSP and PM_(10) concentrations are found to be in the range from 1 to 5.8 μg m^(-3), potentially accounting for a significant fraction of the airborne particulate organic material that has not been identified to date by GC/MS techniques. Results show that up to 5−12% of the allergenicity of atmospheric total suspended particulate matter samples at Long Beach and Rubidoux, CA, is attributable to paved road dust emissions. In an industrial area of urban central Los Angeles where there is less proximity to vegetation and domestic activities, the paved road dust contribution to airborne allergen concentrations is lower, accounting for approximately 0.5% of the total allergenic activity of the atmospheric particle samples. In conclusion, paved road dust when entrained into the atmosphere by passing traffic is a source of allergen exposure for the general population and could be more important in areas with more abundant vegetation or with closer proximity of populations to major highways than is the case for the Southern California air monitoring sites studied here

Meteorological influences on respirable fragment release from Chinese elm pollen

Exposure to airborne pollen from certain plants can cause allergic disease, leading to acute respiratory symptoms. Whole pollen grains, 15&ndash;90 &mu; m-sized particles, provoke the upper respiratory symptoms of rhinitis (hay fever), while smaller pollen fragments capable of depositing in the lower respiratory tract have been proposed as the trigger for asthma. In order to understand factors leading to pollen release and fragmentation we have examined the rupture of Chinese elm pollen under controlled laboratory conditions and in the outdoor atmosphere. Within 30 minutes after immersion in water, 70% of fresh Chinese pollen ruptures, rapidly expelling cytoplasm. Chinese elm flowers, placed in a controlled atmosphere chamber, emitted pollen and pollen debris after a sequential treatment of 98% relative humidity followed by drying and a gentle disturbance. Immunologic assays of antigenic proteins specific to elm pollens revealed that fine particulate material (D p &lt; 2 &mu; m) collected from the chamber contained elm pollen antigens. In a temporal study of the outdoor urban atmosphere during the Chinese elm bloom season of 2004, peak concentrations of pollen and fine pollen fragments occurred at the beginning of the season when nocturnal relative humidity (RH) exceeded 90%. Following later periods of hot dry weather, pollen counts decreased to zero. The Chinese elm pollen fragments also decreased during the hot weather, but later displayed additional peaks following periods of more moderate RH and temperature, indicating that pollen counts underestimate total atmospheric pollen allergen concentrations. Pollen fragments thus increase the biogenic load in the atmosphere in a form that is no longer recognizable as pollen and, therefore, is not amenable to microscopic analysis. This raises the possibility of exposure of sensitive individuals to pollen allergens in the form of fine particles that can penetrate into the lower airways and pose potentially severe health risks.<br /

Links between pollen, atopy and the asthma epidemic

Pollen allergy has been found in 80&ndash;90% of childhood asthmatics and 40&ndash;50% of adult-onset asthmatics. Despite the high prevalence of atopy in asthmatics, a causal relationship between the allergic response and asthma has not been clearly established. Pollen grains are too large to penetrate the small airways where asthma occurs. Yet pollen cytoplasmic fragments are respirable and are likely correlated with the asthmatic response in allergic asthmatics. In this review, we outline the mechanism of pollen fragmentation and possible pathophysiology of pollen fragment-induced asthma. Pollen grains rupture within the male flowers and emit cytoplasmic debris when winds or other disturbances disperse the pollen. Peak levels of grass and birch pollen allergens in the atmosphere correlated with the occurrence of moist weather conditions during the flowering period. Thunderstorm asthma epidemics may be triggered by grass pollen rupture in the atmosphere and the entrainment of respirable-sized particles in the outflows of air masses at ground level. Pollen contains nicotinamide adenine dinucleotide phosphate (reduced) oxidases and bioactive lipid mediators which likely contribute to the inflammatory response. Several studies have examined synergistic effects and enhanced immune response from interaction in the atmosphere, or from co-deposition in the airways, of pollen allergens, endogenous pro-inflammatory agents, and the particulate and gaseous fraction of combustion products. Pollen and fungal fragments also contain compounds that can suppress reactive oxidants and quench free radicals. It is important to know more about how these substances interact to potentially enhance, or even ameliorate, allergic asthma.<br /

Studies on C3a_(hu) Binding to Human Eosinophils: Characterization of Binding

C3a purified to chemical homogeneity from human serum binds preferentially to human eosinophils > neutrophils. Little or no binding is found with human platelets. Maximum binding to eosinophils at 37 °C occurs within 15 min. Dilution of ^(125)I-C3a by either cold C3a or washing away unbound ^(125)I-C3a and reincubating at 37 °C reveals a T_(1/2) of ∼30 min. C3a_(desArg) neither binds to eosinophils nor inhibits the binding of ^(125)I-C3a. The binding of C3a to human eosinophils may reflect a physiologic role of C3a in eosinophil motility or function