PERSONAL TOTAL AND RESPIRABLE ENDOTOXIN AND (1→3)-β-D-GLUCAN CONCENTRATIONS IN RACEHORSE STABLES IN SYDNEY, AUSTRALIA

Abstract

Ample evidence indicates that exposure to industrial, farm and home environments, and specifically to airborne, organic particle-associated bacterial endotoxin, plays an important role in the pathogenesis of acute and chronic inflammatory airway diseases and airflow obstruction in humans. Variable concentrations of total and respirable endotoxin have been determined in grain, cotton and wood chip industries as well as in housing for pigs, chickens and cows, and domestic environments contaminated by pets, vermin and cigarette smoke. A threshold limiting value (TLV), for 8 hour-5day exposure, as low as 4.5–10 mg/m3 of airborne endotoxin in these environments has been proposed for induction of airway inflammation in humans, although exposure to much higher concentrations (100 to 200 ng/m3) usually are necessary to induce general respiratory symptoms and disease. Concentrations of (1→3)-β-D-glucan also has been found in occupational and home environments and probably exerts synergistic or additive effects when inhaled along with organic particles. However, a TLV for glucan has not been determined. Personnel working in racehorse stables are potentially exposed to high levels of airborne organic particles, particularly during long periods (3–4 hours–7 day week) when stables are cleaned and horses are fed (twice daily) and when horses are being groomed within looseboxes. However, concentrations of endotoxin have not been measured in racehorse stable environments and levels of exposure for stable workers are unknown. Extrapolating information gained from epidemiological studies performed on horses in the racehorse industry may be useful as a guide to exposure levels potentially encountered by people working in racehorse stables and whether or not these levels may be high enough to induce airway inflammation. A case control study, nested within a cohort study, was performed in order to identify factors associated with neutrophilic inflammation of the proximal lower airways in young Thoroughbred racehorses housed in racetrack stables in Sydney, Australia. During the study, personal samples (n = 112) of total and respirable particles were collected onto glass fibre micro-pore filters using standardised Institute of Occupational Medicine attachments and personal cyclone impactors respectively. Measurements were conducted for approximately 5-hours during and after feeding and grooming (but not during loosebox cleaning) using a pump flow rate of 2L/minute. Standard endotoxin and (1→3)-β-D-glucan specific assays were used to determine concentrations in respirable and total particle samples. In addition, tracheal aspirate (TA) samples were collected using a guarded catheter and standardised endoscopic technique. Confounding variables (eg., training management factors, horse variables, infectious agents, stable factors and environemental variables) also were determined and data were analysed using univariable and multivariable regression modelling (SAS version 8). The range, mean and median endotoxin and (1→3)-β-D-glucan concentrations are presented in Table 1. There was a significant exposure-response relationship between respirable endotoxin concentration, but not respirable (1→3)-β-D-glucan concentration, and percentage of neutrophils in TA samples in racehorses (P = 0.002). Similar measurements were not performed in stable workers. In conclusion, although these measurements were not made during peak particle generation, personal exposure concentrations found in the breathing zone of horses may be representative of exposure levels for humans working in horse stables and in the case of respirable endotoxin may reach concentrations high enough to induce airway inflammation in humans.