Effects Of Ammonia Exposure Research Articles

EFFECT OF CHRONIC EXPOSURE TO GASEOUS AMMONIA ON THE NASAL TURBINATES OF GNOTOBIOTIC PIGS

Pigs reared in and stock persons working in intensive production systems are continuously exposed to ammonia released by microbial degradation of animal excrement. Experimental studies have shown that exposure to this gas, at concentrations comparable to those encountered in buildings used for the intensive rearing of swine, increases the severity of the clinical disease progressive atrophic rhinitis in pigs by facilitating colonization of the upper respiratory tract by toxigenic Pasteurella multocida. During the course of these studies it was observed that mild turbinate atrophy also occurred in pigs from control groups exposed to ammonia but maintained free from P. multocida and Bordetella bronchiseptica. To determine whether exposure to ammonia is detrimental to the normal anatomical development of the mammalian nasal cavity, a study was conducted using gnotobiotic piglets. Twenty-one gnotobiotic piglets were derived from two sows by hysterectomy. Each litter was split into two groups, and the four groups were accommodated separately in sterile positive-pressure isolators supplied with high-efficiency particulate air (HEPA) filtered air. From 1 wk of age onward the air in the isolators housing one of the groups from each litter was modified by the addition of ammonia at a concentration of 9.1 and 15.7 ppm. The air supply to the isolators housing the littermate groups was not modified. At 6 wk of age all the pigs were euthanatized. The effect of ammonia exposure on the morphology of the nasal cavity of the pig was assessed by image analysis of a cross section of the pig's snout. Pigs exposed to ammonia were found to have a mild but statistically significant level of turbinate atrophy when compared to nonexposed lit termates. Histological examination revealed that prolonged ammonia exposure evoked changes to the mucous membranes lining the nasal cavity, characterized by epithelial hyperplasia with micro-abscess formation, goblet-cell hypoplasia, and inflammatory cell infiltration. Mild degenerative changes within the bony core of the ventral turbinate were also apparent, with a decline in the population of osteoblasts and simultaneous osteoclast proliferation. Group analysis revealed a correlation between the severity of turbinate atrophy and the increase in the number of osteoclasts per unit area of bony core (p<.05). These findings could explain why mild turbinate atrophy is seen on some pig units deemed free from pathogenic bacteria associated with the clinical disease atrophic rhinitis.

Ammonia adsorption and decomposition on the GaAs(100)-c(8 × 2) surface

The effect of ammonia exposure and substrate temperature on the reaction of ammonia with GaAs(100)-c(8 × 2) has been studied using temperature programmed desorption (TPD), X-ray photoelectron spectroscopy (XPS), and high resolution electron energy loss spectroscopy (HREELS). TPD data indicate that thermal decomposition of ammonia occurs at moderate temperatures (250 K). Above 250 K, recombinative desorption of ammonia is the dominant reaction mechanism. The appearance of the NH 2 deformation mode at low exposure and temperature indicates thermal decomposition of ammonia on the GaAs(100)-c(8 × 2) surface.

The effect of ammonia exposure on gill structure of the rainbow trout (Salmo gairdneri)

Gill structure has been studied in fish exposed to various ammonia concentrations. Gill damage resulting from exposure to acutely lethal concentrations was relatively minor and unlikely to have been a primary cause of death. Alternative toxic mechanisms have been discussed. Following long‐term exposure to ammonia there were severe histopathological changes in gill structure and oxygen uptake may have been seriously impaired. A high incidence of disease was also observed.