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In normal dogs and in dogs treated with 20 or 30 U.S.P. parathyroid extract for 5 and 34 days, respectively, the glycosaminoglyeans of compact bone tissue were identified using the cetylpyridinium chloride precipitation method, and the concentrations of total hexosamines and the hexosamines corresponding to cetylpyridinium chloride precipitable acid glycosaminoglycans were determined. Further, the glyeosaminoglycan pattern of the epiphyseal plate and the incorporation of asS-sulphate into the glycosaminoglycans of bone tissue and epiphyseal cartilage after administration of asS-sulphate in vivo was studied.In compact bone tissue, the hexosamines corresponding to acid glycosaminoglycans constituted approximately one third of the total hexosamine concentration and approximately 0.0510.06% of the total dry weight. The main component of the acid glycosaminoglycans in bone was chondroitin-4-sulphate. This was sulphated to a higher degree and also of a higher molecular weight than the chondroitin sulphate of the epiphyseal cartilage, which in accordance with earlier investigations was found to have infrared characteristics of both chondroitin-4-sulphate and chondroitin-6-sulphate, with the former dominating. The molecular weights of the main part of bone chondroitin sulphate ranged from approximately 45,000 to 56,000. A small component of the bone glycosaminoglycans was hyaluronic acid.Large regularly recurring differences in the specific activity of fractions with differences in molecular weight in the chondroitin sulphate of bone tissue and epiphyseal cartilage were noted.Treatment of the dogs with parathyroid extract gave no effect on the molecular weights of the chondroitin sulphate of the bone matrix or of the epiphyseal cartilage. Nor was there any unequivocal effect on the concentrations of total hexosamines or on the acid glycosaminoglycans. No evident stimulatory or depressant effect on the incorporation of 3~S-sulphate into the chondroitin sulphate or in the molecular distribution of newly sulphated and/or synthesized molecules of the chondroitin sulphate within these tissues oceured.

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Aluminium potroom workers have been reported to develop severe pneumoconiosis and bronchial hyperreactivity. The influence of inhalation of aluminium oxide and fluorides on the alveolar milieu was studied by bronchoalveolar lavage (BAL) in 14 male non-smoking potroom workers; 28 non-smoking healthy volunteers served as controls. The total numbers, concentrations, and proportions of various alveolar cells did not differ between the groups. The concentrations of albumin and fibronectin in BAL fluid were significantly higher (p < 0-01 for both) in the exposed workers, reflecting an increased alveolar capillary permeability and an activation of alveolar macrophages (AMs). The concentration of angiotensin converting enzyme, another AM marker, was, however, decreased (p < 0O01) in the workers. The concentration of hyaluronan, a fibroblast marker, did not differ between the groups. AMs from workers had a decreased capacity (p < 005) to interact with yeast C3b particles but not to ingest them. The expression of HLA-DR and OKM I on the cell surfaces of AMs were equal in the two groups. The BAL findings were not accompanied by restrictive lung disease in the workers. The fact that only a discrete alveolitis was found in the potroom workers may be due to a low grade ofexposure to alumina and fluorides and to frequent use of respiratory protection equipment.Aluminium potroom workers are exposed to alumina (aluminium oxide) dust and to particulate and gaseous fluorides. Aluminium plant employees may develop severe pneumoconiosis'-3 and bronchial hyperreactivity.' No relation between atopic constitution and the development of airways obstruction in potroom workers has been observed.9During the past decade bronchoalveolar lavage (BAL) has made possible the study of the alveolar milieu with regard to cells and soluble components under the influence of various agents. For example, the effect of smoking on cells and non-cellular substances has been well documented in several studies.'0The BAL technique also offers the opportunity to study the effects of occupational exposure to various agents potentially harmful on the alveolar space; those exposed to alumina have not to our knowledge been investigated.

Papain has been found to have a very swift and powerful effect on epiphysial cartilage in growing animals of various species (HuLTH 1958; HULTg and WESTE~-BO~ 1959a; ENGFELDT, HULTH and WESTERBO~ 1959; E~GFELDT and WESTE~-BORN 1960a; WESTEnBOR~ 1961). A single dose of papain, injected intravenously, produces histologically detectable changes within ten minutes. The lesions conform to a specific pattern, a reparative stage beginning after approximately 24 hours and the cartilage showing a normal organization after 15--30 days, Various experimental studies employing histologic, autoradiographic, microradiographic and biochemical methods have demonstrated that papain releases chondroitin sulphate from cartilage matrix and concomitantly damages the cartilage cells. Tile effect of repeated injections of papain has also been studied: such treatment results in permanent lesions of the growth zones of long bones, sometimes followed by premature ossification of these zones and dwarfism (HuLT~ and WESTE~BO~ 1959b).As regards rickets the lesions in the growth zones of the long bones occupy the forefront of interest. Although numerous workers have devoted attention to these pathologic changes, employing various morphologic, biophysical and biochemical methods, the mechanism of origin of the different lesions in the growth zones has not yet been fully elucidated (for references vide E~GFELDT and ZETTERSTR(955 1955; FOLLIS 1958;BALL 1960;ENGFELDT and HJERTQUIST 1960).The aim of the present investigation has been to study raehitie growth zones, utilizing knowledge of the action of papain upon normal epiphysial cartilage. The effects of both single and multiple doses of papain in rachitie rats were investigated by histologic, autoradiographic and microradiographic methods. Material and Methods.The experimental animals were rats six to seven weeks old. Some were normal and others had rickets induced by a rachitogenic diet ad modum B~UNIus (1961) or HJERTQUIST (1961 a), initiated at the age of three weeks.Two different types of experiments were conducted, one type involving single doses of papain and the other repeated doses. I. Rats Treated with a Single Injection o~ PapainA 1 per cent solution of crude papain in NaC1 was administered intraperitoneally in a single dose equivalent to 6,5 mg per rat. Radioactive sulphate (SJS2, t~adiochemicM Centre, Amersham, England) was injected intraperitoneally in a dose of 1 mC per rat.10"

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