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[Asbestosis and microfiber role].

Based on the predominant content of thin and short asbestos fibres in lung and mesothelioma tissues, it was recently stated (2005) that such fibres "appear to contribute to the causation of human malignant mesothelioma". In another study of the same year it was stated that fibres in the order of few microm length and 0.2 microm diameter are the sole able to induce mesothelioma. This scientific conclusions entail some implications from practical point of view. The enormous amount of information gained on asbestos in the last decades is based on the definition of a fibre as an alongated particle with an aspect-ratio of at least 3:1, a diameter < or = 3 microm and a length > or = 5 microm. These parameters were used up today to define occupational and in some case non-occupational limits. In which way can "reference" values be established if all lengths or only fibres shorter than 5 microm are considered? Nowadays we have no answer. Secondly, assuming a prevalent role of such fibres especially in mesothelioma cases, how can reliable estimates of past exposure obtained in a medico-legal context, since they have never been counted? Morever, how might he the employer responsibility assessed since short fibres were not measured by definition pathogenic, and this not measured, nor were there appropriate filtering systems up to the middle of the '80?

Asbestos↗
PubMed1991

A landmark case in asbestosis.

The first published account of disease attributed to occupational asbestos exposure was that of Nellie Kershaw, who died in 1924. The circumstances relating to that case are described and explanations are given for its not having a greater impact on policy at that time. This case, starting in 1898, is set in the context of missed opportunities for preventing a major public health hazard. The effects of this hazard are still being witnessed today.

Adult↗
PubMed1991

Asbestosis in New Jersey.

A survey was conducted of 1,079 individuals reported by New Jersey hospitals to the New Jersey State Department of Health. Forty-eight percent of the respondents indicated that they had not received financial compensation for their work-related disease; 415 different sources of exposure to asbestos were identified.

Asbestosis↗
PubMed1990

Mass, number and size of lung fibres in the pathogenesis of asbestosis in sheep.

After long-term asbestos inhalation, the lung tissue burden is much less for chrysotile (CHRY) than for crocidolite (CRO) exposure. Nonetheless CHRY does not appear to be less fibrogenic. To study mechanisms responsible for the low retention of CHRY and the relationships with fibrogenesis, 15 sheep received a single intratracheal injection of either CHRY or CRO. Exposures in 100 ml saline consisted of 100 mg of 1-micron latex beads for the five control sheep, 100 mg UICC CRO fibres for the five CRO sheep and 100 mg UICC B CHRY fibres for the five CHRY sheep. Bronchoalveolar lavage (BAL) was carried out at months 2, 4, 6 and 8 after exposure and necropsy at month 8. BAL and tissue samples were analysed for fibres by transmission electron microscopy. At month 2, mass concentration in BAL was 108 +/- 30 ng/ml for CRO and 0.6 +/- 0.1 ng/ml for CHRY. BAL CRO decreased afterward but BAL CHRY did not. The mass concentration in the lung at month 8 was 40.6 +/- 8.7 ng/mg dry tissue for CRO and 11.5 +/- 7.0 ng/mg for CHRY. BAL fibrogenic activity at month 8 assessed by macrophage fibronectin production was less than 0.2 ng/10(6) cells/24 h in control sheep, 5 +/- 2 in CRO sheep and 11 +/- 2 in CHRY sheep (P less than 0.05 CRO vs CHRY). Histologic score of tissue injury fibrosis was 0 in control sheep, 1.9 +/- 0.3 in CRO sheep and 2.8 +/- 0.1 in CHRY sheep (P less than 0.05). At necropsy, the number size distribution of fibres per microgram of tissue from the (CRO)/(CHRY) sheep was respectively: (127 +/- 54)/(15 +/- 14) for fibres less than 5 microns, (18 +/- 17)/(32 +/- 14) for fibres greater than 5 microns, (1.6 +/- 8)/(7 +/- 13) for fibres greater than 20 microns. This study documented that the low pulmonary retention of CHRY was largely related to the faster alveolar clearance rate of CHRY mass. Fibrogenicity of CHRY remained higher and appeared to be related at least in part to the preferential retention of long and very long CHRY fibres.

Animals↗
PubMed1989

Changes in lymphocyte function and lung histology during the development of asbestosis and silicosis in the mouse.

In order to study changes in lung histology and lymphocyte function during the development of pneumoconiosis, three groups of Balb/c mice were intratracheally instilled with either saline, chrysotile asbestos or silica particles and then sacrificed at different times. Asbestos-instilled mice showed collagen deposits at 2 months while silica-instilled mice showed severe fibrosis at that time. Stimulation of splenic cells with LPS was not affected by instillation of the toxic particles. Stimulation with PHA and ConA, however, induced increased responses especially at 3 and 6 months after instillation of asbestos or silica. A diminution of mitogen-induced proliferation was observed in aged mice. There was no correlation between changes in splenic cell proliferation and development of fibrosis. Asbestos fibers added in vitro, inhibited PHA and ConA-induced proliferation, partially due to prostaglandin (PG) production and to the presence of the fibers during the assay. When asbestos fibers were removed by washing, no inhibition was observed. Moreover, actual stimulation of proliferation was noted when PG production was inhibited in vitro with indomethacin. In contrast, in vivo treatment of asbestos-instilled mice with indomethacin had no effect on the development of lung pathology.

Animals↗
PubMed1989

Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis.

Recent investigations of the fundamental mechanisms of the mineral dust diseases have substantially increased our understanding of the pathogenesis of the pneumoconioses. In all the mineral dust pneumoconioses, the initial early lung lesion is a fibrosing macrophagic alveolitis. The additional contribution of other lung cell populations is currently under investigation and may identify specific processes for each of the pneumoconioses. Clinical investigations have also progressed with new tools such as Gallium-67 lung scanning, bronchoalveolar lavage analyses, and CT scanning of the thorax; their established values are reviewed in this paper, and areas where progress is needed are considered. The clinical progress in the mineral dust diseases is clearly linked to the basic understanding of the mechanisms of these diseases.

Asbestosis↗
PubMed1989

[Exposure to asbestos dust and asbestosis of employees in a Thüringen rubber industry].

131 exposed people by dust of talc in rubber industry in Thuringia were examined by contrast to a same no examined group of working people. The asbestos in talc did cause in 26 (19.8%) cases of exposed people a pneumoconiosis. The occupational disease was admitted. The time of development was between 20 and 40 years. We can found the chronic bronchitis and demages of ventilation much more in cases long time exposed people and by smokers. The following conclusions are: the renunciation of application of talc with asbestos, measures to fight against dust, the instruction of direction and of working people about the danger of asbestos and the dispensatory care for life.

Adult↗