Groups of approximately 120 male and 120 female Fischer 344 rats and C57BL/6 X C3H F1 mice were exposed by inhalation to 0, 2.0, 5.6, and 14.3 ppm of formaldehyde gas 6 hr/day, 5 days/week, for 24 months. This exposure period was followed by up to 6 months of nonexposure. Interim sacrifices were conducted at 6, 12, 18, 24, 27, and 30 months. Significant formaldehyde-induced lesions were restricted to the nasal cavity and proximal trachea. The distribution and severity of these lesions were concentration dependent. Rhinitis, epithelial dysplasia, and squamous metaplasia occurred in all exposure groups of rats and in the intermediate and high exposure groups of mice. There was regression of rhinitis, dysplasia, and metaplasia at 27 months (3 months postexposure) in the 14.3- and 5.6-ppm groups of mice and in the 2.0- and 5.6-ppm groups of rats. Squamous cell carcinomas were observed in the nasal cavities of 103 rats (52 females and 51 males) and 2 male mice exposed to 14.3 ppm and in 2 rats (one male and one female) exposed to 5.6 ppm of formaldehyde gas. Formaldehyde inhalation was also weakly associated with an increase in the frequency of polypoid adenomas in the nasal cavity of male rats.

https://cancerres.aacrjournals.org/content/canres/43/9/4382.full.pdf

Carcinogenicity of Formaldehyde in Rats and Mice after Long-Term Inhalation Exposure

In this chapter the host range of foot-and-mouth disease (FMD) under natural and experimental conditions is reviewed. The routes and sites of infection, incubation periods and clinical and pathological findings are described and highlighted in relation to progress in understanding the pathogenesis of FMD.

Foot-and-mouth disease: host range and pathogenesis.

This article outlines the principles of radiobiology that can explain the time of onset, duration, and severity of the complex reactions of the lung to ionizing radiation. These reactions have been assayed biochemically, cell kinetically, physiologically, and pathologically. Clinical and experimental data are used to describe the acute and late reactions of the lung to both external and internal radiation including pneumonitis, fibrosis and carcinogenesis. Acute radiation pneumonitis, which can be fatal, develops in both humans and animals within 6 months of exposure to doses greater than or equal to 8 Gy of low LET radiation. It is divisible into a latent period lasting up to 4 weeks; an exudative phase (3-8 weeks) and with an acute pneumonitic phase between 2 and 6 months. The latter is an inflammatory reaction with intra-alveolar and septal edema accompanied by epithelial and endothelial desquamation. The critical role of type II pneumonocytes is discussed. One favored hypothesis suggests that the primary response of the lung is an increase in microvascular permeability. The plasma proteins overwhelm the lymphatic and other drainage mechanisms and this elicits the secondary response of type II cell hyperplasia. This, in its turn, produces an excess of surfactant that ultimately causes the fall in compliance, abnormal gas exchange values, and even respiratory failure. The inflammatory early reaction may progress to chronic fibrosis. There is much evidence to suggest that pneumonitis is an epithelial reaction and some evidence to suggest that this early damage may not be predictive of late fibrosis. However, despite detailed work on collagen metabolism, the pathogenesis of radiation fibrosis remains unknown. The data on radiation-induced pulmonary cancer, both in man and experimental animals from both external and internal irradiation following the inhalation of both soluble and insoluble alpha and beta emitting radionuclides are reviewed. Emphasis is placed on the data showing that alpha emitters are at least an order of magnitude more hazardous than beta/gamma radiation and on recent data showing that the more homogeneous the irradiation of the lung, the greater is the carcinogenic hazard which contradicts the so-called "hot particle" theory.

Radiation effects in the lung.

An electrostatic induction technique was used to determine both drop size distribution and concentration of bacteria in the film drops produced by bubbles bursting at the surface of a suspension of Serratia marcescens. Film drops are produced from the collapse of the thin film of water that just before bursting separates the air in the bubble from the atmosphere. Bubbles of 1.7-mm diameter produced from 10 to 20 film drops which ranged from <2 mum to over 30 mum in diameter. Half the drops were <10 mum. For bubbles rising a distance of less than 2 cm through the bacterial suspension, bacterial enrichment factors in the drops were between 10 and 20. Electrostatic methods can be used to determine the enrichment of bacteria in film drops as a function of bubble size and distance of rise through the bacterial suspension.

Water-to-Air Transfer and Enrichment of Bacteria in Drops from Bursting Bubbles.

Publisher Summary This chapter discusses the chemical, physicochemical, and biological properties of mineral fibers. Among the most important occupational air pollutants are particles of coal, quartz, and fibers of asbestos, which are inhaled by miners and exposed industrial workers. Mineralogically, asbestos is divided into two classes: serpentine and amphibole. The former is a sheet silicate, whereas the latter is built up of double chains of tetrahedra. Chrysotile is the principal asbestos member of the serpentine family, whereas all other asbestos minerals belong to the amphibole group. Chrysotile asbestos is usually worked relatively near the surface by open-cast pit methods. Once the overburden has been cleared, explosives are used to release large tonnages of rock and fiber, the latter accounting for only a few percent of the parent rock. Crude asbestos, together with associated mother rock is conveyed to sorting stations, where waste rock is rejected and the ore undergoes a series of crushing and grinding operations. Fiber bundles of widely different lengths are inevitably mixed together. Subsequent screening results in a rough separation into grades but such screening is too imperfect to remove all the shorter fibers from the longer grades and even the lower grades contain a few long fibers.

Mineral Fibers: Chemical, Physicochemical, and Biological Properties

Chronic pneumonitis caused by phosgene. an experimental study.

Fibrous quartz, chrysotile asbestos, and tremolite talc dust, all of respirable particle size, injected intratracheally, produced polypoid proliferative inflammations within smaller air-conducting tubes as well as more peripherally. With time, the inflammatory tissue became converted into coUagenous scars which often caused permanent deformities of bronchi and bronchioles. After intratracheal injection of a fibrous dust such as synthetic chrysotile, ceramic aluminum silicate, silicon carbide, glass, or brucite, the main pulmonary response was a macrophage reaction with minimal stromal participation. In addition, within 4 days after the injection, there were foci of polypoid proliferative inflammation but limited to the more peripheral respiratory bronchiole and alveolar ducts. Because these polypoid lesions did not collagenize and did not destroy the anatomic integrity of the air spaces, and because the lesions were reversible, the dusts calling forth this type of response must be classed as biologically ...

The pulmonary response to fibrous dusts of diverse compositions.

CHAPTER 4 – Experimental Studies on Deposition of Inhaled Aerosols

One hundred eighty-six rats and 202 hamsters, that survived the respective time periods when the first lung cancer was diagnosed in each species, had been given an exposure of 3000 R or 4000 R of x-irradiation applied externally to the chest. About 43% of the rats, but only 2% of the hamsters, developed lung cancer. To enhance the prevalence of lung cancer, some of the irradiated animals were injected intratracheally with 9, 10-dimethyl-1, 2-benzanthracene (DMBA). Lung cancer prevalence in irradiated animals injected with DMBA was no higher than that in irradiated animals not so injected. Intratracheal injections of DMBA in nonirradiated rats did not result in tumor production but, in nonirradiated hamsters, DMBA caused a 6% prevalence of lung cancer. The mortality rate of both animal species showed a more than additive effect in animals given the higher x-ray dosage plus intratracheal injections of either DMBA or iron oxide alone. The lung cancers in the irradiated rats predominantly affected bronchi (86%) and were mostly adenocarcinomas (88%). The cancers were generally intramural and were covered by an intact and normal surface epithelium. Their origin appeared to be from aberrant intramural glands. These glands are not found in the bronchi of germ-free rats but do occur in bronchi thickened by severe endemic chronic bronchitis.

Experimental carcinogenesis bronchial intramural adenocarcinomas in rats from x-ray irradiation of the chest

Emphysema and pneumoconiosis. A comparative quantitation of dust content of pneumoconiotic rodent lungs with and without emphysema.

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