Mists, inhalation exposure

A review of exposures to mineral oil mist averaging below 15 mg/m (but higher in some jobs) in several industries disclosed a striking lack of reported cases of illness related to these exposures. A smdy of oil mist exposures in machine shops, at mean concentrations of 3.7mg/m and maximum of llOmg/m showed no increase in respiratory symptoms or decrement in respiratory performance attributable to oil mist inhalation among men... 

Occupational exposure to chromium(VI) primarily as mist/aerosol can result in respiratory effects. Animal studies have reported respiratory effects following exposure to chromium(VI) or chromium(III) mists and particulates. Exposure to chromium in ambient air is mainly to chromium(III) adhered to dust particles (see Section 5.4.1). The possibility that inhalation exposure to chromium in the environment, from industrial sources, or at hazardous waste sites could result in respiratory effects cannot be ruled out. 

An MRL of 0.000005 mg chromium(VI)/m3 has been derived for intermediate-duration inhalation exposure to chromium(VI) as chromium trioxide mist and other dissolved hexavalent chromium aerosols and mists. The MRL is based on a LOAEL of 0.002 mg chromium(VI)/m3 for upper respiratory effects in humans in the occupational exposure study by Lindberg and Hedenstiema (1983) which spanned both intermediate and chronic durations. 

Chromium(VI) Carcinogenic risk from inhalation exposure Chromic acid mists and dissolved chromium(VI) aerosols RfC Chromium(VI) particulates RfC 1.2x102 pg/m3 8x10-6 mg/m3 1x1 O 4 mg/m3 IRIS 2000b... 

Information regarding death of humans after inhalation exposure to DNOC is limited. A case report of a spray operator who inhaled a dense DNOC mist for an unspecified, but apparently acute, duration noted that he died after lapsing into a coma while being treated in a hospital (van Noort et al. 1960). In a survey of 133 spray operators who applied DNOC to cereal crops 5 days per week for 6 weeks, 4 developed signs of acute poisoning (not otherwise specified), one of whom died (Bidstrup et al. 1952). The amount or concentration of inhaled DNOC was not reported in the survey. 

DNOC is rapidly absorbed by the respiratory tract in humans and animals. A serum DNOC concentration of 1,000 pg/mL was detected in a spray operator 24-36 hours after inhaling a dense DNOC mist for an acute duration (van Noort et al. 1960). The worker subsequently died. Because the spray operator had previous dermal exposure to DNOC, the acute inhalation of dense DNOC mist probably caused the serum DNOC level to spike to lethal levels. A blood DNOC concentration of 60 pg/g was detected in a spray operator who had periodically inhaled an unknown amount of DNOC for 5 weeks (Pollard and Filbee 1951). The blood sample was collected after a 2-day period of no exposure. In addition, a DNOC peak urinary level of 22 mg was detected on the third day after the patient was admitted to the hospital, and a total of 89.9 mg DNOC was eliminated in the urine over 20 days. While these data indicate absorption after inhalation exposure, there was also possible dermal absorption. In an occupational exposure study involving DNOC manufacturers, winter-washer sprayers, and cereal-crop sprayers, a correlation between blood DNOC levels and the symptoms and signs of poisoning was observed (Bidstrup et al. 1952). Blood DNOC levels <10-20 p g/g were not generally associated with signs of toxicity, while concentrations greater than 44 pg/g resulted in several illnesses. 

Kerosene may enter the water or soil environment as a result of regular use (e.g., evaporation of pesticide solvent), from spills during use or transportation, or from leaking storage facilities. The relatively low vapor pressure of kerosene makes inhalation exposure unlikely under ordinary occupational conditions unless conditions of poor ventilation exist. The combustion product of burned kerosene, carbon monoxide, is of real concern when kerosene heaters are not vented. Exposure to kerosene mist can occur as kerosene is often applied in the form of a spray. Eye and skin contact with kerosene and kerosene mists and vapors can occur. The exposure pathway usually of... 

Exposure to crude oil can occur through both direct contact with the material and contact with environmental media contaminated with crude oil. The primary route of exposure in the environment to crude oil is direct dermal contact with liquid oil. In the workplace, the primary route of exposure is also dermal contact. Inhalation exposure to crude oil could occur through the production of oil mists or through inhalation of the volatile fraction of the crude oil. Exposure to crude oil through contact with environmental media also constitutes significant routes of exposure. This can occur at spill sites, in former oil fields developed into other uses, or areas of natural oil seeps. Dermal contact or incidental ingestion of soil contaminated with crude oil, as well as the inhalation of dust from crude oil-contaminated soil are common at crude oil contaminated sites. Both human and animal exposures can occur when crude oil is released into the aquatic environment. 

Picloram is either a colorless powder or crystalline solid having very low vapor pressure, making inhalation exposure unlikely unless the dust is inhaled. Exposure to picloram occurs mainly through its manufacture and its use as a herbicide in forests. Environmental exposures in humans occur when forest visitors or others not directly involved in spray operations come in contact with spray or sprayed foliage, inhale spray mist, eat plants or animals contaminated with the herbicide, or drink water containing the herbicide. A suggested no-adverse-effect level is 1.05 mg 1. ... 

The acute oral toxicity of Folpet for rats was not reached at 10 g/kg, for mice it was 2440 mg/kg. It does cause skin irritation in rabbits the acute dermal toxicity for rabbits was not reached at 5 g/kg according to one source, but according to another its dermal LC50 of 22.6 g/kg was reported for rabbits. Folpet is considered slightly toxic by ingestion. It is not considered as an eye irritant to rabbits. Acute inhalation exposure to Folpet may cause irritation of the mucous membranes. Inhalation of dust or spray mists and contact with the eyes can also result in local irritation. 

Human health Sulfuric acid is corrosive to all body tissues. Inhalation can paralyze the respiratory system, contact with eyes may result in loss of vision, and skin contact may result in severe bums and necrosis. Swallowing may cause severe injury or death. Between one teaspoonful and half an ounce of the concentrated acid may be fatal if swallowed, and an even smaller quantity may be fatal if inhaled. Chronic exposure may cause tracheobronchitis, stomatitis, conjunctivitis, and gastritis. Gastric perforation and peritonitis may occur and may be followed by collapse of the circulatory system. Pulmonary fibrosis, bronchiectasis, and emphysema have been reported from acute exposure to fuming sulfuric acid and sulfuric acid mist. Chronic exposure usually results in erosion of the teeth, particularly the incisors. 

Workers in the metals treatment industry are exposed to fumes, dusts, and mists containing metals and metal compounds, as well as to various chemicals from sources such as grinding wheels and lubricants. Exposure can be by inhalation, ingestion, or skin contact. Historically, metal toxicology was concerned with overt effects such as abdominal coHc from lead toxicity. Because of the occupational health and safety standards of the 1990s such effects are rare. Subtie, chronic, or long-term effects of metals treatment exposure are under study. An index to safety precautions for various metal treatment processes is available (6). As additional information is gained, standards are adjusted. 

Beryllium, beryllium-containing aUoys, and beryUium oxide ceramic in soHd or massive form present no hazard whatsoever (31). SoHd shapes may be safely handled with bare hands (32) however, care must be taken in the fabrication and processing of beryUium products to avoid inhalation of airborne beryUium particulate matter such as dusts, mists, or fumes in excess of the prescribed workplace exposure limits. Inhalation of fine airborne beryUium may cause chronic beryUium disease, a serious lung disease in certain sensitive individuals. However, the vast majority of people, perhaps as many as 99%, do not react to beryUium exposure at any level (33). The biomedical and environmental aspects of beryUium have been summarized (34). 

The primary routes of entry for animal exposure to chromium compounds are inhalation, ingestion, and, for hexavalent compounds, skin penetration. This last route is more important in industrial exposures. Most hexavalent chromium compounds are readily absorbed, are more soluble than trivalent chromium in the pH range 5 to 7, and react with cell membranes. Although hexavalent compounds are more toxic than those of Cr(III), an overexposure to compounds of either oxidation state may lead to inflammation and irritation of the eyes, skin, and the mucous membranes associated with the respiratory and gastrointestinal tracts. Skin ulcers and perforations of nasal septa have been observed in some industrial workers after prolonged exposure to certain hexavalent chromium compounds (108—110), ie, to chromic acid mist or sodium and potassium dichromate. 

The toxicity of a substance is its capacity to cause injury once inside the body. The main modes of entry into the body by chemicals in industry are inhalation, ingestion and absorption through the skin. Gases, vapours, mists, dusts, fumes and aerosols can be inhaled and they can also affect the skin, eyes and mucous membranes. Ingestion is rare although possible as a result of poor personal hygiene, subconscious hand-to-mouth contact, or accidents. The skin can be affected directly by contact with the chemicals, even when intact, but its permeability to certain substances also offers a route into the body. Chemicals accorded a skin notation in the list of Occupational Exposure Limits (see Table 5.12) are listed in Table 5.2. Exposure may also arise via skin lesions. 

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