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Pulmonary effects

Pulmonary effects 1.86 ppm for 75 min affects central nervous system 100 ppm for 1 min affects skin (human). [Pg.158]

Aluminium is the most abundant element of the lithosphere. Although a large number of persons are exposed world-wide to Al, the incidence of pulmonary effects is low (Schaller et al. 1994). In the 1970 s the effect of Al appearing in dialysis solutions on the central nervous system has become weU known. Increased Al could also be detected in several brain regions of patients with Alzheimer s disease. For the determination in biological materials the most widely used method is GF-AAS. [Pg.205]

In summary, intratracheal instillation of CNTs has shown that their potential in eliciting adverse pulmonary effects is influenced by exposure time, CNT dose, CNT biopersistence, surface defects, and metal contamination [71, 72]. Despite the use of surfactants, all studies showed that intratracheal instillation caused major difficulties due to the agglomerative nature of CNTs in a biological environment. More realistic exposure methods, namely inhalation rather than intratracheal administration, are therefore needed for determining the pulmonary toxicity [59, 65, 73]. Several investigations have been performed by using administration different from intra-... [Pg.185]

Shvedova, A.A. and Kagan, V.E. (2010) The role of nanotoxicology in realizing the helping without harm paradigm of nanomedicine lessons from studies of pulmonary effects of single-walled carbon nanotubes. Journal of Internal Medicine, 267 (1), 106—118. [Pg.212]

A casualty with mild to moderate pulmonary effects less than 6 hours postexposure, or a casualty with moderately severe or severe pulmonary signs and symptoms after 6 hours postexposure. [Pg.154]

Pulmonary effects are usually delayed from 2 to 24 hours. Exposure to very high concentrations may produce immediate symptoms. Generally, the more rapid the onset of symptoms, the more grave the prognosis. [Pg.266]

Burleigh-Flayer, H. and Y. Alarie. 1988. Pulmonary effects of repeated exposures to paraquat aerosol in guinea pigs. Fundam. Appl. Toxicol. 10 717-729. [Pg.1187]

Asthma rates in children in Southern California are high and oxidant pollution levels are likewise high. It is important to determine the relationship between the two. It is also important to determine whether there are chronic pulmonary effects produced by either these oxidants and/or particulate pollution. Since children spend more time outdoors than adults and since they exercise more while outdoors, the added assault from increased ventilation may be of importance. The studies feature a comprehensive exposure assessment that has led to a better understanding of the relationship between exposure and effects. It is also important to identify sub-populations of children and adults who are more susceptible to air pollution-related respiratory effects if they exist. Altered susceptibility could be based on genetic or non-genetic mechanisms (nutritional status for example). Both the epidemiologic and chamber studies provide opportunities to examine issues of hypersusceptibility and to determine the reasons for it if it exists. [Pg.274]

After skin is exposed to HN-2 an epidermal rash develops within approximately an hour. If initial exposure is very low, a rash may not develop. As with HN-1, HN-2 exposure is cumulative. If a person receives multiple low-level exposures, a rash will eventually appear. Blistering will begin about 12 hours after the onset of the skin rash. As with other blister agents, great irritation results when HN-2 vapor or liquid mixes with sweat and flows to tender skin areas (e.g., armpits, buttocks, crotch). Pulmonary effects from exposure to HN-2 are not as severe as for distilled mustard. Dry-land drowning syndrome can occur as the lungs flood with mucus, dead tissue, and blood. The victim dies from a combination of asphyxiation and heart failure. [Pg.84]

Respiratory Effects. Pulmonary edema was observed in a patient after an attempted suicide with endrin and was thought to be due to chemical pneumonitis following aspiration of aromatic hydrocarbons contained in the ingested formulation. The authors state that the hydrocarbons may have been the cause of the pulmonary effects (Runhaar et al. 1985), since hydrocarbon-induced chemical pneumonitis is a well established clinical entity. [Pg.32]

Environmental tobacco smokes (ETS) tobacco smoke irritation to mucous membranes chronic and acutes pulmonary effects, cardiovascular effects carcinogenic. [Pg.368]

Drug activity related to proposed indication Secondary pharmacodynamics Pharmacology summary Pharmacology conclusions Safety pharmacology Neurological effects Cardiovascular effects Pulmonary effects Renal effects... [Pg.418]

In Vitro Mediator Release. Although no pulmonary effects have been demonstrable in guinea pigs following inhalation of bract extract (104), contraction of isolated guinea pig ileum by extracts (105,106) has been reported. Aqueous extracts of cotton, jute, flax, and hemp cause contractions of isolated guinea pig ileirni or tracheal muscle preparations which are similar in time of onset and duration to those produced by... [Pg.154]

Of interest is the experimental approach whereby ozone is delivered solely to one lung. The observation of pulmonary effects in the unexposed lun indicates that there are extrapulmonary effects of ozone at edema-togenic concentrations. However, only the exposed lung appears to develop tolerance to later ozone exposure and to exhibit impairment of bacterial defense mechanisms. ... [Pg.362]

Other Systemic Effects. Fever has been reported in children following ingestion of kerosene (Akamaguna and Odita 1983 Aldy et al. 1978 Dudin et al. 1991 Mahdi 1988 Majeed et al. 1981 Nouri and Al-Rahim 1970 Saksena 1969 St. John 1982). In one study, fever was reported with pulmonary complications for children and adults who had ingested kerosene (Subcommittee on Accidental Poisoning 1962). It is not known whether the fever was secondary to the pulmonary effects. [Pg.57]

For oral exposures, different fuel oils have differing lethality profiles in rats. Acute lethal doses in rats were reported to be 12,000 mg/kg for kerosene (Muralidhara et al. 1982) and 47,300 mg/kg for JP-5 (Parker et al. 1981). However, an oral dose of 12,200 mg/kg of Deobase was not lethal in rats (Muralidhara et al. 1982). Although differences in the oral toxicity of fuel oils and differences in species thresholds of toxicity may exist, the oral toxicity of fuel oils is relatively low. The intestinal absorption of fuel oils is also relatively low, and aspiration, with its resultant pulmonary effects, is the primary risk from the ingestion of fuel oils. [Pg.83]

Toxicology. Exposure to aluminum may cause subtle neurological effects, and massive inhalation of aluminum dusts may cause pulmonary effects. [Pg.36]

Toxicology. Chlorine is a potent irritant of the eyes, mucous membranes, and skin pulmonary effects range from respiratory irritation to edema. Chlorine reacts with tissue water to form hydrochloric and hypochlorous acids. [Pg.138]


See other pages where Pulmonary effects is mentioned: [Pg.167]    [Pg.167]    [Pg.304]    [Pg.335]    [Pg.918]    [Pg.299]    [Pg.120]    [Pg.184]    [Pg.187]    [Pg.59]    [Pg.18]    [Pg.1164]    [Pg.164]    [Pg.230]    [Pg.38]    [Pg.72]    [Pg.365]    [Pg.336]    [Pg.697]    [Pg.77]    [Pg.54]    [Pg.78]    [Pg.79]    [Pg.343]   
See also in sourсe #XX -- [ Pg.216 ]




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