Lung effects

Kuhlmann O, Hofmann HS, Muller SP, Weiss M (2003) Pharmacokinetics of idarubicin in the isolated perfused rat lung effect of cinchonine and rutin. Anticancer Drugs 14 411—416. 

Sakagami M, Byron PR, Rypacek F (2002) Biochemical evidence for transcy-totic absorption of polyaspartamide from the rat lung effects of temperature and metabolic inhibitors. J Pharm Sci 91 1958-1968. 

DeLucia, A. J., P. M. Hoque, M. G. Mustafa, and C. E. Cross. Ozone interaction with rodent lung Effect on sulfhydryls and sulfhydryl containing enzyme activities. J. Lab. ain. Med. 80 559-566, 1972. 

Adams et al. 1952). After 5 weeks of an exposure sufficient to induce liver cirrhosis and altered vitamin A concentration in several tissues of the rat, wet lung weight was increased by 10%, but lung vitamin A content remained normal (Chapman et al. 1992). As it appears that lung injury is secondary to renal injury, then the absence of lung effects in animals may be because animals are also less susceptible to the renal injury produced by carbon tetrachloride than are humans. 

Other lung effects including chronic bronchitis and reduced lung function have been observed in workers breathing nickel. Current levels of nickel in workplace air are much lower than in the past, and few workers have symptoms from nickel exposure. 

Compared to rats, mice were more resistant to the development of lung lesions following nickel exposure. In this study, rats were exposed to 0, 0.5, 1, or 2 mg nickel/m as nickel oxide, 0, 0.11, or 0.73 mg nickel/m as nickel subsulfide, and 0, 0.03, 0.06, or 0.11 mg nickel/fti as nickel sulfate. Mice were exposed to 0, 1, 2, or 3.9 mg nickel/m as nickel oxide, 0, 0.44, or 0.88 mg nickel/rh as nickel subsulfide, and 0, 0.06, 0.11, or 0.22 mg nickel/m as nickel sulfate. Lung effects were observed in both rats and mice at all concentrations following exposure to nickel oxide and nickel subsulfide, and at concentrations >0.06 mg nickel/m for rats and mice exposed to nickel sulfate. Based on a NOAEL of 0.03 mg nickel/m for rats exposed to nickel sulfate for 2 years (NTP 1996c), a chronic-duration inhalation MRL of 2x10 " mg nickel/m for soluble nickel compounds was calculated as described in the footnote to Table 2-1. 

Contact of BZP with the eyes or skin may cause severe irritation and possible burns. If it is inhaled, it may cause severe irritation of the respiratory tract with sore throat, coughing, and shortness of breath, or even chemical burns. Prolonged respiratory exposure may cause delayed lung effects, including fluid in the lungs with breathing difficulty. 

B. Rehn et al., Investigations on the inflammatory and genotoxic lung effects of two types of titanium dioxide Untreated and surface treated. Toxicol. Appl. Pharmacol. 189, 84—95 (2003)... 

RDDR is a multiplicative factor used to adjust an observed inhalation particulate exposure concentration of an animal to the predicted inhalation particulate exposure concentration for a human based on a MMAD of 0.28 pm and a geometric standard deviation of 1.63, lung effects (TH or thoracic region) RDDR calculated to be 2.1576 using Table H-l (EPA, 1990—older version of inhalation dosimetry methodology used to calculate RDDR because MMAD <0.5 pm, so cannot use the EPA, 1994 program). 

This toxin manifested its primary acute effects on the lungs and eyes of the victims who came in contact with the gas. It is believed that MIC released from the plant killed 2,000 - 3,000 lives overnight and further larger numbers of people, estimated as 15,000, died within the next few years. It is also believed that the toxin is responsible for chronic health effects in an additional 100,000 to 150,000 survivors. Chronic lung effects, i.e., pulmonary fibrosis, currently appear to be the main cause of morbidity and mortality among the surviving population. A total number of victims, awarded compensations, counted for almost 600,000. 

Q8 Because Mandy s airways were constricted and obstructed, she was not able to empty her lung effectively during expiration and C02 was retained. Increased arterial C02 decreases arterial pH. 

SAFETY PROFILE Poison by inhalation, ingestion, intraperitoneal, and skin contact routes. Human systemic effects by inhalation lacrymation and lung effects. A systemic irritant. Mutation data reported. A severe eye and skin irritant. Extraordinary precautions against fumes are advised. 

For more information about lung effects from plutonium and a review of the hazards associated with alpha-emitting radionuclide exposure, see the ATSDR Toxicological Profile for Plutonium (ATSDR 1990e) or Appendix D of this profile. 

DMM exists at room temperature as a liquid with high volatility. This is in contrast to the solid state of pure MMM. Together with its lipophilicity, these physical qualities enable high concentrations of DMM to be rapidly absorbed by the skin and lungs. Effectively, these routes circumvent first-pass elimination, thereby prolonging the systemic circulation of DMM and extending its residence time in the body. 

Chronic inhalation exposure results in severe lung effects that are characterized by asthma-like reactions characterized by dyspnea, wheezing, and bronchial constriction. The US EPA has neither established an RfC (for inhalation exposure) nor an RfD (for oral exposure) for TDI. 

Chloroacetophenone (CN) is a white crystalline solid with an apple-blossom odor. It is also known as tear gas or Mace . CN acts directly on mucous membranes to produce intense ocular and respiratory irritation as well as burning and pain of the eye, nose, throat, and lungs. Effects can include blepharospasms (i.e., eye blinking), conjunctivitis, sneezing, coughing, secretions, nasal congestion, and a sense of suffocation. The onset of some symptoms is immediate and persists for up to 20 min after the individual leaves the contaminated atmosphere. The primary cause of death related to CN is a result of inhalation effects on the pulmonary system. 

This topic is included because of its potential growth and development. Interest in this has exploded in the last several years. Absorbed drug can be addressed from several viewpoints (1) effect of systemically absorbed bronchodilator on bronchodilation (or other lung effect), ordinarily achieved by local deposition, and (2) utilization of the lung as a route for systemic delivery for treatment of nonpulmonary diseases. 

Absorption of Drugs Given for Local Lung Effect... 

Martonen TB, Katz IM. Deposition patterns of aerosolized drugs within human lungs effects of ventilatory parameters. Pharm Res 1993, 10, 871-878. 

Castranova V, Bowman L, Wright JR, et al. 1984. Toxicity of metallic ions in the lung Effects on alveolar macrophages and alveolar Type II cells. J Toxicol Environ Health 13 845-856. 

HUMAN HEALTH RISKS EPA group B2 probable human carcinogen Acute Risks irritation of skin, eyes, mucous membranes and upper respiratory tract Chronic Risks CNS damage, blood disorders, liver, kidney and lung effects. 

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