Clinical respiratory effects

Respiratory Effects. The only information located regarding respiratory effects in humans associated with lead exposure was a case report of a 41-year-old man who was exposed to lead for 6 years while removing old lead-based paint from a bridge. At the time of the initial assessment, his PbB level was 87 pg/dL, and he complained of mild dyspnea for the last 2-3 years. No abnormalities in respiratory function were seen at clinical examination, so it is not possible to conclude that his respiratory symptoms were related to exposure to lead (Pollock and Ibels 1986). 

The study in which eight exercising subjects were exposed to concentrations at 250, 500, or 1,000 ppm for 4 h and one subject was exposed at these concentrations for 6 h (Utell et al. 1997) is relevant to the derivation of the AEGL-1. The absence of any measurable adverse effect indicates that these concentrations are below those defined by the AEGL-1. No symptoms, clinical signs, or respiratory effects were associated with these exposures. It should be noted that EKG tracings indicated that the heart responded in a normal manner for all exposures, even during exercise. 

The data base for HCFC-141b is extensive and contains studies with human subjects as well as several mammalian species. The study with human subjects was well conducted and addressed clinical symptoms, respiratory effects, cardiotoxicity, hematology and clinical chemistry effects, and pharmacokinetics. The study with humans established a no-effect level (AEGL-1) that may be conservative, because a lowest-observed-effect level was not attained. The AEGL-1 of 1,000 ppm is supported by the animal data, which show an absence of effects at concentrations that are higher by a factor of 10. Animal studies addressed both acute and chronic exposure durations as well as neurotoxicity, genotoxicity, carcinogenicity, and cardiac sensitiza... 

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. 

Respiratory Effects. Although no respiratory effects have been reported in humans following dermal exposure exclusively to 3,3 -dichlorobenzidine, upper respiratory infection and sore throat were among the principal reasons for visits to a company s medical clinic by workers who handled 3,3 -dichlorobenzidine (Gerarde and Gerarde 1974). However, there is no conclusive evidence that these effects were due specifically to 3,3 -dichlorobenzidine exposure. Workers may have been exposed to this and/or other agents by both inhalation and dermal routes. 

Respiratory effects There have been occasional reports of clinically significant respiratory depression associated with buprenorphine. 

No respiratory effects were associated with exposure to 2,3,7,8-TCDD-contaminated herbicides in a group of Vietnam Air Force veterans involved in Operation Ranch Hand examined more than 10 years after the war (Wolfe et al. 1985). In the 1987 follow-up (USAF 1991), no association was found between the initial or current serum level of 2,3,7,8-TCDD and incidences of asthma, bronchitis, pleurisy, pneumonia, or tuberculosis abnormal spirometric measurements were often associated with CDD blood levels, but according to the authors (USAF 1991), the differences in the mean level between high- and low-exposure subjects were not clinically important. The authors suggested that these findings may have been related to the association between 2,3,7,8-TCDD and body fat because obesity is known to cause a reduction in vital capacity. 

The overall evidence from acute, intermediate, and chronic duration studies in experimental animals indicates that the respiratory system is a target for acrolein. These results agree with the clinical picture observed in a case of accidental human exposure to acrolein, in which the respiratory effects were prevalent and persisted for several months after exposure (Champeix et al. 1966). 

Voisin C, Aerts C, Pommery-Dutriez N, et al. 1981. Effects of gaseous pollutants on alveolar macrophages An in-vitro cytotoxicity test using cellular cultures in gas phase. In Meeting European Society for Clinical Respiratory Physiology, Gothenburg, Sweden, June 2-5, 1981. Eur J Respir Dis Suppl 62 187-188. 

Organic Mercury. Limited information was located regarding respiratory effects in humans after oral exposure to organic mercury. Two boys who died after eating meat from a hog that had eaten seed treated with ethylmercuric chloride developed bronchopneumonia and edematous alveolitis, and required artificial ventilation (Cinca et al. 1979). Bronchopneumonia was also identified as the cause of death in four adults and one infant who died as the result of methylmercury poisoning in Iraq during 1972 (Al-Saleem and the Clinical Committee on Mercury Poisoning 1976). It is unclear whether these respiratory effects were the result of direct effects on the respiratory system or were secondary to other effects. 

Respiratory Effects. A case report and a clinical study of 2,4-DNP reported increased respiratory rates at very high single doses (>10 mg/kg [exact doses not specified] and 46 mg/kg followed by another 46 mg/kg 1 week later) (Cutting et al. 1933 Tainter and Wood 1934). This effect is secondary to the elevation of body temperature and basal metabolic rate by 2,4- DNP. Pulmonary edema was seen in a man who died after ingesting the sodium salt of 2,4-DNP in two doses of 46 mg/kg 2,4-DNP 1 week apart (Tainter and Wood 1934). The body temperature was greatly elevated, and the authors concluded that the autopsy findings were similar to those seen in heat stroke. Other case reports have also reported respiratory effects in patients who died after taking... 

In a study of 2-butoxyethanol acetate, Wistar rats and New Zealand white rabbits were exposed to a saturated vapor-air mixture of approximately 400 ppm for 4 hours, and then observed for 14 days after exposure (Truhaut et al. 1979). No clinical signs of respiratory distress were noted for either species. When the animals were sacrificed at the end of 2 weeks, no gross pathological lesions were observed in respiratory tissues of either rats or rabbits. No histological examinations were performed. In the intermediate-duration experiments in this study, in which both gross and histological examinations were performed, no respiratory effects were noted in either rats or rabbits after intermittent exposure (5 days per week, 4 hours per day) to 400 ppm 2-butoxyethanol acetate for 1 month or to 100 ppm 2-butoxyethanol acetate for 10 months (Truhaut et al. 1979). 

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