Respiratory impairment

Cotton Dust Exposure and Chronic Respiratory Impairment An Epidemiological Controversy... 

In contrast to the documented effect of cotton dust on acute responses, the causation of chronic respiratory effects in occupationally exposed subjects has not been established. The OSHA cotton dust standard is based on the premise that sustained exposure may result in chronic respiratory problems. To test this hypothesis, the pertinent literature is reviewed and discussed in an attempt to decide if convincing epidemiological documentation exists to support a cause and effect connection between prolonged dust exposure and chronic respiratory impairment. There appears to be a need for additional studies to clarify this important aspect of occupational medicine. 

The pulmonary fibrotic changes develop slowly over the years, often progressively even without further exposure, and their radiographic detection is a direct correlate of their extent and profusion. In some cases minor fibrosis with considerable respiratory impairment and disability can be present without equivalent x-ray changes. Conversely, extensive radiographic findings may be present with little functional impairment. 

Simple CWP often occurs concomitantly with chronic bronchitis and emphysema. Although CWP is associated with several respiratory impairments, it is not associated with shortened life span the importance of this benign condition is the fact that it is a precursor of progressive massive fibrosis (PMF). However, simple CWP does not progress in the absence of further exposure. 

Use cautiously in people with acute or chronic respiratory impairment, particularly children, because phenothiazines may suppress the cough reflex. If hypotension occurs, epinephrine is not recommended because phenothiazines may reverse its usual pressor effect and cause a paradoxical further lowering of blood pressure. Because these drugs have an antiemetic action, they may obscure signs of intestinal obstruction, brain tumor, or overdosage of toxic drugs. 

Respiratory impairment was observed, which included labored breathing and irritation (Haskell Laboratory 1961). 

In an acute-duration inhalation exposure study, groups of 4 male albino ChR-CD rats were exposed to 5, 11, 26, 27, 72, or 370 ppm HDI for 4 or 8 hours. Rats survived a 4-hour exposure to 72 ppm but showed severe respiratory impairment and cyanosis during exposure. No other hematologie pathology was described (Haskell Laboratory 1961). 

Deaths due to oral exposures were reported to occur at very high doses in laboratory animals (>940 mg/kg). The cause of death in many cases was not reported however, respiratory impairment may have been responsible (Haskell Laboratory 1961). Due to the limited data available, it is not known if the vehicle plays a role in oral HDI toxicity in laboratory animals. As with the irrhalation studies deseribed above, using small nttmbers of animals in testing lethal oral eoneentrations makes deriving a firm LD50 diffieult. Larger doses of HDI placed topically also resulted in death (Thome et al. 1987). 

Analgesic efficacy and clinical use Levallorphan (Leimgruber et al., 1973) is an opioid antagonist with a minor agonistic component and practically no analgesic action. It has been used as one of the first relative pure antagonists for the treatment of opioid overdose, to reverse opioid central depression and to antagonize opioid-induced respiratory impairment (Foldes et al., 1969). 

Nine deaths have been reported in children with Prader-Willi syndrome receiving growth hormone. Pfizer issued a safety warning for growth hormone and Prader-Willi syndrome after reviewing seven deaths in male subjects (89). There was an association with severe obesity and severe respiratory impairment. 

BEIs are the concentrations of chemicals that are most likely to be observed in specimens (blood or urine) collected from healthy workers who have been exposed to chemicals to the same extent as workers with inhalation exposure at the TLV. The exceptions are the BEIs for chemicals for which the TLVs are based on protection against nonsystemic effects (such as irritation or respiratory impairment) where biomonitoring is desirable because of the potential for substantial absorption via an additional route of entry (usually the skin). The BEI generally indicates a concentration below which nearly all workers should not experience adverse health effects (ACGIH 2001). 

Warburg O (1956) On respiratory impairment in cancer cells. Science 124 269-270... 

Hussein, M.H., Daoud, G.A., Kakita, H., Kato, S., Goto, T., Kamei, M., Goto, K., Ozaki, Y., Ito, T., Fukuda, S., Kato, I., Suzuki, S., Hashimoto, T., Togari, H. Effect of polymyxin B-immobilized fiber hemoperfusion on respiratory impairment, hepatocellular dysfunction, and leucopenia in a neonatal sepsis model. Pediatr Surg Int 26 (2010) 187-193. 

Spicer, J. I. and R. E. Wever. 1991. Respiratory impairment in crustaceans and molluscs due to exposure to heavy metals. Comp. Biochem. Physiol. 100C 339-342. 

Intramuscular levomepromazine in combination with an intravenous benzodiazepine has been said to increase the risk of airways obstruction, on the basis of five cases of respiratory impairment in patients who received injections of psychotropic drugs (630). The doses of levomepromazine were higher in the five cases that had accompanying airways obstruction than in another 95 patients who did not. 

Because of the frequency of co-administration of benzodiazepines with neuroleptic drugs, it is important to consider possible adverse effects that can result from such combinations. In a brief review, emphasis has been placed on pharmacokinetic interactions between neuroleptic drugs and benzodiazepines, as much information on their metabolic pathways is emerging (166). Thus, the enzyme CYP3A4, which plays a dominant role in the metabolism of benzodiazepines, also contributes to the metabolism of clozapine, haloperidol, and quetiapine, and neuroleptic drug plasma concentrations can rise. Intramuscular levomepromazine in combination with an intravenous benzodiazepine has been said to increase the risk of airways obstruction, on the basis of five cases of respiratory impairment the doses of levomepromazine were higher in the five cases that had accompanying airways obstruction than in another 95 patients who did not (167). 

Case 1. On July 13, 1995, a 7-month-old girl was brought to an emergency department because of respiratory arrest but could not be resuscitated. The cause of death was listed by MCMEO as bronchopulmonary dysplasia associated with environmental hyperthermia. She had been receiving home nursing care for congenital respiratory impairment. A window air conditioner was being installed at the time of her death. 

M (increased percentage (7%) of workers with early signs of respiratory impairment)... 

Bourbeau J, Ernst P, Chrome J, et al. 1988. Relationship between respiratory impairment and asbestos related pleural disease in an active workforce [Abstract]. Am Rev Respir Dis 137 (Suppl) 92. 

Harkin TJ, McGuinness G, Goldring R, et al. 1996. Differentiation of the ILO boimdary chest roentgenograph (0/1 to 1/0) in asbestosis by high-resolution computed tomography scan, alveolitis, and respiratory impairment. J Occup Environ Med 38 46-52. 

Wang X, Yano E, Nonaka K, et al. 1997. Respiratory impairments due to dust exposure A comparative study among workers exposed to silica, asbestos, and coalmine dust. Am J Ind Med 31 495-502. 

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