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C L Braun

Publications and source records attributed to C L Braun.

6 recordsLinked to original sources
PubMed1994

Respiratory allergy: hazard identification and risk assessment.

Various chemicals and proteins of industrial importance are known to cause respiratory allergy, with occupational asthma being the most important manifestation of the disease. This paper describes clinical syndromes, mechanisms associated with occupational respiratory hypersensitivity, and methods available currently for the prospective identification of potential respiratory allergens. Certain classes of chemicals are commonly associated with occupational respiratory allergy. There is insufficient information, however, to predict respiratory sensitization potential from analysis of structure alone, although reactivity with proteins is likely to be relevant. As yet there exist no fully validated or widely applied predictive methods or internationally harmonized guidelines. The most promising predictive animal methods are the mouse IgE test and guinea pig models. Work in mice has focused upon events occurring during the induction phase of sensitization following primary encounter with the test chemical. In contrast, guinea pig models have been used primarily to identify respiratory allergens (chemicals or proteins) as a function of elicitation reactions induced in previously sensitized animals. Given the possible serious health manifestations of respiratory allergy, early identification of respiratory sensitizers is urgently required. The two methods should, as a priority, be developed further and the production of a detailed protocol for these methods be undertaken to facilitate further validation. Together, this information will allow for two types of risk assessment associated with respiratory allergy: the risk that exposure to a material will (1) induce sensitization in an individual and (2) elicit allergic reactions in a previously sensitized individual.

Allergens↗
PubMed1990

Biological monitoring of carbon disulfide.

The aim of this study was to investigate the relation between exposure to carbon disulfide, as measured by personal air sampling, and the excretion of 2-thiothiazolidine-4-carboxylic acid (TTCA) in urine. The subjects of investigation were 29 workers involved in the production of viscose rayon fibers. The average exposure level was 12.6 mg/m3 (range less than 1-66). The present Dutch occupational exposure limit ("MAC-value") is 60 mg/m3. After logarithmic transformation of the data, the following linear regression equation was found: log (TTCA) = 0.84 log (CS2) - 1.10, wherein TTCA is expressed as mmol/mol creatinine and CS2 as mg/m3. The correlation coefficient was 0.95. Neither the hepatic drug-metabolizing capacity (antipyrine clearance) nor the degree of obesity (Quetelet index) influenced the relationship significantly. On basis of the equation it was possible to establish tentative biological limit values corresponding to the respective occupational exposure limit values. The calculated biological limit value of 0.77 mg/g creatinine (= 0.57 mmol/mol creatinine) corresponds, with 95% confidence, to time-weighted average of air concentration lower than the TLV level of 30 mg/m3.

Air Pollutants, Occupational↗
PubMed1988

Effect of antacid and H2 receptor antagonists on the intestinal absorption of folic acid.

Intestinal folic acid transport is a saturable process with a pH optimum of 5.5 to 6.0. Because of the possible effects of antacids and acid-lowering drugs on the pH of the proximal small intestine, the influence of these drugs on folic acid absorption was studied by using tritium-labeled pteroylmonoglutamic acid (PGA) in 30 subjects (21 women, nine men) of 56 to 89 years of age. Both cimetidine and an antacid containing aluminum and magnesium hydroxide reduced folate absorption from a liquid formula meal (p less than 0.01, p less than 0.001, respectively). Although ranitidine also caused a fall in folic acid absorption from the liquid meal, the change was not statistically significantly different from when PGA was given with the meal alone. Both histamine receptor antagonists tended to maintain a high intraluminal pH in the proximal small intestine after meals, which in part could explain the inhibition of folate absorption. However, neither drug was found to chemically interact with folic acid, and neither drug inhibited the dihydrofolate reductase. The antacid was found to precipitate folic acid at a pH of greater than 4.0, thus removing it from the aqueous phase. This appears to be the explanation for the lowered folate absorption in the presence of antacid. Although the effects of these drugs on reducing folic acid absorption were relatively small, such reductions could become clinically significant in chronic antacid or H2 receptor antagonist use or intensive antacid or H2 receptor antagonist use by individuals eating diets that are marginal in folate content.

Aged↗