PubMed · 1960846
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1991. Chloroethane.. https://pubmed.ncbi.nlm.nih.gov/1960846/
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Although there has been a dramatic increase in awareness about the contributions of the work environment to asthma, many aspects of this illness remain to be explored in further detail. This article focuses on issues that need to be better understood. Data are reported that describe newly recognized agents in the workplace that have been shown in a sophisticated manner to induce asthma. In addition, data that further describe the mechanisms of occupational asthma and information regarding the management of occupational asthma are given. Important problems yet to be resolved include whether those who develop occupational asthma from different agents are likely to have different outcomes, whether screening is likely to have a significant effect on the outcome (and, if so, what is the best approach to screening), and identification of a clear definition of the role of immunologic-mediated parameters as they relate to the initiation of asthma attributable to low molecular weight agents and patient outcome. There is little information about "safe" levels of exposure that protect all workers. Data (such as underlying specific immunologic or genetic markers) are lacking that might aid in predicting which workers are likely to be sensitized by low molecular weight agents. This abbreviated list of unresolved issues makes the study of occupational asthma a fertile field for research.
We studied mutations in exon 3 of the hypoxanthine-guanine phosphoribosyltransferase (HPRT) locus in 113 6-thioguanine-resistant T-cell clones derived from coke-oven workers and control subjects in order to analyse possible changes in the mutational spectrum associated with the exposure to polycyclic aromatic hydrocarbons (PAHs). In 99 mutants, HPRT exon 3 was analysed by means of genomic polymerase chain reaction (PCR) and single-strand conformation polymorphism (SSCP). Products for which SSCP indicated the presence of a mutation were further analysed by DNA sequencing. In addition, HPRT cDNA from 14 clones was analysed by reverse transcription (RT) PCR and DNA sequencing. In total, 18/113 mutants (16%) had a mutation in exon 3. This frequency was similar in PAH-exposed (9/57) and non-exposed (9/56) subjects. Base substitutions caused 14 mutations at 13 different sites. Three +/- 1 bp frameshifts and one 6 bp deletion were identified. No significant differences between PAH-exposed and non-exposed workers were observed in this limited mutational spectrum. These results indicate that deletions/insertions at the HPRT exon 3 account for 22% of the mutations, and base substitutions for 78%.
In 1998, the Iowa Department of Public Health (IDPH) and Iowa State University (ISU) Extension Department, with the assistance of local health departments, investigated a series of carbon monoxide (CO) poisonings associated with the use of liquified petroleum gas (LPG)-powered forklifts in light industry. In each episode, forklifts emitting high CO concentration levels were operated in inadequately ventilated warehouse and production facilities, which resulted in high CO accumulations. Employees at each site developed symptoms of CO poisoning, and some employees received inadequate or inappropriate medical care. This report summarizes the investigations and provides recommendations to prevent such incidents.