[Indoor air quality and adult asthma]. / Pollution de l'air intérieur et asthme chez l'adulte.

INTRODUCTION: Asthma is a chronic inflammatory disease of the airways. The recent increase in its global prevalence suggests a possible role of environmental factors such as indoor air pollution. In 2000, according to the Institute Of Medicine, there was insufficient evidence to determine whether or not an association existed between high priority indoor air pollutants, listed by the French Indoor Air Quality Observatory, and asthma. The objective of this paper is to describe the current state of knowledge on the links between exposure to high priority indoor air pollutants and exacerbations of adult asthma. METHOD: A review of the Medline database has been undertaken of the following pollutants: formaldehyde, benzene, acetaldehyde, volatile organic compounds, particles (PM2.5, PM10) and diethylhexyl-phthalate. The studies were classified by type and source of pollutant. RESULTS: Twenty-three studies were included in the analysis. Most of the observational studies have shown an association between pollutants (by type and source) and adult asthma. The best documented pollutants were formaldehyde and volatile organic compounds. No studies were found on acetaldehyde and diethylhexyl-phthalate. CONCLUSION: The analysis of the literature is complicated on account of the difficulty of comparing different studies. However, since the synthesis performed in 2000, the existence of a link between chemical indoor air pollutants and increased respiratory symptoms appears to be reinforced. It seems necessary to adopt preventive health measures while pursuing scientific research on this topic.

Induction of platelet aggregation after a direct physical interaction with diesel exhaust particles.

BACKGROUND: There is a proven link between exposure to traffic-derived particulate air pollution and the incidence of platelet-driven cardiovascular diseases. It is suggested that inhalation of small, nanosized particles increases cardiovascular risk via toxicological and inflammatory processes and translocation of nanoparticles into the bloodstream has been shown in experimental models. We therefore investigated the ability of diesel exhaust particles (DEP) to interact physically and functionally with platelets. METHODS: The interaction of DEP and carbon black (CB) with platelets was examined by transmission electron microscopy (TEM), whereas the functional consequences of exposure were assessed by measuring in vitro and in vivo platelet aggregation via established methods. RESULTS: Both DEP and CB were internalized and seen in proximity with the open canalicular system in platelets. DEP induced platelet aggregation in vitro whereas CB had no effect. DEP induced Ca(2+) release, dense granule secretion and surface P-selectin expression, but not toxicologic membrane disruption. Low concentrations of DEP potentiated agonist-induced platelet aggregation in vitro and in vivo. CONCLUSIONS: DEP associate physically with platelets in parallel with a Ca(2+) -mediated aggregation response displaying the conventional features of agonist-induced aggregation. The ability of DEP to enhance the aggregation response to platelet stimuli would be expected to increase the incidence of platelet-driven cardiovascular events should they be inhaled and translocate into the blood. This study provides a potential mechanism for the increased thrombotic risk associated with exposure to ambient particulate air pollution.

Methods to detect clonal gene rearrangements in lymphomas and leukemias.

The process of lymphocyte differentiation involves structural alterations of specific genes including those for the immunoglobulin (Ig) and T-cell receptor (TCR) antigen genes. This process occurs very early in the differentiation of B- and T-lymphocytes and involves an ordered program for splicing and rearranging segments of these genes, depending on cell lineage and level of differentiation. Specific DNA cutting and splicing enzymes result in the removal of a number of constant, joining, and variable segments of the Ig and TCR genes. Rearrangement of the VDJ and C segments occurs randomly during the process of B- and T-cell development; hence, the resultant gene rearrangement varies from cell to cell. This results in a unique rearrangement of these genes that encode for a specific Ig or TCR protein. A clonal population of lymphocytes, however, will have a specific molecular structure of rearrangements. Identification of this clonal population is central to the diagnosis of lymphomas and lymphocytic leukemias, because virtually all forms of lymphoid malignancies contain rearrangements of one or more antigen receptor genes. Furthermore, as a clonal expansion, an individual neoplasm will contain the identical rearranged gene throughout the population, serving as a unique clonal marker (1). However, it is important to be aware that lymphocyte clonality is not equivalent to malignancy (2). Benign and reactive conditions may show monoclonal rearrangements. Correlation with histology and immunophenotypic studies is important in order to establish a definitive diagnosis of malignancy. Similarly, the absence of clonal gene rearrangement may be seen in cases that appear malignant by histologic and immunophenotypic criteria. In these instances, it is important to be aware of technical limitations of the assays and sampling errors, which may result in a false-negative result.

Assessment of left ventricular function using serum cardiac troponin I measurements following myocardial infarction.

The prognosis and extent of injury to the myocardium have previously been assessed by increased serum creatine kinase (CK) MB levels. We report findings from 39 consecutive, acute myocardial infarction (AMI) patients presenting 4.5 h (range, 0.7-12.1 h) after the onset of chest pain. We compared CK MB mass (upper reference limit, 5.0 ng/ml) and cardiac troponin I (cTnI; upper reference limit, 0.8 ng/ml) (Stratus II, Dade International) in serial serum specimens obtained over 36 h after chest pain from AMI patients; within 6 h after onset of chest pain. While the appearance of the kinetics of CK MB and cTnI were similar during the initial 24 h following the onset of chest pain, cTnI was increased significantly (p < 0.05) over CK MB after 9 to 12 h. Half-life determinations (mean+/-S.D.) in 22 of the 39 AMI patients demonstrated a significantly (p < 0.01) shorter half-life in non-Q-wave infarcts [t1/2 6.8 h (+/-5.6)] vs. Q-wave infarcts [t1/2 20.4 h (+/-10.7)]. Further serial time versus marker (mean+/-S.D.) results were significantly correlated (p < 0.001, r = 0.66). Sixteen of twenty patients assessed by echocardiography had an abnormal left ventricular ejection fraction (LVEF); mean 37.6 (S.D. 15.2)%, ranging from 15.4 to 67.6%. LVEF was significantly and inversely correlated to peak CK MB (r = .50, p = 0.03), as well as to peak cTnI (r = 0.46, p = 0.04). Based on these findings, cTnI shows excellent promise as a useful marker of infarct size, for the assessment of left ventricular function, and may potentially replace CK MB as the cardiac-specific marker for AMI detection.

Needle localization of non-palpable breast lesions.

Screening mammography identifies suspicious, non palpable mammary lesions. Mammographic needle localization (MNL) is currently being used to facilitate excision biopsy of these lesions. Thirty-two patients underwent biopsies of the breast after MNL for non-palpable lesions. Mammographic indications for biopsy consisted of microcalcifications (48%), mass or abnormal density (21%) or mass+abnormal density (24%). The carcinoma was identified in four cases (12%). Two of these were in situ, one was microinvasive and one was frankly invasive. Three were treated with a modified radical mastectomy. One of these non palpable lesion demonstrated nodal metastasis but none showed distant metastasis. All radiologically detected abnormalities were removed and confirmed with repeat radiology. No complications were identified. MNL effectively localizes non-palpable lesion of the breast and compliments accurate diagnosis and treatment of early carcinoma of the breast.