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Biomedical subjects

L Dal Vecchio

Publications and source records attributed to L Dal Vecchio.

13 recordsLinked to original sources
PubMed1994

Does n-heptane cause peripheral neurotoxicity? A case report in a shoemaker.

Subjective and electrophysiological signs relating to the central and peripheral nervous systems developed in a shoemaker, a few months after beginning work at home. Signs of central nervous system involvement rapidly disappeared after the end of the exposure, whereas those of mild peripheral neuropathy lasted for several months. The glue used contained a variety of solvents including ethylacetate, cyclohexane, methylcyclohexane, methylethylketone and others; n-hexane was not detected, whereas, unusually, n-heptane was. This exposure was reproduced experimentally in the same work room and the solvent air level did not exceed the American Conference of Governmental Industrial Hygienists threshold values. A tentative conclusion is that the toxic effects on the peripheral nerve are likely to be due to n-heptane.

Adult↗
PubMed1990

"Intrinsic" positive end-expiratory pressure in stable patients with chronic obstructive pulmonary disease.

We have assessed "intrinsic" positive end-expiratory pressure (PEEPi), during quiet breathing in 18 patients with chronic obstructive pulmonary disease (COPD) in stable condition. Ventilatory flow, lung volume, oesophageal (Poes), gastric (Pga), and transdiaphragmatic pressure (Pdi) were measured. PEEPi was measured as the pressure difference (delta Poes) between the onset of the inspiratory effort, indicated by the start of the Pdi swing, and the point corresponding to zero flow. PEEPi was present in all of the 18 COPD patients, and averaged 2.4 +/- 1.6 cmH2O. The maximum transdiaphragmatic pressure (Pdi,max) was also measured and averaged 81.5 +/- 17.4 cmH2O. Following a randomized sequence, ten patients then inhaled an adrenergic agonist (fenoterol 1.6 mg), and eight patients the corresponding placebo. Fenoterol, but not placebo, caused a significant increase in forced expiratory volume in one second (FEV1) (+34%, on average), associated with a significant decrease in PEEPi (-63%, on average) and a significant improvement in Pdi,max (+19%, on average). We conclude that: 1) intrinsic PEEP can be present in stable COPD patients due to increased airflow resistance; 2) fenoterol improved diaphragmatic strength (Pdi,max) in our COPD patients, possibly due to a decrease in lung volume.

Aged↗
PubMed1988

Occupational asthma due to isocyanates.

162 subjects who had been exposed to isocyanates, who had developed symptoms during the exposure period, or in the evening or night and, therefore, had a history compatible with isocyanate-induced asthma, were studied with inhalation challenge testing to isocyanates (toluene diisocyanate and methylene diphenyl diisocyanate) and methacholine, because they were suspected of having occupational asthma. None of these subjects had symptomatic asthma before employment. The diagnosis of occupational asthma was delayed (duration of symptoms before diagnosis: 3.9 +/- 0.4 yrs). Isocyanate-asthma documented by a positive inhalation challenge to isocyanates was present in 57.4% of the subjects. A higher degree of airway responsiveness to methacholine was present in subjects with a positive isocyanate inhalation challenge compared to subjects with a negative challenge (Gmean and GESM: 0.407 (1.14) vs 0.942 (1.14) mg). The majority of the subjects complained of shortness of breath and cough. The low proportion of atopic subjects (21.5%) and of smokers (7.5%), and the high proportion of subjects with the late component in the asthmatic reaction (71%) appear to be common features in this disease.

Adult↗
PubMed1987

Occupational asthma due to ebony wood (Diospyros crassiflora) dust.

A 47-year-old man developed a specific late asthmatic reaction after occupational-type exposure to ebony wood dust. Intradermal skin test to an aqueous extract of ebony wood did not give any immediate or late response. The challenge with ebony wood dust was therefore the only method of confirming the cause of asthma. The mechanism underlying this asthmatic reaction remains unknown.

Asthma↗
PubMed1986

Toluene diisocyanate-induced asthma without airway hyperresponsiveness.

Six workers with occupational asthma due to toluene diisocyanate (TDI) were studied. For each worker a detailed clinical and occupational history was taken, and lung function measurement and skin intradermal tests for common allergens were carried out. Methacholine inhalation challenge was performed before TDI inhalation, and 8 h after TDI inhalation. Methacholine challenge was within normal limits when performed before TDI inhalation, but went into the asthmatic range after TDI inhalation. These cases provide evidence that asthma can be induced by toluene diisocyanate in the absence of airway hyperresponsiveness. They further demonstrate that an isolated negative methacholine inhalation test cannot be used to exclude sensitization to TDI. Screening and follow-up studies on workers exposed on TDI require serial measurements of airway responsiveness and of variable air-flow obstruction.

Adolescent↗
PubMed1985

Prednisone inhibits late asthmatic reactions and the associated increase in airway responsiveness induced by toluene-diisocyanate in sensitized subjects.

To determine whether late asthmatic reactions and the associated increase in airway responsiveness induced by toluene diisocyanate (TDI) are linked to airway inflammation, we investigated whether they are inhibited by prednisone. Ten "sensitized" subjects were studied in 2 sets of experiments. In the first set, each subject was given no treatment and was studied before and for 8 h after exposure to TDI. In the second set, 2 to 4 wk later, each subject was studied before treatment and then during treatment with prednisone (50 mg once a day for 3 days, orally), both before and after exposure to TDI. To assess late asthmatic reactions to TDI, we measured FEV1 immediately before and after exposure, then hourly for 8 h. To assess changes in airway responsiveness, we measured the provocation dose (mg) of methacholine causing a 20% decrease in FEV1 (PD20FEV1) before and 8 h after exposure to TDI. When the subjects received no prednisone treatment, TDI caused late asthmatic reactions and increased airway responsiveness. By contrast, when the subjects received prednisone, TDI caused no late asthmatic reaction or increased airway responsiveness. Prednisone did not change baseline airway caliber or airway responsiveness. These results suggest that late asthmatic reactions and the associated increase in airway responsiveness induced by TDI in "sensitized" subjects may depend on the development of a steroid-responsive acute inflammatory reaction within the airways.

Adult↗
PubMed1985

Combined asthma and alveolitis due to diphenylmethane diisocyanate (MDI) with demonstration of no crossed respiratory reactivity to toluene diisocyanate (TDI).

Two workers, who developed asthmatic symptoms, were studied with inhalation provocation tests using diphenylmethane diisocyanate (MDI) and toluene diisocyanate (TDI). The subjects showed specific asthmatic reactions to MDI challenge (more than 20% fall in FEV1), and one also had an alveolar response. Alveolitis was suggested by fever, basal crackles, increased neutrophil counts in venous blood and in bronchoalveolar lavage. The asthmatic reaction to MDI challenge was associated with an increase in airway responsiveness to methacholine in both subjects. We conclude that MDI is a cause of asthma and/or hypersensitivity pneumonitis in workers exposed to diphenylmethane diisocyanate.

Adult↗
PubMedDate not supplied

Prednisone, indomethacin and airway responsiveness in toluene diisocyanate sensitized subjects.

We investigated whether late asthmatic reactions and the associated increase in airway responsiveness induced by toluene diisocyanate (TDI) in sensitized subjects are inhibited by indomethacin and/or prednisone. Four sets of experiments were conducted in five subjects sensitized to TDI. To assess late asthmatic reactions to TDI, FEV1 was measured immediately before and after exposure to TDI and then hourly for 8 h. To assess change in airway responsiveness, the provocative dose (mg) of methacholine that caused a decrease in FEV1 of 20% (PD20FEV1) before treatment, and then before and after exposure to TDI was measured. In the first set of experiments, each subject was given no treatment and was studied before and 8 h after exposure to TDI; in the other two sets, each subject was studied before treatment, then during treatment with indomethacin (50 mg q.i.d. for 3 days, orally) or prednisone (50 mg once a day, for 3 days, orally), both before and 8 h after TDI exposure. In a fourth series of experiments, each subject was again given no treatment and studied before and 8 h after TDI. When the subjects were given no treatment or indomethacin, TDI caused late asthmatic reactions and increased airway responsiveness to inhaled methacholine. In contrast, when the subjects were given prednisone, TDI caused neither late asthmatic reactions nor increased airway responsiveness. Treatment with indomethacin and prednisone did not change baseline FEV1 and airway responsiveness. These results suggest that release of prostaglandins does not contribute to late asthmatic reactions and the associated increase in airway responsiveness induced by TDI. Inflammatory mediators inhibited by prednisone but not by indomethacin may be involved.

Adult↗
PubMedDate not supplied

[Exposure to glues containing technical heptane: a clinical and electrophysiological study].

Polyneuropathy caused by n-hexane contained in glues was, until recently, the typical occupational disease of shoemakers. Glues no longer contain large concentrations of this solvent, and in some cases, it as been completely replaced by other hydrocarbons. The authors investigated the health status in a group of shoemakers using glues containing 35% technical heptane. The same glue, not containing n-hexane, was used by a shoemaker who worked at home; she developed an otherwise unexplainable peripheral polyneuropathy. For each of the 16 subjects, the following procedures were carried out: environmental sampling, biological monitoring for Mek and heptane metabolites, a neurological and electromyographic examination. No neurological abnormalities were found in the workers that could be attributable to occupational exposure, probably due to the low level environmental contamination (< 100 mg/m3 n-heptane) found in the 7 factories and workshops studied where acceptable hygiene conditions existed. The time course and ratio of urinary metabolites of heptane were also studied, the latter showing a predominance of 2- and 3- heptanol in the initial phase and 2-5 heptandione at the end of the work week; probably, the presence of other solvents, such as Mek, can modify the ratio of metabolites and consequently the formation of neurotoxic compounds could result.

Adhesives↗
PubMedDate not supplied

[Decrease in the n-hexane risk in shoe manufacturing industry].

In recent years the composition of the glues used in the shoe manufacturing industry in the "Riviera del Brenta" area (northern Italy) has changed considerably, with a gradual reduction of n-hexane. This fact emerged from a survey of 337 gluing stations in 105 shoe factories where 104 different commercial products containing organic solvents were found. The determining element in this change was the substitution of technical hexane with other refinery products which have a low n-hexane content (< 5%). There was a possible health risk due to n-hexane exposure in about only 10% of the gluing stations and in about 8% of commercial products, where mixtures of technical hexane are used. Ethyl acetate, cyclo-hexane, hexane isomers, methyl ethyl ketone, heptane and acetone are among the solvents most frequently used. This change means that assessment of glue composition will be necessary before beginning a health monitoring programme of the exposed population.

Adhesives↗
PubMedDate not supplied

[Ulnar neuropathy at the elbow in workers using column sewing machines: case reports and follow-up].

Fifteen cases of ulnar nerve neuropathy at cubital tunnel level were observed in women aged between 16 and 37 years employed in shoe factories. The women operated column sewing machines resting their elbows on the work table. Past evidence showed that the interval between the beginning of work and onset of neuropathy was generally more than one year but less than that for similar diseases observed in other jobs where arthritis of the elbow played a more important role and the average age was higher. It can therefore be supposed that arthritis in these shoes workers was of less significance, whereas local trauma, which was not prevented by the use of small soft cushions under the elbows (4 out of the 15 subjects had been using them for some time), seemed of greater importance. A period of less than one year (in one case only a few days) was deemed due to the presence of a pre-existing neuropathy of the elbow which had so far been asymptomatic. Cases treated within six months of onset showed marked improvement. However, rapidly worsening symptoms, independent of the degree of damage reached, often led to early treatment with favourable outcome in a short time, while slow and insidious onset brought a longer prognosis. The primary prevention suggested is to instruct workers as to the correct work posture, i.e., avoiding resting the elbows on the work table. As a secondary preventive measure, bearing in mind the need of early diagnosis and treatment, medical check-ups every six months are proposed.

Adolescent↗