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D A Purser

Publications and source records attributed to D A Purser.

8 recordsLinked to original sources
PubMed1992

The evolution of toxic effluents in fires and the assessment of toxic hazard.

Toxic hazard in fire depends upon three factors: the fire growth curve (mass loss rate of materials, kg/min) and volume dispersal (kg/m3), the yields of toxic products (e.g. kg CO/kg fuel burned) and the toxic potency of the products (exposure dose needed to cause toxic effects, e.g. lethal dose of CO in ppm.min). The first and second sets of data are obtainable from large-scale tests or small-scale tests and mathematical modelling, the third and some information on the second are derived from toxicity studies of combustion products in small-scale tests or of individual fire gases. Small-scale toxicity test data on materials expressed as lethal mass loss exposure doses (LCt50 g min m-3) can be used in Fractional Effective Dose (FED) hazard assessments, providing the decomposition conditions of the test reproduce those in the fire being examined; principally either non-flaming oxidative, early well-ventilated flaming, or vitiated post-flashover. Although bioassays are needed for a full toxicity assessment, it is now possible to predict the toxic potency of materials to some extent from analytical data alone. The suitability of the small-scale test decomposition conditions are determined in terms of non-flaming or flaming behaviour, temperature (or radiant flux), CO2/CO ratio and oxygen concentration. Existing small-scale test methods provide reasonable models for materials under non-flaming oxidative and early flaming conditions, although the data base for the latter is poor. Only the DIN 53436 method is able to model vitiated post-flashover decomposition conditions, but data for this condition are almost non-existent.

Animals↗
PubMed1987

Classification of dangerous substances and pesticides in the European economic community directives: a proposed revision of criteria for inhalation toxicity.

Criteria for the classification of dangerous substances with respect to their inhalation toxicity were originally proposed by the European Economic Community (EEC) on the basis of a 1-hr LC50, as were the similar United Nations (UN) "transport" criteria. Both sets of criteria have since been amended for a 4-hr LC50, but whereas the UN criteria limits have been decreased to compensate for the increased exposure time, the EEC limits have not. This has introduced an anomaly into the EEC classification scheme whereby substances are classified more severely than they were previously. The EEC scheme is now out of line with the UN criteria and other international guidelines and gives a much more stringent toxicity classification for individual substances by inhalation than by the oral route, as well as causing an unjustifiable duplication of animal tests. This anomaly has led to a proposal by the Federal Republic of Germany for revised criteria. This paper examines the scientific basis for the relationship between inhalation exposure duration and toxicity, and for a comparison of the LD50 and LC50 classifications for individual substances. It is concluded that the proposed German revised classification scheme is more in line with the UN transport criteria and international guidelines and provides a rational basis for a classification scheme for inhalation toxicity. The classification criteria therefore should be harmonized by a revision of the EEC classification limits for inhalation toxicity.

Aerosols↗
PubMed1983

Effects of lead exposure on peripheral nerve in the cynomolgus monkey.

The relationship between blood lead concentration and nerve conduction velocity has been examined, using the cynomolgus monkey as a model for human lead poisoning, with lead dose and blood lead concentration maintained under controlled conditions, to determine whether nerve conduction velocity could be used as an objective measure of the effects of lead on the nervous system at subclinical concentrations. Five cynomolgus monkeys were maintained at a blood lead concentration of 90-100 micrograms Pb/100 ml for nine months by daily oral dosing with lead acetate (12-15 mg Pb/kg body weight). Motor nerve conduction velocity in the ulnar nerve was measured, together with blood lead concentrations. Blood lead concentrations were proportional to lead intake, reaching a stable level within one to two weeks. Lead did not accumulate in the blood, and blood lead concentrations were found to decrease to a maintained plateau from initial high concentrations during the first seven days of dosing. The animals showed no clinical or behavioural evidence of lead poisoning at any time during the study, although there was a progressive decrease in blood packed cell volume, haemoglobin concentration, and erythrocyte concentration. The maximal motor nerve conduction velocity of the ulnar nerve remained constant throughout the study, although changes were observed in the conduction velocity of slowly conducting nerve fibres. At termination, intranuclear inclusions were found in the renal tubular cells of all animals as were focal areas of myelin degeneration in the ulnar and sciatic nerves.

Animals↗
PubMed1979

The toxicity and renal handling of paraquat in cynomolgus monkeys.

The acute intravenous and oral toxicity of single doses of paraquat dichloride was studied in the cynomolgus monkey. Renal handling and effects upon renal function were also investigated following an oral dose of [14C]paraquat. Clinical signs consisted of vomiting, anorexia and dyspnoea. By 48 h all animals showed signs of acute renal failure with oliguria, high plasma urea and SGPT levels and metabolic acidosis. Animals dosed orally showed similar, though less severe, signs to those dosed intravenously. The oral LD50 was approx. 70 mg paraquat cation/kg. Following an oral dose plasma levels peaked by 2 h, but were constant from 12 h to 24 h. Paraquat clearance was high initially and exceeded the creatinine and urea clearance, but fell off markedly after 14 h as renal failure developed. By 18 h urine production had ceased. It is concluded that acute renal failure and acute pulmonary damage are the main causes of death, with interstitial pulmonary fibrosis being a factor in animals surviving the acute phase.

Absorption↗
PubMed1978

Effects of chronic inhalation of dimethyl ether in the rat.

Dimethyl ether (DME) is a colourless gas with an ethereal odour. It is used mainly as a liquid refrigerant and an aerosol dispersant. Little or no data exist on the toxicology of this material. In the present study, groups of male and female rats were exposed to 0.02%, 0.2% and 2% v/v of DME in air, 6 h/day, 5 days/week for 30 weeks. At the end of the study the high-dose level male rats showed a significant reduction on liver weight compared with the control group; this was accompanied by raising SGPT levels. In high-dose female rats there was no significant effect on liver weight but the SGPT levels were raised above control values. No histological abnormalities were observed in the liver or in any other organ.

Aerosols↗
PubMedDate not supplied

Effects of carbon monoxide on behavior in monkeys in relation to human fire hazard.

Although studies have been made of the behavioral effects of low levels of carbon monoxide in man, there is little information on the behavioral incapacitation resulting from short exposures to high concentrations likely to be encountered in fires. Monkeys, trained to perform behavioral tasks during exposures to 900 ppm carbon monoxide, were seriously affected after 20 to 30 min exposure, achieving carboxyhemoglobin levels of 25-30%. The tests were as sensitive as tests in man for detecting psychomotor deficits induced by carbon monoxide, and measurements of carbon dioxide production presented a more sensitive method for detecting early deficits. It is concluded that a man exposed to 1000 ppm carbon monoxide while engaged in light activity (e.g., walking) could be seriously affected within 30 min.

Animals↗
PubMedDate not supplied

Intoxication by cyanide in fires: a study in monkeys using polyacrylonitrile.

It is suspected that hydrogen cyanide (HCN) may be an important factor in incapacitating fire victims, but the effects of sublethal exposures are not well characterized. Also, the incapacitating effects of fire atmospheres result from exposure to a mixture of toxic products so that the contribution from each component is difficult to determine. The mechanisms of incapacitation in monkeys exposed to the pyrolysis products of polyacrylonitrile (PAN) were compared to those resulting from low level HCN gas exposures. The physiological effects of the PAN atmospheres were almost identical to those of HCN gas alone. They consisted of hyperventilation, followed by loss of consciousness after 1-5 min, bradycardia with arrhythmias and T-wave abnormalities, and were followed by a rapid recovery after exposure. Hydrogen cyanide is considered to be the major toxic product formed by the pyrolysis of PAN. It is suggested that HCN may produce rapid incapacitation at low blood levels of cyanide in fires, while death may occur later due to carbon monoxide poisoning or other factors.

Acrylic Resins↗