Occupational Poisoning Research Articles

Adsorptive power of different activated charcoal samples of some metals at various pH

Activated charcoal still plays a very important role in toxicology [1–4]. Even though recent findings suggest that it might be replaced by more specific resins, charcoal will probably remain indispensible both as an a specific external antidote, and as an internal antidote for haemoperfusion [5, 6]. One aspect which is still poorly understood is the adsorption of metals by charcoal because of the rarity of acute intoxications, the very high distribution volumes with low plasma levels, and difficulty in defining the chemical state of the solution. In spite of these limitations, our interest was focused on the adsorption of some heavy metals, i.e. Cd, Cu, Pb, and Zn. These metals are frequently the cause of occupational intoxications which very often show a chronic feature, though acute events can occur, and antidotal treatments generally are not sufficient. There is insufficient knowledge of the intermediate phases of heavy metal distribution and of the nature of the bounds these metals form with plasma carriers. The aim of this study is to evaluate the adsorption of these ions by charcoal in water, before extending the research to the adsorption of the above-mentioned ions in plasma. The charcoal samples were with or without coating; we pre-tested each for methylene blue adsorptive capacity according to Ph. Eur. [7] and assayed their 1 g/100 ml suspensions in 1 mg% w/v solutions of the four metals. The assays were done at 2.3±1 °C pH 1.2–4.8 to avoid precipitation which can occur above pH 5. Adsorptive power was quantified after 5-15-30-60 min incubation by differential determination of each element by atomic adsorption. The results showed that, as the pH increased within the narrow acidic range, the adsorption capacity of all charcoal samples was related to the increasing amount of complex ions of one or two OH −. In particular, as the adsorption rate is dependent upon the physicochemical state of each metal at the above solution pH, Cd and Zn were least adsorbed because they are only in their Cd ++ and Zn ++ forms, whereas Cu and Pb were most adsorbed as the Cu ++ and Pb ++ forms are present only in traces. Raw activated charcoal >50 mesh showed higher adsorptive capacity than granulated charcoal coated with hydroxy-ethylmetacrylate (Norit). The coating material caused a 10–25% decrease in adsorption. A petroleum pitch based bead-type active carbon, of very hard 0.6 mm spherical beads and coated with collodion (Asahi Medical Co.), exhibited very high adsorptive power, almost comparable to the highest level exhibited by the raw activated crushed charcoal. In view of the effective detoxication and prevention of poisoning observed, the pH range studied seems to be large enough to permit an estimate of the adsorption power of raw charcoal in the gastric medium and to provide a preliminary evaluation of the use of covered charcoal in haemoperfusion. Finally the isotherms provide the desired metal:charcoal ratio to achieve the highest adsorption with the most suitable charcola.(See diags. on facing page). ▪

The haematological and biochemical pattern in occupational organic solvent poisoning and exposure

A haematological and biochemical investigation was undertaken in 122 consecutive male patients with suspected organic solvent poisoning due to exposure to a mixture of organic solvents such as turpentine, toluene and xylene. Sixty-four healthy solvent exposed and 91 healthy non-exposed male volunteers were used as controls. The only statistically significant differences were that in the patients (B)-leucocytes and S-creatinine were lower than in the controls. (B)-monocytes were higher in all exposed groups than in the controls. S-creatine kinase was higher in patients actually exposed at the examination time, than in all other groups. B-hemoglobin, B-erythrocytes, (B)-Erc-reticulocytes, (B)-hematocrit, (B)-MCHC, (B)-MCV, (B)-Lkcs-differential count except monocytes, (B)-thrombocytes, B-sedimentation rate, P-orosomucoid, P-immunoglobulins (IgG, IgA and IgM), S-alanine amino transferase, S-urate, U-glucose, U-albumin and U-hemoglobin were unchanged. It is concluded that there was no characteristic haematological and biochemical pattern that could be of value in the individual diagnosis of organic solvent poisoning. The patients and the controls were seen as out-patients. In all groups studied, more than 10% of the results of reticulocytes, leucocytes, sedimentation rate, orosomucoid and creatine kinase exceeded the upper level of the reference interval, which is based on in-patients. New reference intervals for these 5 analyses, valid for ambulantly examined subjects, should be worked out.

Lead exposure reduction in workers using stabilizers in PVC manufacture: effects of a new encapsulated stabilizer

The handling of lead-containing powdered stabilizers may be associated with excessive lead exposure and occupational lead poisoning. An encapsulated stabilizer has been designed, which is shown to result in a marked reduction in air lead levels and a concommitant decrease in blood lead concentrations in a group of blender operators manufacturing PVC electrical cable coating.

Toxicology of selenium: a review.

The concentration of selenium in soil, water, or minerals is site specific. World or regional averages are of little practical value. In one report from the front range area of Colorado, average selenium concentrations in bodies of standing water were from 0.3 to 15.8 micrograms Se per liter of water. In some aquatic organisms there is a strong correlation between the Se content of the water ant that of the body tissues; in others no such correlation obtains. Some organisms bioaccumulate Se by factors as high as 1300 to 3800. In most fish the amount of Se in the flesh seems to depend on the amount in the food taken in; there are exceptions, however. Aquatic organisms from seleniferous regions bioconcentrate selenium so as to reach total body levels of 60 micrograms Se per gram or up to 100 micrograms Se per gram of liver. There seems to be no evidence for "biomagnification" of selenium by aquatic organisms. Selenium exerts a strong protective action against the poisoning effects of many heavy metals (lead, cadmium, arsenic, and mercury, for example) and of some organic toxicants (paraquat, for example) in birds, mammals, and man. Data on man are sketchy. Selenium is released into the environment from the burning of coal. No identifiable hazard to man or to plants and animals useful to man can, at this time, be attributed to this source. Selenium is poisonous to man and animal in large amounts. It is a necessary micronutrient for many animals in small amounts; it may also be a needed micronutrient for man, but the data are sparse. The usual American diet contains adequate selenium for human health. Occupational selenium poisoning is mostly accidental and rare.

Factors limiting injury from pesticides.

Factors are discussed that may limit injury from pesticides whether the victims are exposed occupationally, through other intentional uses, or simply accidently. Emphasis is placed on choice of methods fitted to the problems revealed by dependable vital statistics for each country. In general, good labeling of pesticides is the most important single factor in their safe use. Regulation of use combining agricultural advice to the farmer with surveillance of his practices in the handling of pesticides often is the best way to minimize occupational poisoning and restrict residues on crops brought to market. To be successful, these and other aspects of education must be directed toward the improvement of human health. International organizations may be the best source of practical solutions simply because of the range of their experience.

The battle against occupational lead poisoning in Finland. Experiences during the 15-year period 1964--1978.

Occupational lead poisoning has been greatly reduced as a problem in Finland during the 1970s. Case-finding efforts and increased awareness of plant physicians first caused an increase of the incidence with a peak of 89 reported cases in 1974. A sharp decline followed, and, although about 30 mild cases are still reported annually, classical clinical poisoning hardly exists anymore. An extensive regular monitoring program covering 8,000--10,000 blood lead (PbB) analyses a year also shows that exposure levels have been reduced. In 1977 only 70 PbB values, or 1%, were in excess of 70 micrograms/100 ml, and 243 values (4%) exceeded 60 micrograms/100 ml. All such values came from workers employed by less than 30 workplaces, and several of them belonged to workers monitored more than once a year. It is proposed that the general development of occupational health in Finland is to a great extent reflected in this favorable development; however, since special research, educational and informative efforts have been devoted to the lead problem, it may well be that these measures have also influenced the outcome. The results show that, on a nationwide scale, the lead problem can be coped with much more effectively than one has been apt to think. Hence the nonfeasibility of lowering maximum permissible exposure levels has been put in serious doubt. There is no reason to allow unnecessarily high exposure in the vast majority of workplaces only because a small minority has technical difficulties.

Occupational lead poisoning in the United States: clinical and biochemical findings related to blood lead levels.

Dose-response relationships between blood lead levels and toxic effects have been evaluated in 160 lead workers in two smelters and a chemicals plant. Blood lead levels ranged from 0.77 to 13.51 mumol/litre (16-280 microgram/dl). Clinical evidence of toxic exposure was found in 70 workers (44%), including colic in 33, wrist or ankle extensor muscle weakness in 12, anaemia (Hgb less than 8.69 mumol/litre (Hb/4) or 14.0 gm/dl) in 27, elevated blood urea nitrogen (greater than or equal to 7.14 mmol/litre or 20 mg/dl) in 28, and possible encephalopathy in two. No toxicity was detected at blood lead levels below 1.93 mumol/litre (40 microgram/dl). However, 13% of workers with blood lead levels of 1.93 to 3.81 mumol/litre (40-79 microgram/dl) had extensor muscle weakness or gastrointestinal symptoms. Anaemia was found in 5% of workers with lead levels of 1.93-2.85 mumol/litre (40-59 microgram/dl), in 14% with levels of 2.90 to 3.81 mumol/litre (60-79 microgram/dl), and in 36% with levels greater than or equal to 3.86 mumol/litre (80 microgram/dl). Elevated blood urea nitrogen occurred in long-term lead workers. All but three workers with increased blood urea nitrogen had at least four years occupational lead exposure, and nine had received oral chelation; eight of this group had reduced creatinine clearance, and eight had decreased renal concentrating ability. These data support the establishment of a permissible biological limit for blood lead at a level between 1.93 and 2.90 mumol/litre (40-60 microgram/dl).

Polyneuritis incidence in shoe factory workers: cases report and etiological considerations.

This study describes an outbreak of polyneuropathies in an artificial leather shoe factory. Thirty-seven females employed in the factory were examined; clinical findings and hematochemical data suggest a possible role of tricresylphosphate (TCP) in the genesis of these polyneuropathies. A high percentage of subjects evidenced definite signs of upper-motor neuron involvement, which appeared at an early or late stage of the disease. A statistically significant (P less than .001) reduction of red-blood-cell acetylcholinesterase (AChE) was found in the subjects. The ascertained upper-motor neuron involvement suggests a connection with previously described intoxications by TCP- by ingestion or occupational poisoning. The reduction of AChE seems attributable to TCP, and not to n-hexane, whose anti-AChE activity has never been demonstrated.

Need for alertness to neuropsychiatric manifestations of inorganic mercury poisoning

Inorganic mercury as a cause of a characteristic psychiatric syndrome is sometimes not recognized by diagnosticians. The recent opportunity to examine some hospital laboratory employees who had been exposed to inorganic mercury from working with the Van Slyke blood gas apparatus has impressed upon us the likelihood that cases of this occupational intoxication may be overlooked when a diagnostician is concluding that a patient's symptoms are due to neurosis or functional psychosis. Several of these people had been told by a physician that it was “just nerves.” Nine individuals, ranked in order of number of typical symptoms and signs, showed a significant positive rank order correlation with their ranking in mgm of Hg per liter of urine.

Prophylactic chelation therapy in occupational lead poisoning: a review

Chelating agents are useful in the therapy of acute overexposure to lead. However, prophylactic use of chelating agents, particularly under conditions of continued exposure to lead can be harmful to health. Potential adverse effects include kidney damage, symptomatic lead poisoning, increased absorption of lead from the gastrointestinal tract and disruption in the metabolism of trace metals other than lead. Prophylactic chelation is an unacceptable medical practice which cannot be condoned.

Excreção urinária de fenol em trabalhadores de indústrias de calçados expostos ao benzeno

Foi utilizada a excreção urinária de fenol como indicador biológico de exposição profissional ao benzeno, em uma amostra populacional de 79 trabalhadores de indústrias de calçados no município de Franca, SP, Brasil e em 65 pessoas que realizam trabalhos domésticos com colas, contendo benzeno, para indústrias de calçados no município de São Paulo. Os valores médios encontrados, respectivamente 6,5 e 4,2 mg/g de creatinina, permitiram caracterizar diferentes graus de exposição. A primeira população (trabalhadores de indústrias de calçados de Franca), pôde ser considerada como um todo, pelo menos, no ((período pré-patogênico" da intoxicação profissional pelo benzeno.

Occupational lead poisoning, animal deaths, and environmental contamination at a scrap smelter.

Occupational lead poisoning and environmental contamination were evaluated at a lead scrap smelter. Thirty of 37 employees (81 per cent) has blood lead levels of greater than or equal to 80 mug/100 ml, indicating unacceptable absorption, and 35 had free erythrocyte protoporphyrin (FEP) levels greater than 60mug/100ml rbc, indicating toxicity of lead on heme metabolism in red blood cells; eight current and previous employees had been hospitalized with lead colic, and another with encephalopathy. Levels of lead in surface soil (1,800 ppm) and vegetation (20,000 ppm) at the smelter were high and decreased with distance. Animals on nearby pasture had died, and lead levels in the blood, milk, and hair of large and small animals were elevated. Adults living within 100 meters of the smelter had higher blood and hair lead levels than controls, who lived at greater distances, but there was no evidence in them of lead toxicity.

Worker reentry safety. VII. A medical overview of reentry periods and the use of urinary alkyl phosphates in human pesticide monitoring.

Physicians working in rural areas would be the first to acknowledge the limited quality of care available to the agricultural worker. Occupational health specialists, too, would agree that the implementation of conventional occupational health practices in agriculture is at best fragmentary and at worst in some areas practically nonexistent. Farming today is highly mechanized and has become an occupation with numerous attendant hazards. Occupational pesticide poisoning is one of the more important of these hazards and one which has not been adequately categorized. Systemic pesticide poisoning and exposure are the result either of pesticide applicational process or the result of the thinning or picking processes. In the former, the worker at some time or other comes into contact with the pesticide concentrate and illness results either because of accidental spillage malpractice or inadequate protection. Resultant illness is usually severe, rapid on onset, and usually singly. The case fatality rate is higher in applicator poisoning than in picker poisoning. Applicator poisoning has been observed in loaders, sprayers, formulators, and manufacturers. The second category occurs as a result of work contact with the diluted pesticide on the foliage. Illnesses are milder, occur in clusters, are more common in dry and more arid areas, and the case fatality rate is low. The phenomenon is seen in workers who are picking or thinning crops and the illness is called “picker or thinning poisoning.”

Standards for the prevention of occupational lead poisoning.

(1971). Standards for the Prevention of Occupational Lead Poisoning. Archives of Environmental Health: An International Journal: Vol. 23, No. 4, pp. 245-248.

Industrial Toxicol _j and the Prevention of Occupational Poisoning in the Chemical Industry

Industrial Toxicol _j and the Prevention of Occupational Poisoning in the Chemical Industry

1103. Occupational poisoning by ethyleneimine: Thiess, A. M. (1965). Gesundheitsschädigungen und Vergiftungen durch Einwirkung von Äthylenimin. Arch. Tox.21, 67

1103. Occupational poisoning by ethyleneimine: Thiess, A. M. (1965). Gesundheitsschädigungen und Vergiftungen durch Einwirkung von Äthylenimin. Arch. Tox.21, 67

Spectrographic determination of manganese in blood, urine and feces

Spectrographic determination of manganese quantity in blood, urine and feces of normal male has been studied, in order to examine the occupational manganese poisoning, because of its trace amonut of contents, restriction of the sampling quantity and also of easy operation of the sample. Sample blood was dried, and sample urine and feces were dried to ashes, and they are discharged between graphite powder electrode, either copper or lithium carbonate being used as an internal standard material and crater graphite electrode with alternating current are of 220V, at 68A and the calibration was made according to the Seidel density method.The results show that it is determined in the range of 0.01ppm with 24 ml of sample bIood and 0.001ppm with feces, with 1020% precision.

Clinical Toxicology of Commercial Products.

This substantial book is subtitled Acute Poisoning—Home and Farm . This is an understatement for two reasons: (1) the data here may be also applicable to chronic poisoning, and (2) the book will also be useful in patients with industrial or occupational poisoning. We often buy a book partly with the intention of reading it but especially to have it on hand when a specific situation sends us to refer to the literature. An example mav be a dermatology text bought by the internist. But a vast difference applies to a book on toxicology, for it is too late to refer to it when the need arises. Countermeasures must be taken at once. For that reason the reader should assess the toxicology text at leisure and become so familiar with the book that one will be able to find a reference when one is confronted with a dangerously sick patient. And

The Successful Prevention of Lead Poisoning in the Glazing of Earthenware in the North Staffordshire Potteries

In 1572 an extensive epidemic of disease characterized by severe abdominal colic, later identified as lead poisoning, occurred in France in the province of Poitou. Citois named the disease colica Pictonum, that is the colic of the Pictones, the ancient Celtic tribe who inhabited the area. There-after the term was used generically for lead poisoning, otherwise plumbism or saturnism. The origin of the poisoning was traced to the practice of vintners who sophisticated sour acid wines with lead oxide. This adulteration restored the sweetness of the wine by the formation of sugar of lead, lead acetate. Similar outbreaks of poisoning were traced to the same fraudulent practice in the wine-growing districts of Germany and Spain. The preparation and storage of food and drink in containers of pewter and lead glazed earthenware resulted in accidental contamination of the substances, the consumption of which caused acute and chronic plumbism. Among the most frequently lead-contaminated liquors was Devonshire cyder, hence Devonshire colic. Occupational lead poisoning was described among lead miners and smelters in the mid-sixteenth century. Thereafter the disease was observed in a wide variety of trades and processes. The subject was comprehensively reviewed by Tanquerel des Planches in 1839. Among the workmen frequently affected were dippers in the pottery industry where lead oxide and lead carbonate were constituents of the glaze. The disease appeared as a serious problem among dippers and their assistants in North Staffordshire, the centre of the manufacture of earthenware and china in Great Britain. The manifestations of the disease included colic, convulsions, paralysis of limbs, blindness, and general emaciation. Female lead workers suffered excessively from abortions and miscarriages and many of their infants died of fits. The situation became so serious that the Government were compelled to enquire into the problem through a succession of Commissions. Meantime the manufacturers experimented to discover methods of glazing their products without lead or with lead in the relatively harmless fritted state of low solubility lead glazes. The progress of the investigations and remedial measures are followed in detail leading to the final conquest of lead poisoning among dippers and their assistants.

TOXICOLOGIC PROPERTIES OF THE ORGANOPHOSPHORUS INSECTICIDE DIMETHOATE.

The results are presented of extensive toxicological studies on the systemic organophosphate insecticide dimethoate, and compared with published results from other laboratories. It behaves as a typical indirect anticholinesterase, by conversion in the liver to at least four short-lived active metabolites, whose hydrolysis products are rapidly excreted, mainly in the urine. The acute oral toxicity of dimethoate is low in mammals but higher in avians. Dermal absorption is notably slow and dermal toxicity correspondingly low. Cumulative dosing of rats and guinea-pigs gave no cholinesterase inhibition at 0·7 and 4 mg./kg./day respectively. Dietary feeding to growing rats caused no cholinesterase inhibition at 0·5 mg./kg./day and no other effect at 10 times this dose. The main plant metabolite is identical with one formed in the liver, and comparative feeding tests with normal dimethoate and that partly metabolized in vegetation showed that residue analysis determined total hazard. Tests on humans, some with ³²P-labelled material, confirmed that metabolism and urinary excretion are very rapid, that skin absorption is very slow, and that at least 2·5 mg., and probably up to 18 mg., could be ingested daily for at least three weeks without cholinesterase inhibition or other effects. Vapour hazards proved negligible. Oral toxicity was not potentiated by any of 17 other insecticides. The earliest detectable effect of dimethoate poisoning was always erythrocyte cholinesterase inhibition. Symptoms of poisoning could be effectively treated by atropine but not by oxime therapy. No known cases of occupational poisoning have occurred during five years9 commercial usage of dimethoate.