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At least 19 recordsLinked to original sources
PubMed1977

Thermodynamics and toxicity of sulfuric acid mists.

The hygroscopic nature of sulfuric acid mist has not been totally appreciated in previous toxicological work. Sulfuric acid mist, by adsorption or desorption of water, equilibrates rapidly with the relative humidity of its environment. The measured particle diameters of a given sulfuric acid mist will increase in size as the particles adsorb water on entering the respiratory tract. For a dry climate of 5% relative humidity, sulfuric acid mist particles will triple in size in the respiratory tract. At 60% relative humidity, particles will double in size, while particles in humid regions will increase very little. In the respiratory tract, the particles will deposit according to their size at 98% relative humidity. In order to compare toxicity data for sulfuric acid mist, relative humidity must be carefully recorded throughout the experimental procedure.

Adsorption↗
PubMed1977

Effects in rats and guinea pigs of short-term exposures to sulfuric acid mist, ozone, and their combination.

Ozone and the oxides of sulfur are common environmental pollutants. The acute pulmonary lesions caused by ozone and sulfuric acid mist in rats and guinea pigs have been characterized. Rats are not affected by sulfuric acid mist in concentrations up to 100 mg/m3 except for reduced body weight at the higher doses. A true alveolitis develops in guinea pigs exposed to more than 20 mg/m3 sulfuric acid mist. The ozone lesion is primarily confined to the terminal bronchioles and proximal alveoli. In combination studies with up to 2 ppm ozone and up to 10 mg/m3 sulfuric acid mist, the pulmonary lesion and lung/body weight data were essentially the same as in exposure to ozone alone, and the number of statistically significant synergistic effects in rats and guinea pigs was about what one would expect to observe by chance alone.

Aerosols↗
PubMed1977

Experience with a high output sulfuric acid aerosol generator.

Experience with a high output sulfuric acid aerosol generator suitable for large chamber exposure studies is described. Sulfuric acid aerosol is produced by combining sulfur trioxide (SO3)(g) vapor with water vapor in the exposure chamber air supply. The mass output of the generator is stable over long periods, and the mass median aerodynamic diameter of the aerosol produced is in the submicron size range (0.3-0.6 micrometer).

Aerosols↗
PubMedDate not supplied

Effect of chronic inhalation of sulfuric acid mist upon mucociliary clearance from the lungs of donkeys.

The effect of chronic inhalation exposures to sulfuric acid mist upon mucociliary clearance from the lungs was studied, using the donkey as an analogue for man. Four animals were exposed 1 hr/day, 5 days/week, for 6 months. The mean mass concentration of acid mist was 102 microgram/m3 for two animals, and 106 microgram/m3 for the other two. The mass median aerodynamic diameter was approximately 0.5 micrometer. Clearance was monitored by serial, external in vivo measurements of the retention of an insoluble, radioactively tagged ferric oxide aerosol which was inhaled following exposure to the acid mist. Bronchial clearance became erratic within the first week of exposure; rates were significantly different, usually slower than control on many test days, although the degree of response varied among the four animals. Two animals exhibited a sustained impairment of clearance towards the end of the 6-month exposure period and continued to have erratic clearance during a 3-month follow-up period. No changes in the regional deposition of the ferric oxide occurred during the course of the study in any of the animals. It is proposed that alterations in bronchial mucociliary clearance may be an early, if not the first, physiologic effect resulting from the inhalation of sulfuric acid mist, and this may be a factor in the pathogenesis of chronic bronchitis in populations exposed to the sulfur oxide-particulate-complex in the ambient air, which often includes sulfuric acid.

Aerosols↗
PubMedDate not supplied

The effects in rats and guinea pigs from six months exposures to sulfuric acid mist, ozone, and their combination.

Rats and guinea pigs were exposed to 0.5 ppm ozone, 10 mg/m3 sulfuric acid mist, or their combination for 6 hrs/day, 5 days/week for six months. Exposure-related microscopic alterations were seen in the lungs of guinea pigs exposed to ozone alone or in combination with sulfuric acid mist. No other microscopic lesions were present in either rats or guinea pigs. No biologically meaningful synergistic effects were noted in animals exposed to the combination of ozone and sulfuric mist.

Aerosols↗
PubMed1978

Simplified fat extraction with sulfuric acid as cleanup procedure for residue determination of chlorinated hydrocarbons in butter.

A new cleanup procedure is described for chlorinated hydrocarbon residues in butterfat. The method is based on the dropwise addition of H2SO4 to a fat solution column and continuous removal of the lipids and the acid. The cleanup of 0.25-2.0 g fat requires only 10-40 ml sulfuric acid and 12-17 ml petroleum ether. There is no need for any further cleanup step, solvent evaporation, or centrifugation. The method is easy to standardize and is suitable for automation. At least 30 fat samples can be cleaned up manually by one analyst in one day. Recoveries were complete (greater than 90%) for polychlorinated biphenyl compounds and for 13 chlorinated pesticides of 16 examined. The method was tested on chlorinated hydrocarbon residues in commercial butter and the results were compared with those obtained with the acetonitrile method. The versatility and limitations of the method were investigated by varying the sulfuric acid strength, initial fat solution concentration, and column dimensions.

Butter↗
PubMed1979

Embryotoxicity of inhaled sulfuric acid aerosol in mice and rabbits.

The effect of inhaled sulfuric acid (H2SO4) on embryonal and fetal development was assessed in CF-1 mice and in New Zealand white rabbits. Both species were exposed for 7 hr/day to 0, 5, or 20 mg H2SO4/m3 during the period of major organogenesis (mice, days 6 through 15 of gestation; rabbits, days 6 through 18 of gestation). Little evidence of toxicity was seen in the fetuses of mice or rabbits exposed to H2SO4. Slight maternal toxicity was seen at 20 mg H2SO4/m3 in both species. Teratogenicity was not observed in either mice or rabbits exposed to H2SO4.

Administration, Intranasal↗
PubMedDate not supplied

Respiratory tract lesions in guinea pigs exposed to sulfuric acid mist.

Guinea pigs were exposed inhalation chambers to 25 mg/m3 sulfuric acid mist 6 h/d for 2 d, and the acute respiratory effects were correlated by light and electron microscopy. This concentration of acid was selected since lower concentrations result in only slight effects while higher concentrations result in death. By light microscopy, the most prominent pulmonary lesion at 48 h was segmental alveolar hemorrhage and edema accompanied by proliferation of alveolar macrophages and type 2 pneumocytes. The segmental distribution of the pulmonary lesion was reaffirmed by scanning electron microscopy, while transmission electron microscopy showed injury to the distal airways and changes in the vascular endothelium.

Aerosols↗
PubMed1979

Toxicity of 0.4- and 0.8-microm sulfuric acid aerosols in the guinea pig.

To determine mortality caused by inhaled sulfuric acid mist, groups of Hartley guinea pigs 2-3 mo old were exposed for 8 h to graded concentrations of aerosols of 0.4 or 0.8 microm mass median aerodynamic diameter. Relative humidity during exposures was maintained at 70-80%. Based on probit analysis, the concentration required to produce 50% mortality (LC50) for deaths to 21 d after exposure was 30 mg/m3 for the 0.8-microm aerosol. For the 0.4-microm aerosol, the LC50 was above 109 mg/m3, the highest concentration obtainable at that particle size. At both particle sizes, the animals either tended to develop severe dyspnea and die minutes (0.4 microm) or hours (0.8 microm) thereafter or appeared nearly unaffected. Lesions in animals that died as a results of 0.4-microm exposures were restricted to hyperinflation; animals that died as a result of 0.8-microm exposures also showed hemorrhage and transudation. No gross or histopathologic changes were observed in animals that appeared unaffected during exposure. Differences in total and/or regional respiratory tract deposition may account for the different responses to the two aerosols.

Aerosols↗
PubMed1978

Effects of sulfuric acid aerosol on cardiopulmonary function of dogs, sheep, and humans.

Submicronic aerosol of sulfuric acid (H2SO4) originates from the burning of fossil fuels and discharge of vapor from the automobile engine equipped with the catalytic converter. This study was conducted to determine whether brief exposure to this aerosol in high concentrations adversely affects the cardiopulmonary system. In all studies, submicronic aerosol of sodium chloride was used as a control. Anesthetized dogs that breathed H2SO4 aerosol in concentrations up to 8 mg per m3 showed no effects on respiratory resistance, static lung compliance, and functional residual capacity. A 4-hour exposure to H2SO4 aerosol (4 mg per m3) produced no significant changes in mechanics of breathing, functional residual capacity, pulmonary and systemic arterial blood pressures, cardiac output, heart rate, and arterial blood gas tensions. Conscious sheep that breathed H2SO4 aerosol in concentrations up to 14 mg per m3 for 20 min had no alteration of tracheal mucous velocity in an immediate 3-hour follow-up period or 5 to 10 days later. Conscious sheep that breathed H2SO4 aerosol (4 mg per m3) for 4 hours had no significant alteration of tracheal mucous velocity immediately and 2 hours thereafter. Both normal and asthmatic adults breathing H2SO4 aerosol in concentrations up to 1 mg per m3 for 10 min showed no significant alteration of lung volumes, distribution of ventilation, ear oximetry, dynamic mechanics of breathing, oscillation mechanics of the chest-lung system, pulmonary capillary blood flow, diffusing capacity, O2 consumption, and pulmonary tissue volume. No delayed effects in pulmonary function nor exacerbation of bronchial asthma were observe during a follow-up period of a few weeks. The present study indicates that single exposure to submicronic H2SO4 aerosol does not produce an immediate or a delayed adverse effect on cardiopulmonary function in anesthetized dogs, conscious sheep, and normal and asthmatic adults.

Aerosols↗
PubMedDate not supplied

Effects in rats and guinea pigs of six-month exposures to sulfuric acid mist, ozone, and their combination.

Rats and guinea pigs were exposed to 0.5 ppm O3, 10 mg/m3 sulfuric acid (H2SO4) mist, or their combination for 6 h/d, 5 d/wk for 6 mo. Microscopic alterations were seen in the lungs of guinea pigs exposed to O3 alone or in combination with H2SO4 mist. No other microscopic lesions were present in either rats or guinea pigs. No biologically meaningful synergistic effects were noted in animals exposed to the combination of O3 and H2SO4 mist.

Aerosols↗
PubMed1976

Hepatic metabolism of N-hydroxy-N-methyl-4-aminoazobenzene and other N-hydroxy arylamines to reactive sulfuric acid esters.

Hepatic cytosols catalyzed a 3'-phosphoadenosine 5'-phosphosulfate (PAPS)-dependent O-sulfonation of N-hydroxy-N-methyl-4-aminoazobenzene (N-HO-MAB) and of several other N-hydroxy arylamines. The presumed product from N-HO-MAB, N-methyl-4-aminoazobenzene-N-sulfate, reacted with added guanosine to yield N-(guanosin-8-yl)-N-methyl-4-aminoazobenzene, with methionine to form a sulfonium derivative that decomposed to yield 3-methylmercapto-N-methyl-4-aminoazobenzene, and with ribosomal RNA to give a bound derivative. N-Methyl-4-aminoazobenzene was converted to N-(guanosin-8-yl)-N-methyl-4-aminoazobenzene in concerted N-oxidation and O-sulfonation reactions conducted aerobically with a fortified 10,000 X g rat liver supernatant. In the absence of an added nucleophile, metabolically formed N-methyl-4-aminoazobenzene-N-sulfate (or the nitrenium ion from this unstable ester) was reduced by N-HO-MAB to form N-methyl-4-aminoazobenzene; the N-HO-MAB was oxidized, probably through a nitrone intermediate, to yield products that included N-hydroxy-4-aminoazobenzene and formaldehyde. An analogous reaction was noted between N-benzoyloxy-N-methyl-4-aminoazobenzene and N-HO-MAB in the absence of cytosol and PAPS. Hepatic N-HO-MAB sulfotransferase activities were in the order: male rat greater than female rat, male rabbit, male guinea pig, male mouse greater than male hamster. Male rat kidney and small intestine cytosols had low activities; the other tissues studied had little or no activity. Hepatic sulfotransferase activities for N-HO-MAB and N-hydroxy-N-acetyl-2-aminofluorene displayed different pH optima and inhibitor and activator responses. The rates of PAPS-dependent rat liver cytosol-catalyzed esterification of N-hydroxy-N-ethyl-4-aminoazobenzene, N-hydroxy-4-aminoazobenzene, and N-hydroxy-1- and 2-naphthylamine were 20 to 50% of that for N-HO-MAB. Activities for trans-N-hydroxy-4-aminostilbene, N-hydroxy-2-aminofluorene, N-hydroxyaniline, and N-hydroxy-N-methyl-N-benzylamine were not detected. No microsomal reduced nicotinamide adenine dinucleotide-dependent reduction or reduced nicotinamide adenine dinucleotide phosphate-dependent oxidation or cytosolic transferase reactions for N-HO-MAB, except the above-described PAPS-dependent reaction, were detected in rat liver.

2-Naphthylamine↗