THE CHEMICAL ENVIRONMENT 835

1451. Acute toxicity of sulfolane Brown, V. K. H., Ferrigan, L. W. & Stevenson, D. E. (1966). Acute toxicity and skin irritant properties of sulfolane. Br. J. ind. Med. 23, 302.

Sulfolane (tetramethylene sulphone; I) is a useful industrial solvent. A study of its acute toxicity and skin irritant properties suggests that I should present no occupational hazard.

The acute oral LDso in rats and mice was found to be 2.1 and 1.9-2.5 g/kg, respectively, and in both species, death (preceded by convulsions) was caused by anoxia. No specific pathological lesions were revealed on post-mortem examination. The acute percutaneous toxicity in rats is also very low (LDso>3"8 g/kg). Repeated application of I to the skin of rabbits and guinea-pigs produced no skin irritation or histological damage. Topical and intradermal tests in guinea-pigs revealed the absence of a sensitization response. I produced only a very mild transient conjunctivitis when instilled into the eyes of rabbits.

The authors conclude that on the basis of its very low acute toxicity and its lack of skin irritancy and sensitization potential, I should be reasonably safe to handle.

1452. Experimental nitrogen dioxide poisoning Cutlip, R. C. (1966). Experimental nitrogen dioxide poisoning in cattle. Path. vet. 3, 474.

The steadily increasing pollution of the atmosphere with nitrogen dioxide (NO2) is a matter of some concern, since even moderately low occupational exposure to this toxic agent causes lung irritation followed by pulmonary oedema (Cited in F.C.T. 1967, 5, 267). Experimental poisoning of animals also causes lung damage, and the lesions appear to be typical of those occurring in field cases of bovine pulmonary adenomatosis (BPA). To find whether NO2 is actually the causatwe factor in the aetiology of BPA, a study has been made of the clinical and pathological alterations produced in c~/ttle poisoned with NOv

Inhalation of NO2 for 5 min daily caused methaemoglobinaemia (due to nitrite formation in vivo) and severe dyspnoea which resulted in death 11-25 days after the initial exposure. Some of the pulmonary lesions such as oedema, emphysema and obliterative bronchiolitis were similar to those occurring in BPA. However, other pathological changes induced by NO2 have not been observed in BPA and include the following: infarcts amd massive fibrin deposition in the lungs, necrosis of proximal convoluted tubules and infarcts of the kidneys, as well as other vascular changes such as haemorrhage and thrombi in nervous tissue. These findings suggest that NO2 is not involved in the pathogenesis of BPA. One of several pulmonary irritants could cause the non-specific lung lesions seen in this disease.

1453. More cases of contact texti le dermatitis Martin-Scott, I. (1966). Contact textile dermatitis. (With special reference to fire proof fabrics). Br. J. Derm. 78, 632.

In addition to the known dermatitic effects of some dyes and formaldehyde resins (Cited in F.C.T. 1964, 2, 622), synthetic fibres may themselves cause contact dermatitis. Four such cases are now reported. One girl and one woman developed recurrent skin rashes when wearing undyed nylon clothes, an effect which disappeared when they ceased to wear the offending garments. Both gave positive patch tests with formaldehyde as well as with undyed nylon. The two other cases, both in young girls, were due to the wearing of Proban-fireproofed Winceyette nightdresses. In one, skin sensitization resulted immediately in an urticarial rash, but in the other it took 4 months in a hot climate for extensive derma- titis and subsequent blister formation to appear. Only one of the gifts was sensitive to formaldehyde. Nevertheless, the author emphasizes the very low incidence of contact eczema from Proban-treated fabrics. These cases were the first to be encountered in 4 yr, while in the original patch-test programme only one very mild skin reaction occurred a m o n g 256 volunteers.