A randomized trial of dehumidification in the control of house dust mite.

BACKGROUND: House dust mites (HDM) are sensitive to humidity. Few studies have adequately examined the potential of dehumidification in reducing HDM numbers. OBJECTIVE: The study examined the effect of portable domestic dehumidifiers, and a behavioural programme to reduce humidity, on HDM counts and HDM allergen levels. METHODS: A randomized controlled trial was undertaken. A total of 76 homes were allocated to three groups that received a portable domestic dehumidifier, a behavioural programme, or no intervention. Humidity, temperature, HDM counts (trap and vacuum samples), HDM allergen, and other details of the home environment were measured on four occasions over a period of 1 year. Interventions and measurements were concerned predominantly with one bedroom. RESULTS: There was a reduction in relative humidity in the dehumidifier group, but not the behavioural group. A decline in HDM trap counts was observed for all three groups. Change scores did not indicate that the dehumidifier group had a greater decline than the other groups. A secondary analysis examining presence or absence of HDM showed a shift from households having HDM at baseline to households not having HDM in the final round for some trap measures. Change score analysis indicated that this shift was greater in the dehumidifier group compared with other groups. The dehumidifier group did not show a greater decline in HDM allergen than that seen in the other two groups. CONCLUSION: Neither the dehumidifier nor the behavioural intervention had a major effect on HDM counts or allergen levels. However, the study did have a number of limitations relating to size, timing of intervention, and running of the dehumidifiers. The secondary data analysis may indicate some effect of dehumidification, but clearly this effect was small. There is a need for more information on the effects of reducing ambient humidity on the distribution of HDM within their habitats.

Structural studies on bioactive compounds. 4. A structure-antitumor activity study on analogues of N-methylformamide.

A series of derivatives of N-methylformamide (NMF), an experimental antitumor agent, has been prepared, having the general formula R3C(X)NR1R2 where R1 = H, CH3, CD3, CH2CF3, CH2CH2Cl, cyclopropyl, C2H5, CH2OH, CH2OR, CH2N(CH3)2; R2 = H, CH3; R3 = H, CF3, CCl3, CH3, Ph, NHCH3, N(CH3)2; and X = O, S, NH. A further short series of "push-pull" olefins of the general formula R1R2C = CHNR3R4 has been synthesized where R1 = H, CH3 and R2 = H, NO2, CN, CHO, CH3 and R3 = H and R4 = H, CH3, morpholino. These compounds have been tested for activity against the M5076 ovarian sarcoma and the TLX5 lymphoma in mice. NMF was by far the most potent agent of both series with activity against both tumors. Some other compounds showed weak activity, but there is a rigorous structural requirement for activity and most analogues were inactive. Certain members of the series exist as equilibrium mixtures of rotamers about the amide or pro-amide bonds as shown by NMR.

N-Methylformamide (NSC 3051): a potential candidate for combination chemotherapy.

N-Methylformamide (NMF) was found to be non-toxic to the bone marrow as reflected in the absence of leukopenia in mice, even when the marrow had been compromised by prior administration of cyclophosphamide. Thus recovery from the leukopenic nadir after 160 mg/kg of cyclophosphamide was unaffected by 200 mg/kg X 10 of NMF. This combination, given to animals bearing the M5076 sarcoma, proved to have an additive antitumour effect as measured by tumour growth delay and was superior to the antitumour effect of two doses of cyclophosphamide, a regime which prolonged the leukopenia. Furthermore, the hepatotoxicity of NMF was not augmented by the addition of cyclophosphamide. When hepatotoxicity was induced in BALB/c mice bearing the NMF-resistant ADJ/PC6A plasmacytoma, cyclophosphamide fully maintained its antitumour effect. The results show NMF to be a highly specific antiproliferative agent with potential for use in the therapy of patients with a compromised bone marrow and/or in combination chemotherapy.