Trends in patch-test results and allergen changes in the standard series: a Mayo Clinic 5-year retrospective review (January 1, 2006, to December 31, 2010).

BACKGROUND: Patch testing is essential for identification of culprits causing allergic contact dermatitis. OBJECTIVE: We sought to identify trends and allergen changes in our standard series during 2006 to 2010, compared with our previous report (2001-2005). METHODS: We conducted a retrospective review of patch-test results. RESULTS: A total of 3115 patients were tested with a mean of 73.0 allergens. Since our prior report, 8 allergens were added to the standard series; 14 were deleted. Significantly higher rates of allergic positive reaction were documented for carba mix, 3%, and Disperse Orange 3, 1%. Rates were lower for 10 allergens: neomycin sulfate, 20%; gold sodium thiosulfate, 0.5%; hexahydro-1,3,5-tris(2-hydroxyethyl)triazine, 1%; disperse blue 124, 1%; disperse blue 106, 1%; diazolidinyl urea, 1%; hexylresorcinol, 0.25%; diazolidinyl urea, 1% aqueous; 2-bromo-2-nitropropane-1,3-diol, 0.25%; and lidocaine, 5%. Many final patch-test readings for many allergens were categorized as mild reactions (erythema only). Overall allergenicity and irritancy rates declined significantly since our prior report. Results were generally comparable with those in a North American Contact Dermatitis Group report from 2005 to 2006. LIMITATIONS: This was a retrospective study; there is a lack of long-term follow-up. CONCLUSIONS: Since our previous report, our standard series composition has changed, and overall rates of allergenicity and irritancy have decreased. Notably, many final patch-test readings showed mild reactions.

Impact of domestic air pollution from cooking fuel on respiratory allergies in children in India.

This study undertaken in India was aimed at identifying the effects of the indoor air pollutants SO2, NO2 and total suspended particulate mater (SPM) generated from fuel used for cooking on respiratory allergy in children in Delhi. A total of 3,456 children were examined (59.2% male and 40.8% female). Among these, 31.2% of the children's families were using biomass fuels for cooking and 68.8% were using liquefied petroleum gas. Levels of indoor SO2, NO2 and SPM, measured using a Handy Air Sampler (Low Volume Sampler), were 4.60 +/- 5.66 microg/m3, 30.70 +/- 23.95 microg/m3 and 705 +/- 441.6 microg/m3, respectively. The mean level of indoor SO2 was significantly higher (p = 0.016) for families using biomass fuels (coal, wood, cow dung cakes and kerosene) for cooking as compared to families using LP gas. The mean level of indoor NO2 for families using biomass fuels for cooking was significantly higher in I.T.O. (p = 0.003) and Janakpuri (p = 0.007), while indoor SPM was significantly higher in Ashok Vihar (p = 0.039) and I.T.O. (p = 0.001), when compared to families using LP gas. Diagnoses of asthma, rhinitis and upper respiratory tract infection (URTI) were made in 7.7%, 26.1% and 22.1% of children, respectively. Respiratory allergies in children, which included asthma, rhinitis and URTI, could be associated with both types of fuels (liquefied petroleum gas [LPG] and biomass) used for cooking in the different study areas. This study suggests that biomass fuels increased the concentrations of indoor air pollutants that cause asthma, rhinitis and URTI in children. LP gas smoke was also associated with respiratory allergy.

Hepatotoxic and immunotoxic effects produced by 1,3-dibromopropane and its conjugation with glutathione in female BALB/c mice.

To determine a possible role of glutathione (GSH) conjugation in 1,3-dibromopropane (1,3-DBP)-induced hepatotoxicity and immunotoxicity, female BALB/c mice were treated orally with 1,3-DBP. Based on the liquid chromatography/electrospray ionization-tandem mass spectrometry (LC/ESI-MS) analyses, two forms of S-bromopropyl GSH were observed at m/z 427.9 and 429.9 in the positive ESI spectrum with a retention time of 5.29 and 5.23 min, respectively. Following single treatment of mice with 150, 300 or 600 mg/kg 1,3-DBP for 12 hr, the amount of S-bromopropyl GSH was detected maximally in liver homogenates at 600 mg/kg 1,3-DBP. Hepatic GSH levels were significantly decreased by treatment with 1,3-DBP. In a time course study, production of S-bromopropyl GSH rose maximally 6 hr after treatment and decreased gradually thereafter. The liver weights were significantly increased by treatment with 600 mg/kg 1,3-DBP. When mice were treated orally with 600 mg/kg 1,3-DBP for 12 hr, the activities of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were increased by 365- and 83-fold. In addition, oral 1,3-DBP significantly suppressed the antibody response to a T-dependent antigen at 600 mg/kg 1,3-DBP. 1,3-DBP elevated hepatic levels of malondialdehyde and suppressed the activities of some hepatic enzymes involved in anti-oxidation. Taken together, the formation of GSH conjugate with 1,3-DBP may deplete cellular GSH and, subsequently, produce hepatotoxicity and immunotoxicity via damage to the cellular anti-oxidative system.