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Investigation into the environmental factors associated with the incidence of skin disease following an outbreak of Miliaria rubra at a coal mine.

A retrospective study was undertaken to examine by interactive linear modeling a possible association between environmental conditions and the incidence of skin conditions (excluding athletes foot) in a coal mine following an increase in skin rashes, mainly 'prickly heat' (Miliaria rubra). An increase in the incidence was found with increasing surface temperature and underground air velocity; a decreased incidence with increased underground air quantity (air volume per unit time); whilst the relationship with underground temperature was found to be quadratic with incidence decreasing until 27 degrees C wet bulb (although this is not necessarily the optimum temperature for other purposes) and then increasing. The association between skin incidence and environmental factors was strongest (in terms of variance explained) when the incidence was associated with the environmental conditions of 4 to 8 weeks previously. The constant nature of relative humidity over the period prevented an examination of its relationship with rash incidence. Possible strategies for reducing the incidence of 'prickly heat' are discussed.

Air Pollutants, Occupational↗

The pathogenesis of miliaria rubra. Role of the resident microflora.

Anhidrosis was induced in volunteers by covering the skin with an impermeable plastic film. The degree of sweat suppression and miliaria after a thermal stimulus was directly proportional to the increase in the density of resident aerobic bacteria, notably cocci. No anhidrosis resulted when antibacterial substances were used to prevent the expansion of the microflora. Histological study showed a PAS-positive diastase resistant amorphous mass deep within the acrosyringium after 2 days of occlusion, accompanied by a periductal dermal infiltration of leukocytes. After another 2 days the duct became clogged by an amalgam of degenerating leukocytes. This impaction sloughed after about 3 weeks as a result of epidermal renewal. Colonies of bacteria were never found within the ducts. It is postulated that cocci secrete a toxin which injures luminal cells and precipitates a cast within the lumen. Infiltration by leukocytes creates an impaction which completely obstructs the passage of sweat for several weeks.

Aerobiosis↗

Heat intolerance as a function of percent of body surface involved with miliaria rubra.

Twenty-four heat-acclimatized male volunteers were wrapped as previously described (Am. J. Physiol. 239 (Regulatory Integrative Comp. Physiol. 8): R226-R232, 1980) but to produce miliaria rubra (heat rash) in specific regions of the body. Three experimental rash groups were involved: 1) the torso (17% total skin surface rashed, n = 6), 2) torso and arms (38%, n = 8), or 3) legs (41%, n = 6), while four subjects served as controls. All subjects were reexposed to walking in the heat on the 7th day after unwrapping, and again 14, 21, and 28 days after unwrapping. When compared to responses for the last heat acclimatization day, tolerance time and sweat rate were lower and mean body temperature and delta heat storage significantly higher for experimental rash subjects contrasted to the controls for up to 21 days; however, no significant differences between the three rashed groups were found. The critical amount of surface area for heat intolerance from heat rash appears to be related to the specific region of the body and associated sweating responses; smaller rashed areas of the trunk, because they have greater potential for abundant sweating, may produce similar responses to heat stress as larger rashed areas of the limbs. Heat intolerance due to rash was not resolved until after 21 days.

Acclimatization↗