Building-related factors to consider in indoor air quality evaluations.

Many factors should be considered in an indoor air quality (IAQ) evaluation, and many of these factors are interactive. This article identifies building-related factors that may contribute to IAQ problems. Sixty percent of IAQ problems are related to ventilation and 30% result from air contamination, 20% from inside the building and 10% from outside the building. The remaining 10% are due to miscellaneous other causes (ref. 1). Specific problem areas for each of these categories are discussed in this article. Elements of a proactive management style are also discussed, because management styles can influence how an IAQ episode is handled or prevented.

Environmental control of chemical indoor air quality agents.

Although the number and species of chemicals that can have a causal role in indoor air quality complaints can be enormous, the control methods are limited for most chemical emissions in a building. Because the causal chemical species is often not identified in indoor air quality evaluations, environmental controls for chemical contaminants are generally used. The type of control strategy can be divided into three major categories: emission source control; general dilution and local exhaust; and selective controls. Although general dilution ventilation is the most frequently used control for odors and background building-related chemicals, emission source control is quickly becoming a major control strategy of product manufacturers. As more product emission information becomes available, building interior specifications will soon begin to incorporate these data. In very limited situations, "selective" controls can be used to remove specific contaminants.

Thermoregulatory responses to heat and vibration in men.

To determine if exposure to vibration influences thermoregulation, six healthy Caucasian men, 22-33 years old, were heat-acclimated and then simultaneously exposed to heat and whole-body vibration (WBV). The WBV exposures were divided into two intensity levels, and included tests at frequencies of 5, 10, 16, 30, and 80 Hz. Rectal temperature, local sweat rate, heart rate, and local blood flow were measured. There were no statistically significant differences (p less than 0.05) in rectal temperatures or heart rate as a function of frequency. The mean rectal temperatures for the WBV intensity-level exposures became elevated more quickly than in the control period. WBV produced an initial increase (p less than 0.05) in heart rate over the control level only during the initial 20 min of exposure. There were both intensity- and frequency-dependent WBV relationships in localized blood flows and sweat rates. Vibration appears to reduce the efficiency of the cooling mechanisms during a heat exposure at rest, which results in significant increases in rectal temperatures compared with those from heat exposures alone.

Effect of antigravity suit inflation on cardiovascular, PRA, and PVP responses in humans.

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hydration on some orthostatic and haematological responses to head-up tilt.

Experiments were undertaken to determine the effects of hydration status on a) orthostatic responses, and on b), relative changes in intravascular volume and protein content, during 70 degrees head-up tilt (HUT). Six men underwent 45 min of HUT, preceded by 45 min supine, first dehydrated, and again 105 min later after rehydration with water. Heart rate was consistently lower following rehydration (p less than 0.01), while supine diastolic pressure was higher (p less than 0.02). Systolic pressure fell during dehydrated HUT (p less than 0.01), but not during rehydrated HUT. Postural haemoconcentration, which was reduced after rehydration (p less than 0.001), was accompanied by a decrease in intravascular albumin content (p less than 0.05). Two subjects experienced severe presyncopal symptoms during dehydrated HUT, but not during rehydrated HUT. Thus, it appears that rehydration after fluid restriction improves orthostatic tolerance. Furthermore, extravascular hydration status may be more important than intravascular hydration status in determining orthostatic tolerance.

Reduced tolerance for heat stress environments caused by protective lotions.

There have been complaints of excessive heat after applying skin protective lotions. The purpose of this study was to determine if oil-base or alcohol-base protective lotions interfere with the body's cooling mechanisms during moderate work in heat stress conditions, and if so, then to identify the mechanisms. This was accomplished by evaluating the effect of lotions on thermoregulation as measured by rectal temperatures, local sweat rates, and total water losses during exercise at elevated temperatures. In comparison to the control, after about thirty minutes, the skin lotion tests resulted in a more hyperthermic condition, as measured by rectal temperatures.

Exercise thermoregulation in men after 6 hours of immersion.

Rectal (Tre) and mean skin (Tsk) temperature, skin heat conductance (Ksk), heart rate, and total body sweat rate were measured in 6 men (20-35 years) during 70 min of supine leg exercise (Ta = 23.5 degrees C, rh = 40%) at 50% of their peak O2 uptake (VO2 peak); these data were taken after a 6-h control (C) period in air and after immersion to the neck (NI) in water (34.5 degrees C) for 6 h after overnight food and fluid restriction. After NI mean (+/- S.E.) water balance was -1,285 +/- 104 ml for the 6 h and plasma volume (delta Hb and Hct) decreased by 5.2%. End exercise heart rates after C (141 +/- 3 b X min-1) increased to 148 +/- 3 b X min-1 (p less than 0.05) after NI while Vo2 were both 2.2 L X min-1 Tre increased by 0.5 C degrees (p less than 0.05) between the end of NI and the start of exercise. During exercise following C and NI, delta Tre were +1.0 degrees C and +0.9 degrees C (NS), Ksk were 44 +/- 2 and 43 +/- 1 kcal X m-2 X hr-1 X degrees C-1 (NS), while sweat rates increased from 248 +/- 19 to 366 +/- 52 g X h-1 (p less than 0.05), respectively. Both the total integrated Tre and Tsk curves after NI were higher (p less than 0.05) than for C. These results suggest that, compared with control responses, the equilibrium level of core temperature during submaximal exercise is regulated at a higher level after immersion.

Immersion diuresis without expected suppression of vasopressin.

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20-35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersion experiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at the end of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed when there is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.