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In this study, the authors evaluated the relationship between polycyclic aromatic hydrocarbon--deoxyribonucleic acid (PAH-DNA) adduct levels in workers' peripheral white blood cells (WBCs) and their occupational exposures to coke oven emissions (measured by air and urinary 1-hydroxypyrene [1-OHP]). Personal exposures to smoking, charbroiled food, changing clothes in the workplace, and respirator use were determined by questionnaire. Eighty-nine coke oven workers were divided into 3 exposure groups on the basis of job description: topside workers, cokeside workers, and plant office staff. Referent subjects comprised 63 individuals from the same company who worked at a site remote from the coking plant. The geometric mean (GM) PAH-DNA adduct levels determined from the WBCs of the exposed groups were 6.86, 1.56, and 0.90 adducts/[10.sup.8] nucleotides, respectively (referents = 0.38 adducts/[10.sup.8] nucleotides). GM personal benzene soluble fraction (BSF) exposures for the exposed groups were 483.2 [micro]g/[m.sup.3], 70.1 [micro]g/[m.sup.3], and 43.2 [micro]g/[m.sup.3], respectively (referents = 10.7 [micro]g/[m.sup.3]). There was a significant correlation (p < 0.05) between individual BSF and PAH-DNA adduct levels for the exposed groups. The authors also found a significant correlation (p < 0.05) between urinary 1-OHP levels from the day 2 samples of the exposed groups and their PAH-DNA adduct levels. The logistic-regression model revealed that PAH-DNA adduct levels were significantly different between job categories. The results of this study indicate that BSF exposure is the primary contributor to PAH-DNA adduct levels determined from WBCs., POLYCYCLIC AROMATIC HYDROCARBONS (PAHs) are universal environmental pollutants, particularly in a coke oven plant where coal is pyrolyzed into coke. (1,2) Coking workers with long-term exposure to coke oven emissions [...]

Polycyclic aromatic hydrocarbons, which are carcinogenic and mutagenic to humans, are primary compounds in coke oven emissions generated by the coking process. The authors examined the relationship between coke oven workers' urinary 1-hydroxypyrene levels and their exposure to polycyclic aromatic hydrocarbons, as determined on the basis of work category and pre- and postshift effects in a steel plant in Taiwan. Eighty-eight coke oven workers constituted the exposed group, and 61 office workers in a steel plant located 1.5 km from the coke plant constituted the control group. The benzene-soluble fraction in personal air samples, and 1-hydroxypyrene in urine samples, were measured for 3 consecutive days. The 3-day urinary 1-hydroxypyrene sampling results for topside workers (i.e., those most heavily exposed to emissions) in the coke oven group, and for the control group, as determined from postshift geometric means, were 23.8 [micro]g/gm creatinine and 0.3 [micro]g/gm creatinine, respectively. These values increased to 13.4 and 0.1 [micro]g/gm creatinine, respectively, after an 8-hr work period. The major source of polycyclic aromatic hydrocarbons for the exposed group was occupational; therefore, the closer workers were to the coke oven, the greater their exposure, and, consequently, the greater their metabolite level. Urinary 1-hydroxypyrene levels of the exposed group were 80 times higher than those of the control group. Smoking had no significant effect on the excretion of urinary 1-hydroxypyrene. 1-hydroxypyrene levels in the workers' urine during an 8-day period was cumulative (half-life = 18.6 hr). The authors concluded that it would be desirable to switch highly exposed workers to a low-exposure work area, after a period of rest. In addition, urinary 1-hydroxypyrene was a confirmed, useful biological indicator for exposure to polycyclic aromatic hydrocarbons., POLYCYCLIC AROMATIC HYDROCARBONS (PAHs) are formed from the incomplete combustion or pyrolysis of organic materials, and they are distributed widely throughout the environment. (1) Occupational sources of PAHs include coke [...]

The authors studied electrolyte loss from profuse sweating in soccer-team players and evaluated the relationship between this source of iodine loss and iodine deficiency. Thirteen male soccer-team players and 100 sedentary students from the same high school were evaluated for 8 d, during which the players were training. The authors analyzed 208 sweat samples to determine losses of iodine, sodium, potassium, and calcium in sweat. Excretion of urinary electrolytes by the subjects was also measured. The mean losses of iodine, sodium, potassium, and calcium in sweat following a 1-hr game were 52 [micro]g, 1,896 mg, 248 mg, and 20 mg, respectively; the ratios of sweat loss to urinary daily loss of the four electrolytes were 0.75, 0.2, 1.88, and 0.92, respectively. Urinary iodine was significantly (p [is less than] .02) lower than the normal level of 50 [micro]g/gm creatinine in 38.5% of the soccer players, compared with 2% of the sedentary students. Forty-six percent of the players had Grade I goiter, compared with a mere 1% of the sedentary students (p < .01). The results of the study suggest that loss of iodine through profuse sweating may lead to iodine deficiency, and loss of electrolytes through sweating may have a dietary significance for heat-stressed individuals or for individuals who perform heavy workloads., WHEN HUMANS are exposed to a hot environment or to warm surroundings, a balance can be established between heat production and heat loss. Once the set-point temperature is exceeded, heat [...]