Nonsmokers

Mobilization and Metabolism. The total ascorbic acid body pool in healthy adults has been estimated to be approximately 1.5 g, which increases to 2.3—2.8 g with intakes of 200 mg/d (151—158). Depletion of the body pool to 600 mg initiates physiological changes, and signs of clinical scurvy are reported when the body pool falls below 300 mg (149). Approximately 3—4% of the body pool turns over daily, representing 40—60 mg/d of metabolized, or consumed, vitamin C. Smokers have a higher metaboHc turnover rate of vitamin C (approximately 100 mg/d) and a lower body pool than nonsmokers, unless compensated through increased daily intakes of vitamin C (159). The metaboHsm of ascorbic acid varies among different species. 

The second example of an air pollutant that affects the total body burden is carbon monoxide (CO). In addihon to CO in ambient air, there are other sources for inhalation. People who smoke have an elevated CO body burden compared to nonsmokers. Individuals indoors may be exposed to elevated levels of CO from incomplete combustion in heating or cooking stoves. CO gas enters the human body by inhalation and is absorbed directly into the bloodstream the total body burden resides in the circulatory system. The human body also produces CO by breakdown of hemoglobin. Hemoglobin breakdown gives every individual a baseline level of CO in the circulatory system. As the result of these factors, the body burden can fluctuate over a time scale of hours. 

Model equations can be augmented with expressions accounting for covariates such as subject age, sex, weight, disease state, therapy history, and lifestyle (smoker or nonsmoker, IV drug user or not, therapy compliance, and others). If sufficient data exist, the parameters of these augmented models (or a distribution of the parameters consistent with the data) may be determined. Multiple simulations for prospective experiments or trials, with different parameter values generated from the distributions, can then be used to predict a range of outcomes and the related likelihood of each outcome. Such dose-exposure, exposure-response, or dose-response models can be classified as steady state, stochastic, of low to moderate complexity, predictive, and quantitative. A case study is described in Section 22.6. 

Human (nonsmoker, occupational exposure) Sister chromatid exchange - Seiji et al. 1990... 

Human (smokers and nonsmokers, occupational Sister chromatid exchange - Nagayaetal. 1989a... 

He works as an assistant copywriter in a busy publishing house, and is constantly struggling with multiple deadlines he is an occasional social drinker and nonsmoker he is a single father to a 6-year-old boy... 

Carcinoembryonic antigen (CEA) level may be high. Normal level is less than 3 ng/mL (3 mcg/L) in nonsmokers and less than 5 ng/mL (5 mcg/L) in smokers. 

Carboxyhemoglobin (nonsmoker) Less than 2% 0.01 Less than 0.02... 

Carcinoembryonic antigen A protein normally seen during fetal development. When carcinoembryonic antigen is elevated in adults it suggests the presence of colorectal and other cancers. The normal level in nonsmokers is about less than 2.5 ng/mL, but it can be elevated in smokers and other nonmalignant conditions such as pancreatitis. 

A somewhat related situation can be used to explain the well-publicized lung-cancer inducing effects of P-carotene in heavy smokers. This subpopulation will have low vitamin C levels and hence damage due to smoke components, such as N02 can produce P-CAR which will reach the lung and initiate damage. In nonsmokers, the vitamin C (or other water-soluble antioxidant) is likely to be present in sufficient concentration to preclude this damaging process. Indeed, this speculation has been promoted by the American Chemical Society as the subject of a press release in 1997 (Bohm et al. 1997). 

Increased age and smoking are associated with an increased oxidative stress and depletion of low-molecular weight antioxidants in many tissues including the retina (Beatty et al., 2000). Epidemiological studies indicate that on average, smokers develop late stage AMD 10 years earlier than nonsmokers (Kelly et al., 2004 Klein et al., 1998 Mitchell et al., 2002 Thornton et al., 2005 Tomany et al., 2004). 

Dose-dependent effects of transdermal nicotine on early morning awakening and rapid eye movement sleep time in nonsmoking normal volunteers. J. Clin. Psychopharmacol. 14, 264-7. 

Salin-Pascual R. J., de la Fuente J. R., Galicia-Polo L, Drucker-Colin R. (1995). Effects of transdermal nicotine on mood and sleep in nonsmoking major depressed patients. Psychopharmacology 121, 476-9. 

Staley, J., Krishnan-Sarin, S., Zoghbi, S. et al. Sex differences in [123I]beta-CIT SPECT measures of dopamine and serotonin transporter availability in healthy smokers and nonsmokers. Synapse. 41 275, 2001. 

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