Effect of Tobacco Consumption on Bone Mineral Density in Healthy Young Males N. Ortego-Centeno, 1 M. Mun ˜ oz-Torres, 2 E. Jo ´dar, 1 J. Herna ´ndez-Quero, 1 A. Jurado-Duce, 1 J. de la Higuera Torres-Puchol 1 1 Service of Internal Medicine B, Granada University Hospital, E-18012 Granada, Spain 2 Service of Endocrinology, Granada University Hospital, E-18012 Granada, Spain Received: 30 July 1996 / Accepted: 31 December 1996 Abstract. Smoking is related to a decreased bone mass and increased risk of osteoporotic fractures. Nevertheless, the effect of smoking in males is poorly understood. The pur- pose of this study was to assess the repercussion of smoking on bone mass in otherwise healthy male smokers and its relationship with markers of mineral metabolism and hor- mone profile. We measured bone mineral density (BMD) in 57 healthy males (26 nonsmokers, 31 smokers; aged 20–45 years) by dual X-ray absorptiometry (DXA, Hologic QDR 1000 ) in the lumbar spine and proximal femur. In a subset we measured biochemical markers of bone metabo- lism and hormonal profile. We found significant differences in BMD between heavy smokers (more than 20 cigarettes/ day) and nonsmokers in all skeletal sites. Serum levels of dehydroepiandrosterone sulfate (S-DHEAS) were lower in smokers and correlated with femoral BMD measurements. No significant differences in bone turnover markers were found. Our findings show that smoking by healthy young males is associated with decreased bone mass. Key words: Bone mineral density — Smokers — Healthy men — Mineral metabolism — Sex steroids. Although most studies have been undertaken in women, cigarette smoking is a frequently cited risk factor for osteo- porosis and associated fractures [1–3]. Tobacco was linked to an increased prevalence of vertebral fractures in men in the cohort studies of Seeman and Melton [4] in which the relative risk of vertebral fracture in smokers was 2.3 and was independent of alcohol consumption. We have previ- ously reported a decreased bone mass in premenopausal smokers associated with characteristic changes in the hor- monal profile [5]. However, the mechanism by which smok- ing affects bone in men is unclear. The aim of this study was to assess the repercussions of smoking on bone mass in young males, and to investigate the possible alterations in mineral metabolism and hormone profile associated with cigarette smoking. Subjects and Methods Fifty-seven males from the staff of the University of Granada Hospital and the student body of the University of Granada Medi- cal School and Nursing School participated voluntarily in the study. We excluded those men who were receiving or had re- ceived, during the previous 3 years, medication that may have altered phosphorus or calcium metabolism or bone mass (e.g., thyroid hormone, corticosteroids, androgens, diuretics, antiacids, antiepileptics, or anticoagulants). All of them consumed a normal diet that included at least 500 mg of calcium/day, and drank less than 40 g of alcohol/day. All participants were informed about the nature of the study and gave their consent to participate. The study was approved by our center’s ethical committee. Each participant was assigned to one of two groups depending on whether he was a smoker or nonsmoker. Smokers were con- sidered to have consumed more than eight cigarettes per day for at least 2 years previously. There were 31 smokers and 26 nonsmok- ers; of the former, 20 consumed fewer than 20 cigarettes/day, and 11 smoked 20 or more/day. In a subpopulation of the sample consisting of 15 smokers and 17 nonsmokers, we assessed mineral metabolism parameters and hormone profile. Starting 1 week before the test, all subjects re- ceived a normocaloric, gelatin-free diet supplying known amounts of calcium (800–1000 mg/day) and phosphorus (1000 mg/day). The men were studied over a 3-day period. Fasting blood samples were collected to determine serum levels of calcium (S-Ca), phos- phorus (S-P), creatinine (S-Cr), and alkaline phosphatase (S-AP), and two 24-hour urine collection were used to determine urinary (U)-Ca, U-P, and U-Cr. Renal threshold phosphate (TmP) was calculated from these data. Serum concentrations of midregion parathyroid hormone (S-PTH), calcitonin (S-CT), osteocalcin (S- BGP), estradiol (S-E 2 ), testosterone (S-T), progesterone (S-Prog), dehydroepiandrosterone sulfate (S-DHEAS), and sex hormone binding globulin (S-SHBG) were measured. Free estradiol index (FEI) and free testosterone index (FTI) were calculated from the following formula: total hormone × 1000/SHBG. On the third day, a fasting urine sample was collected to determine urinary hydroxy- proline (U-OHPr) and U-Cr, and the U-OHPr/U-Cr and U-Ca/U- Cr ratios were calculated. Assays were performed as previously described [5]. BMD expressed as g/cm 2 was measured with dual-energy-X- ray absorptiometry (DXA) (Hologic QDR-1000, Walthmam, MA) at the lumbar spine (L2–L4) and at four sites in the proximal femur: femoral neck, trochanter, intertrocanter region, and Ward’s triangle. During spine measurements, the legs were bent at the hip and the lower legs were elevated to minimize lumbar lordosis. For measurements in the femur, a foot support was used so that the leg was positioned at 20°C inward rotation. Our laboratory’s in vivo precision has a long-term coefficient of variation (CV) of 2.2% in the spine, 1.8% in the femoral neck, and 2.3% in Ward’s triangle. Stability of the instrument with time was checked by daily scan of a spine phantom of known composition (Hologic Inc.). * Present address: Service of Endocrinology. University Hospital 12 de Octubre, Madrid, Spain Correspondence to: M. Mun ˜oz-Torres, Plz. Isabel La Cato ´lica 2, 3°, 18009 Granada, Spain Calcif Tissue Int (1997) 60:496–500 © 1997 Springer-Verlag New York Inc.